MORE BIOLOGY; "SYNTHETIC THEORY, CRISIS AND REVOLUTION" (By Maximo Sandin)

Originally published in: Arbor CLVIII, 623-624 (November-December), p.265-300

Translation : Irene Fernández Monsalve

From the very start, Darwinist theory suffered from significant weaknesses acknowledged by its author. Both the observation of natural species and the evidence derived from the fossil record were in direct conflict with two of its core concepts, natural selection and gradual change, giving rise to problems that deeply troubled Darwin and some of his followers.

But these problems, clearly observable, were “solved” in a theoretical way by mathematical population genetics modelling. Consequently, Darwinism consolidated in the middle of this century, in the shape of modern synthetic theory, the evolutionary model widely accepted since then by the scientific community.

Meanwhile, observations from the field of embryology were adding new discrepancies that contributed to a growing divergence between the observed evidence and the theoretical model.

This discrepancy has reached its peak as a result of recent discoveries in molecular genetics, and, especially, in the genetics of development. The implication of mobile elements, endogenous viruses, repeated sequences, homeotic genes, etc., in the transmission of genetic information, and its complex operation during embryonic development, have turned this divergence into a blatant contradiction.

The situation to which biology has been driven by the contradiction between these facts and the fundamental theoretical model corresponds to what Thomas Kuhn defines as a crisis in science.

In this context, the growing clues indicating a viral origin for the above mentioned sequences, in addition to viral self-integration ability in animal and plant genomes, could represent an evolutionary mechanism of an infective character, capable of giving answers to the problems mentioned previously.

The confirmation of this hypothesis would constitute what Kuhn referred to as a “scientific revolution”, with a subsequent change of paradigm, since it would not only affect the evolutionary mechanism, but also its interpretation and meaning.

Population genetics: from mathematics to nature

“But I now admit that in previous editions of my “Origin of Species” I probably attributed too much importance to natural selection or the survival of the fittest. I had not sufficiently considered before the existence of many structures that are neither beneficial nor pernicious, and I believe this to be one of the greatest omissions up to now detected in my work.” C. Darwin, “The Descent of Man”*

Darwin himself initiated the most authoritative criticism of the scientific content of his work. To the progressive loss of weight of natural selection as an evolution-driving mechanism, he added another weak point: gradual change. Amongst doubts and reassertions, he wrote: “Why is it that if species have descended from other species through minute gradations, we do not see innumerable transition forms everywhere? Why is not all Nature in confusion, instead of species being as we see them, well defined?*

In the face of such overwhelming arguments it seems inconceivable that the hypothesis of gradual change in the evolutionary process could survive without serious reconsideration. It is even stranger if we bear in mind that these observations do nothing but support the evidence from the fossil record, since, according to Darwin, if transformations from certain morphologies to others took place in a gradual way, “...the number of links must have been inconceivably large”*. And this is evidently not so. In fact, and just as Darwin himself acknowledged, the most eminent palaeontologists and the greatest geologists of his time advocated species immutability.

In other words, the theory whose objective was to explain the variability existing in nature was finding trouble, form the start, in adjusting to it precisely when it was observed in detail. If, instead of holding on to concepts that satisfied their cultural prejudices, Darwin’s advocates had shared with him his doubts and intellectual honesty, the path followed by evolutionary theory would possibly have been a different one.

But the path was precisely an ever-stronger assertion of the core concepts of natural selection and gradual change, and a progressive distancing from the observation of nature, in other words, the growth and consolidation of population genetics.

The rediscovery of Mendel’s laws, and Fisher, Haldane and Wright’s mathematical models, turned evolution into a process of “gradual change in allele substitution”. In Mayr’s recent words (97): “Mathematicians convincingly demonstrated that even mutations conferring relatively small advantages were favoured by selection, and their findings helped overcome various objections to natural selection.” *

The objections Mayr refers to are, amongst others, those coming from a field to which Darwin had paid special attention, considering it a fundamental source of information about evolution: embryology.

Despite the fact that Haeckel’s “fundamental ontogenetic law” had been discredited by the confirmation that he had forced the similarities between fish, bird and mammal embryos in order to highlight the importance of embryology’s contribution to the study of the evolutionary process, Harrison (37), Weiss (39) and Child’s (41) experimental studies had managed to forge the fundamental concept of the “morphogenetic field”. These “fields” are embryological information areas whose components create a network of interactions that allow each cell to acquire an embryonic potential determined by its position inside each field.

These complex interactions observed in embryos were not easily reconcilable with the (theoretical) mathematical postulates of population genetics. As a result, the geneticist Morgan prevented the publication of Child’s findings, since his works seemed to Morgan to be “outdated” and not “good science” (Mittman and Fausto-Sterling, 89).

In this way, a fundamental field of study for the understanding of evolutionary mechanisms, has until very recently been officially relegated by evolution scholars.

It might seem surprising that the trust placed in mathematical modelling to explain a non-visible phenomenon (evolution) proved strong enough to encourage scientists to ignore contradictory processes, whose existence could be clearly observed in the laboratory. However, the fact is that the social component once more proved to have more weight than scientific arguments. According to Beatty (94), the US Commission for Atomic Energy became one of the most important factors behind population genetics’ hegemony in the study of evolution. Their interest in the genetic effects of radiation made it possible for Dobzhanky, amongst others, to have access to a constant source of finance and collaborators, while the majority of evolution scholars from other fields found serious trouble getting financial support.

There is also a second factor, less well-known but more altruistic, that must be mentioned. According to Paul (88), Dobzhansky and other scientists saw in the population genetics model of adaptation an undermining of the racial and social prejudices that accompanied the concept of “fitness”.

With these precedents what is today known as “modern synthetic theory” emerged. Based on a strictly Mendelian conception of character transmission, its basic premises were:

1. Evolution is a gradual process of allele substitution taking place within a population. The source of variability for these alleles would be point mutations or micromutations.

2. Evolution is a gradual process of allele substitution taking place within a population.

The trust placed in the explanatory capacity of mathematical modelling led Dobzhansky (51) to write: “Since evolution is a change in the genetic composition of populations, the mechanisms of evolution constitute problems of population genetics”

The bases for the view of evolution widely accepted today were thus established: evolutionary change is a gradual process of gene frequency variation within a population, channelled by natural selection. Larger-scale events, ranging from the origin of new species to long-term patterns of evolutionary change, represent exactly the same process over longer periods of time. In Mayr’s (66) words, the evolutionary process “is no more than the extrapolation and extension of events that take place within populations and species” *.

However, this concept soon proved unsound in the very light of population genetics: extrapolating changes in gene frequencies within a species to larger-scale events, that is, to evolution, thus considering speciation as the starting point, soon proved to be seriously problematic.

According to population geneticists’ criteria, the transition from one species to another would imply a substitution of at least a dozen genes. And given the decline in population size necessary for the substitution of one allele for another to take place through the process of natural selection, the consequence would be the extinction of the species. This is what is known as “Haldane’s dilemma”, named after one of the pioneers in the elaboration of mathematical population genetics models.

However, the answer to this mathematical dilemma might be found (strange as it may sound to some people) in the observation of nature: natural selection favours geographical variation of species as an adaptation to specific conditions in the different areas they occupy, but such a diversification is always produced within species. In Goldschmidt’s (40) words: “Subspecies are not incipient species, they are culs-de-sac. Subspecies’ characters are like gradients, whereas the species limit is characterized by a jump, a discontinuity with no intermediate steps in many of its characters” *.

In any case, the fundamental problem does not seem to be that of explaining speciation as a result of natural selection acting upon gene frequency changes. The real “dilemma” is how to extrapolate speciation, in the sense of reproductive isolation, to the great changes in morphological, physiological and genetic organization that have taken place throughout evolution.

In 1977, the French biologist P. Grassé wrote about the confirmation of the natural selection process in nature: “...It is simply the observation of demographic factors, of genotypes, local fluctuations and geographical distributions. Frequently, observed species have remained practically unchanged over hundreds of centuries!” *.

The acknowledgement of this phenomenon has finally been embodied by the “theory of punctuated equilibrium”, formulated by the palaeontogists Eldredge and Gould in 1972. Its hypotheses are :
1. Stasis: most species show no directional change whatsoever during their time on earth. They appear in the fossil record with a very similar aspect to that of their disappearance. Morphological change is generally limited and non-directional.
2. Sudden appearance: in any local area, a species does not arise gradually through constant transformation of its ancestors, but emerges at once and fully formed.

These are the observed facts. Now, let us see their interpretation: the emergence of a new species would take place quickly in “geological terms” (Gould, 94), and its origin would be the result of natural selection acting over small isolated groups in the periphery of the geographical area occupied by the ancestral species. If the new species had acquired certain advantages over the original, it would be able to take over the central area quickly, suddenly appearing, as a result, in the fossil record.

It is important to note that no trace of evidence for this process has yet been found in the fossil record. What is more, we are back at the problem of associating speciation with evolution. Steven M. Stanley puts such a concept in its place in his book “The New Evolutionary Timetable” (1981): “Let us hypothetically suppose that we want to form a bat or a whale, separated from their common ancestor over 10 million years, through a gradual change process [65 million years ago mammals were small undifferentiated animals, and indeed, 50 million years ago Icaromycteris, a bat of current morphology, and Basilosaurus, which a despite its name was an 18 meter whale, already existed]. If one average chronospecies lasts one million years, or even more, and we just have 10 million years available, then we only have ten of fifteen chronospecies ... to form a continuous succession connecting our minute primitive mammal with a bat and a whale. This is evidently absurd. Chronospecies, by definition, gradually go from one to the other, each of them showing very little change. A chain of ten or fifteen of them could take us from a little type of rodent to a slightly different one, maybe representing a new genus, but never from a bat to a whale!” *. In short, if species originate in “geological instants” and undergo practically no changes over long periods of time, it seems clear that the great evolutionary changes (macroevolution) cannot be the result of a simple extrapolation of allele substitutions inside a population. And if gradual change cannot be observed in the fossil record, and if living species show no trace of evidence for it, it seems reasonable to consider the possible existence of another mechanism of change.

This is exactly the same conclusion reached by R. Goldschmidt in 1940: There should be “macromutations”, that is instant mutations with great effect over an individual’s variability. It is probably not necessary to recall the cruel reaction of his “orthodox” colleagues, advocates of synthetic theory. The result of these macromutations, named “monsters without hope” by these colleagues, would not find a partner for reproduction, so that there would be no place for them in the evolutionary process.

However, significant discoveries have been made recently regarding the characteristics of gene expression regulation, showing that a great variety of factors act over the expression of complex groups of genes, and are able to give rise to great phenotypical effects. These discoveries have demonstrated not just that “macromutations” are possible, but also that in the scientific world it is more honest and creative to try to understand an observed phenomenon, even when not all of its mechanisms can be clearly defined, than to distort obvious facts in order to adapt them to the prejudices of the dominant majority.

The fact is that the fundamental problems still unanswered by modern synthetic theory are exactly the same that Darwin posed from the beginning: the stability of living species, and sudden changes in the fossil record.

Scientific model and social model

Karl Popper accused Sigmund Freud’s followers of “wanting to explain everything” on the basis of their theoretical principles. The two fundamental fallacies he attributed to them were, on the one hand, that they only looked for confirmatory examples, ignoring those that did not fit into Freudian theory, and, on the other hand, that they made the theory so flexible that anything could count as a confirmation.

These characteristics, however, do not seem to be exclusive to Freudianism (a less dogmatic theory, on the other hand, for its creator than for some of his followers), and become blatantly obvious each time an attempt is made to construct not even a criticism, but a mere synthesis of the current situation of the “official” theory of evolution. In addition, such a theory shares its arguments and dialectical resources with other doctrines when they become institutionalized. Indeed, synthetic theory seem to have moved from the category of theory to that of doctrine, based on two unquestionable principles that purport to explain all the variability present in living organisms: mutations, of a greater or lesser magnitude but always random, as generators of variability; and natural selection as the channelling agent of that variability. Under this simplified Darwinian cover it is possible to find a wide spectrum of interpretations. “Reactionary” defenders of what Darwin himself referred to as the “narrow interpretation” of natural selection, the “nature of bloody fangs and claws” (that Richard Dawkins (75), for instance, shares with Huxley) can be found at one end, considering DNA the basic unit and aim of evolution. At the other, we find more “liberal” and critical attitudes towards the official doctrine, giving species the category of raw material upon which selection acts, and advocating the abandonment of “strict adaptationism” as evolutionary mechanism (S.J. Gould is a deservedly prestigious representative of this interpretation).

Between these two viewpoints, which we could consider as examples of extreme positions, orthodoxy admits all sorts of gradations and combinations for each specific case, so that there is always a way of adapting the data to the theory. In case this proves to be insufficient, It is also possible to accept “permissible” exceptions, apparently due to their rare occurrence. In this way, many non-adaptive (even “anti-adaptive”) characteristics are justified on the basis of allometry; others, without possible justification, are either explained through pleiotropy or exaptation, the latest invention; the most surprising cases, through genetic drift, and, finally, a greater or lesser dose of neutralism, according to the case, covers the remaining instances.

But the problem with a rule arises when we add up all the exceptions and find a considerably larger number of them than of confirming cases. If we add the “ignored” exceptions (that keep growing day by day) to the officially admitted ones, we will find we are no longer talking about a problem with the theory, but about a serious illness.

Indeed, the biological mechanisms and processes that do not fit easily into synthetic theory keep piling up. As examples, we can cite regulating sequences, mobile elements, repeated sequences, homeotic genes, as well as remarkable regulation mechanisms at the different levels of organisation: at the cellular level, we find an extremely complex system of control made up of proteins that “revise” (check) and “repair” duplication errors, control correct cellular functioning and are capable of self-regulation; at the embryonic development level, morphogenetic fields control, with unbelievable precision, the spatial and temporal process of tissue and organ formation, and are capable of correcting accidents and reconducting the process; and, at the organic level, neuro-endocrine regulation systems connect tissues and organs under the protection of a complex immune system with an amazing capacity of response to foreign agents.

The great precision with which each of these systems operates, and the close interconnection between them all ?in other words, their complex-system nature with elements that cannot act as independent parts? leaves a narrow margin for random errors to act as an evolutionary mechanism. But if we also bear in mind their self-regulation capacity at the cellular and embryonic levels, what room is left for natural selection to act as change-inducer in organisms provoking true evolution?

This question is an old one. Long before these complex control, regulation and repair systems in organisms were known, the problem of the gradual and random appearance of complex organs was already being posed (this question especially worried Huxley). The answers given from within orthodoxy go from the “intelligent doubts” that, for example, Gould (86) shares with Goldschmidt (“...it is too difficult to invent a reasonable sequence of intermediate designs (in other words, of viable and functional organisms) between ancestors and descendants in cardinal structural transitions.” *) to the simplistic answers of R. Dawkins (1986), according to whom the gradual evolution of complex organs “is in no way a problem” since “it is clear that 5% of an eye is better than nothing, and 10% better than 5%”*. Such a “piecemeal” organ emergence would be the direct result of natural selection acting over DNA. In this way, from the “Selfish Gene” perspective, whose objective, according to Dawkins, is to “attain supremacy over other genes”, the action of natural selection over gene sequences can be proven through increasingly complex formulae derived from population genetics (Charlesworth et al., 94), to which the appropriate “selection coefficient” must be added in order to obtain coherent results.

However, from the embryonic development point of view, the direct step from gene to organism, forgetting all about the complex ontogenetic processes through which the genetic program information is executed, “is an unsustainably reductionist approach” (Devillers et al., 90) *, since genome expression during development is a “a system organized in hierarchical interconnected levels whose parts cannot be treated as independent elements”*.

The conclusion to which experts in the genetics of development are driven by new information is that “the role of natural selection in evolution is of little importance. It is simply a filter for inadequate morphologies generated by development.”* (Gilbert et al., 96).

These contradictions keep accumulating from different fields, showing the extremely weak condition the core concept of synthetic theory finds itself in. As early as 1984, Prevosti, in an essay about population genetics, concluded: “...if natural selection is not admitted, it is necessary to look for an alternative mechanism to explain the origin of the information contained in each species’ genetic program, where its functional properties are based. Up to now, such an alternative has not been found.” *

The situation seems to match perfectly what T. Kuhn (1962) defines as a crisis in Science. As a result of the activity of what he refers to as “normal science”, facts that contradict habitual interpretation arise, giving birth to an anomaly. This, in turn, gives rise to a crisis whose only possible solution is a change in the way the problem is viewed and analysed: that is, a change of paradigm.

Indeed the projection of cultural and social values, of a particular way of seeing the world, onto biological phenomena seems to be the fundamental problem underlying these contradictions.

If, as seems to be firmly established, the social and economic concepts of Malthus and Spencer, together with the prevailing world view of the time, were determinant in the birth of Darwinist theory, today the phenomenon has established itself more firmly with the simultaneous strengthening of the economic model based on free competition and chance as driving force, to the extent that it not only affects the theoretical frame of research in biology, but also the objectives and applications of the results.

However, despite the evident, and sometimes “astounding” discoveries derived from these principles, which might induce some people to think that it is now possible to control the mechanisms of life, if the theoretical framework supporting research is a deformation of reality, the results and their interpretation intrinsically carry their own deformation, even though they might appear congruent amongst themselves. In the words of the Sephardic philosopher Benito Spinoza, (“Ética demostrada según el orden geométrico”, 1675), “false ideas, that is, those inadequate and confused, succeed one another with the same necessity as true ones, that is, those clear and distinct.” *.

Paradigm and crisis

Kuhn (62) maintains that the criteria defining a scientific revolution are:

1.-A theory is able to solve the anomaly or anomalies responsible for crisis in the old paradigm, which is then displaced by the new one
2.-This new paradigm preserves, to a great extent, the old one’s specific problem-solving capacity.

If both criteria are met, progress will take place as a result of “quantum leaps” in science, that is, the differences will be qualitative, and not quantitative. A true scientific revolution is then followed by a period of “normal science”, governed by the new paradigm.

It is striking how Kuhn described the functioning of science as one of “punctuated equilibrium” a decade before Eldredge and Gould proposed it as an evolutionary model. However, unlike them, Kuhn understood such a behaviour in a true saltationist sense.

Indeed, the term revolution implies (in the strictest sense) a discrete episode, not a cumulative process. The analysis of theories and explanations throughout history shows that the approach towards different aspects of the same problem, or towards the same problem in different lights, can suddenly offer new solutions. And out of these solved problems new concepts, laws, theories and tools arise, leading us towards a new paradigm through which to view and explain the world. For “even observations change their nature under different paradigms”* (Kuhn, 62), since paradigms include the ontology of what constitutes their essence, their reality.

These observations come into head-on conflict with the view, by now traditional, of science as a steady, cumulative process, as a continuum between the first natural observation and current times, in which explanations, theories and laws have developed through the gathering and linking up of facts and discoveries. A gradual process that can, eventually, be speeded up through technological innovations or new discoveries, and whose progress will lead us, sooner or later, to the ultimate truth.

Nevertheless, the saltationist characteristic of the process of scientific knowledge forces a radical change in perspective. For, as we can see, we are not dealing with a subtle change of approach inside a paradigm, neither is it a question of false saltationism produced by an acceleration of the process of gradual change. Thanks to its own characteristics, and especially because of its consequences, it implies a real change.

The essential differences between these two perspectives display an interesting parallelism with the previously discussed macroevolutionary and extrapolative microevolutionary views of evolution: they confront a global view of the history of scientific knowledge with another that intends to universalise a process limited both in time and space, that is, the progress of empirical science, which we can consider as having “western” roots. And for that reason, from the gradualist, cumulative view, scientific revolutions in a deep, Kuhnian sense, do not exist in biology (Wilkins, 96).

Nevertheless, it is possible that the crisis, (real, in the light of the facts and arguments explained above) will bring about an inevitable change in paradigm. Moreover, we are probably facing the beginning of a revolution.

Crisis and revolution

In 1982, the Welsh astronomer Alfred Hoyle published a book entitled “Evolution from Space”, in which he theorized about the possibility that the strange viral capacities of self-integration in living organisms’ genomes, and of permanence in those genomes as “proviruses”, could be a mechanism for complex gene sequence acquisition, available for their eventual use as a response to or as a consequence of environmental changes or stimuli. Such a mechanism would justify the saltationist phenomena systematically observed in the fossil record, as well as explaining the deep differences in genetic and morphological organization present amongst great taxa.

For this phenomenon to be possible, an indispensable condition must be met: the sequences of viral origin must have a content with biological meaning, that is, they must be sorts of “subroutines” of vital processes.

Naturally, this proposition was ignored by official science, and was even ridiculed by some scientists, especially regarding the “outer space” origin Hoyle attributed to viruses. This was a logical reaction, on the other hand, since both the hypothetical role of viruses and their possible origin place such a proposal completely out of the paradigm, according to which all living organisms on Earth come from the random union of their chemical components and their subsequent evolution, in which natural selection, acting over molecules, has been the driving force from the very origin (Rebec, 94).

What is true, however, is that viruses are strange “organisms” which are not easily situated in the living world. They cannot be classified as “living organisms”, since they are “no more” than a DNA or RNA molecule wrapped up in a protein coat, sometimes of amazingly geometrical shape, that does not grow or feed. They can even crystallize without losing their abilities. They can only exist because they penetrate the cells of living organisms, where they introduce their genetic material, with its relevant information, and use the host’s proteins to make copies of themselves, which can then re-invade other cells, and, on occasions destroy them, thus damaging the receiving organism. This is their pathogenic aspect, which because it is the most easily observable, and because of its consequences, is usually considered as their fundamental nature. Nevertheless, and for unknown reasons, “on certain occasions” their genetic material (in a wide sense) inserts itself at a specific point it recognizes in the host’s genome, and stays there in the form of a “provirus” that can remain silent or code for its own proteins. An interesting aspect of this process is that retroviruses (a kind of RNA virus), once inside the cell, and in order to insert themselves in the host’s genome, transcribe their molecule into DNA through their own “reverse transcriptase”. This enzyme has the special feature of being unable to repair copying errors (unlike cellular replication), so that the inserted DNA molecules contain frequent “mutations” of the original. Another characteristic of this phenomenon, of great interest, is that “proviruses” can be “activated” by external factors, inducing them to escape from their insertion site (on occasions carrying with them cellular DNA fragments) and, after reconstructing their capsid, recover their infectious nature. A series of factors responsible for this activation have been identified: excess or defect of certain nutrients, ultraviolet radiation, and chemical substances foreign to the cell.

It must be admitted that all these characteristics in an organism that is not exactly “living”, sound, at the very least, strange. It is hard to imagine why they are so, and how they have originated. However, in the explanations normally found in textbooks such problems have clear solutions: these viruses are DNA or RNA fragments that “in some random way” (has it happened thousands of times?) have managed to escape from the cell (of different tissues and different taxa?); and, it appears that also “in some way” they have acquired all their complicated abilities, amongst which we find that of inserting themselves at a specific point in the DNA of a certain cell belonging to each species they “infect”.

Yet there is, in addition, another alternative that might convince those who find the previous explanation unlikely: from the “selfish DNA” perspective, viruses could constitute the final result of evolution.

It is surprising how from a scientific doctrine that prices itself on being rational and logical, fundamental problems of this kind are solved with such fragile and superficial “explanations”. The fact is that the line of thought which underlies this attitude is that “there is no need to understand it, as long as it works”, which in addition to not being very scientific, has led to widespread incongruity owing to a confusion between describing a process and understanding it.

As a result, for the moment we will ignore these so called “explanations” and maintain a reasonable doubt. It is necessary to acknowledge our ignorance, and the lack of a coherent scientific explanation of what these organisms on the borderline of the living and non-living world are, and how they have arisen. What does seem possible is to try to understand their significance on the basis of the consequences of their actions, in the light of Hoyle’s hypothesis. In other words, given that their sequences have the ability of self-integration in genomes in an “infective” way (that is, in a considerably large number of individuals), then if proof was found to show that the sequence content expression had “biological meaning” (which would be equivalent to saying that their manifestation was part of normal vital processes), it would be sufficient evidence to induce a serious consideration of their character as transporters of complex genetic information, and therefore of fundamental importance in the evolution of life.

But this is not all. The possible confirmation of such a hypothesis would not mean a mere change of focus in orthodox theory affecting the mechanism responsible for the introduction of variability exclusively. We are not dealing with a simple substitution of the “copy error” mechanism for a viral integration process. The simultaneous integration of sequences with complex biological content (that is, the integration of one complex system into another) in numerous individuals would radically change not just the process and the identity of the new character-creating agent, but also the meaning of the process. The new species would appear suddenly, through a substantial change (exactly as the fossil record reveals) shared by a considerably large number of “infected” individuals, making interfecundity possible. Natural selection would no longer be the “driving force” of evolution. It would simply be the elimination mechanism of faulty designs during extremely long evolutionary stasis periods, during which fit organisms (not “the fittest”) would easily reproduce, with variations in non-essential characters (whose origin, on the other hand, could be retroviral “copy errors”).

In short, we are dealing with a revolution in a strict Khunian sense. First of all, because confirmation of this hypothesis would solve two of the fundamental problems unanswered by the current paradigm:
1.-Saltationist phenomena systematically observed in the fossil record, which would be explained by complex gene sequence integration.
2.-The simultaneous change in a number of organisms high enough to allow for their interfecundity. But in addition, and as a result, the confirmation of such a mechanism would bring about a cascade of changes in numerous interpretations (including the “exceptions”) of described and manipulated biological processes, whose behaviour does not fit easily into conventional theory.

On the other hand, and in a meaningful way, the revolution’s lateral characteristics closely match those described by Kuhn (62). As well as being a hypothesis totally foreign to the existing paradigm, and hard to demonstrate (at least initially), “almost always the men who achieve these fundamental inventions of a new paradigm have been either very young or very new to the field whose paradigm they change”. Indeed, Hoyle’s profession and usual field of study is astrophysics, and regarding youth, it does not have to be a strictly chronological concept. If idealism, generosity and rebellion against conventions, are characteristic of youth (at least there was once a time when it was so), then Sir Alfred Hoyle, is, without a doubt, very young.

Finally, the philosophical consequences of revolution would be a “change of paradigm”, that is, a new way of looking at the nature of events. But it seems reasonable to postpone this aspect until the feasibility of the hypothesis is verified. For the moment, we will stick to confirming the existence of data capable of solving the above mentioned problems. We will have to proceed, as a result, in reverse order to that we are accustomed to: instead of taking an “unquestionable” model as the starting point and trying to force existing facts into that pattern, we will examine and interrelate the data, trying to identify the factors common to them, and finally, attempting to deduce what kind of model they suggest.

The quantum nature of life

Space limitations intrinsic to an essay of this kind force a necessary selection of the most significant data, which might give the impression of a premeditated bias. Nevertheless, customary interpretations of certain events within their own field of study, isolated from the general context and disconnected from their evolutionary meaning, might make them appear exceptional or rare. Therefore, we will try to compensate for such limitations with arguments, rare in the field of biology, but capable of providing a conceptual framework in which to interpret and interrelate certain phenomena that challenge our linear logic. To prevent this resource from appearing unscientific, it is necessary to remember that in his book “Life Itself” (81), Francis Crick posed a problem of a similar kind: “The fundamental facts of evolution are at first glance so strange that they could only be explained through an unconventional hypothesis”*. We are obviously not dealing with a deduction in the logical, linear sense, but with what we could refer to as an “impression”, or an intuition born of some mental product of his remarkable knowledge. But it is certainly not a sentence void of meaning since, indeed, precisely the fundamental facts in evolution are the ones that are the hardest to “fit” in the conceptual frame of conventional theory (assuming we do not limit ourselves to solving these problems with a “dogma of faith” kind of explanation). As fundamental facts we could consider the origin of life on Earth, the origin of the first cell and of the first multicellular organism, the emergence of all the great taxa, known as the “Cambrian explosion”, and the sudden changes in animal and plant organization observed in the fossil record. All of them are becoming harder and harder to explain under the “natural selection acting over random mutations” hypothesis, as knowledge about the complexity and stability of biological processes deepens.

Therefore, we will allow ourselves a brief reference to certain concepts that might provide a theoretical model in which to fit these “fundamental facts”. We will deal with the characteristics or properties of matter in the light of the astounding discoveries of quantum mechanics (not a very adequate name, since the discovered phenomena could be described as anything but mechanic).

As an outline, we can consider three of this discipline’s basic fundamental aspects. The first is that subatomic particles, the ultimate components of matter, do not have “individual entity” (they are not particles in a material sense), they only exist as a function of their relationships with others. In other words, their appearance in the shape of an atom would have had to be simultaneous.

The second is that the energy/matter produced by these “particle systems” are organised in discontinuous “quanta” that go (jump) from the atomic organisation level to the universe. These systems have the particular feature of being themselves formed by lower-level systems (totalities) interacting between themselves, so that “the whole is more than the sum of its parts.”

The third is that electrons possess a dual nature: they are both particles and waves, conditions that are opposite and complementary at the same time. As a result, their state at a given instant can only be expressed as a probability.

These properties, so different to the materialist conception of Newtonian mechanics (this one really is so), are assumed by the scientific community, despite their difficult “visualisation” through our way of thinking and understanding the world.

But given their acceptance as properties of matter, and given that living organisms (including ourselves) are evidently material, it is pertinent to ask whether these properties are a constituent part of the essence of all living organisms, and therefore of their (our) qualities. In such a case, these properties would also condition the mechanisms of the evolutionary process.

Indeed, even though an inevitable reductionism leads to the study of living organisms (or partial aspects of them) as if they were independent entities, it becomes clear that the “independent organism” concept has little real reflection in nature. Living organisms are capable of self-organisation (that is, they can only exist) through intense exchanges with their environment, itself organized as a complexly interrelated, dynamic ecosystem.

Descending to lower levels, organisms themselves are open systems made up of units that construct organs functioning in a co-ordinated fashion with other organs. Each of them is in turn formed by cells ?extremely complex systems including energy transformation mechanisms, information and regulation networks, internal and external structure generation, etc. All these levels have in common the property of the whole as more than the sum of its parts, each of which can only exist if subject to the existence of the others. In this context, genes should least of all be considered as individual entities, since their activity (their identity) depends on the co-ordinated interaction of a considerably large number of regulation proteins, histones, RNA, and even other genes or groups of genes acting in a synchronic fashion.

Consequently, do these properties of matter have any implication whatsoever in the characteristics of the evolutionary process? There are sufficient clues to make us seriously think they do. And a truly spectacular case is a crucial phenomenon for the understanding of evolutionary and biological processes in general: the origin of the eukaryotic cell, and consequently, of the first component systems of living organisms.

The formation of the first eukaryotic cell, that complex network of processes so exquisitely interwoven, finds no easy explanation from the orthodox perspective in terms of a gradual (to a lesser or greater extent) result of random chemical reactions (Gesteland et al., 93). However, this process has been explained by L. Margulis and D. Sagan (85) in such a convincing way that it has joined the small group of evolutionary processes that may be considered as scientifically proven, both from the morphological and functional points of view. The inclusion of a Prochloron-type bacterium, and of aerobic bacteria resembling Paracoccus or Rhodopseudomonas, inside others is admitted as the origin of chlorplasts and mitochondria. The origin of cellular microtubules may be explained in the same way, being identified by the authors with spirochetes.

The interpretation of this phenomenon is explained by the own authors in terms of random and occasional endosymbiotic processes (in other words, a bacterium assimilated others, but did not digest them, acquiring a selective advantage over others). Nevertheless, putting aside the fact that a eukaryotic cell would be hard pushed to exceed bacterial reproductive capacity, a different interpretation is also possible: if the process we could consider as fundamental in the appearance of eukaryotes was produced as a result of the union of various “complex systems”, would it not be possible for this to be the main evolutionary mechanism?. We have already discussed the extreme cellular-process interdependence, and in this sense, bacteria are systems, totalities, what Koestler named holons. This integrity, strange as it may seem, makes it necessary for the emergence of cellular processes to have been simultaneous (totalities, just like the “quanta” of physics, cannot appear gradually). This would explain the sterility of trying to find the origin of life in self-replicating molecules (Rebeck, 94), since it seems clear that the cell is the only natural medium where the complex phenomena making up life can take place.

In fact, bacteria were not only the first living organisms identified on Earth, (according to Carl Sagan, the “speed” of life formation on Earth indicates the process was a probable one) but they were also the creators of the conditions needed for the emergence of life as we know it (see Margulis and Sagan, 95).

Irrespectively of their “taxonomic divisions”, these peculiar “systems” show certain activities very different to the pathogenic nature that is usually attributed to them (amongst them post-adaptive mutations (Cairns, 91)), activities that are always basic for the development of life, in soils, plants, and inside animals (Benoit, 97). And with all probability, there are still many more bacteria, with many more functions, to be discovered.

However, the apparently most surprising, ?but certainly the most coherent? conclusion Margulis and Sagan are driven to by the development of endosymbiotic theory is that living organisms are, after all, more or less modified bacterial aggregates.

It is curious how one might be contributing in a crucial way to a paradigm crisis, without even knowing it. For this model is not a mere contribution to current theory, but the proof for a process that overturns the accepted path of random mutations from the time of the first (unique?) cell. And, above all, it radically changes the meaning of the evolutionary mechanism.

However, the authors themselves do not see this difference in meaning, attributing responsibility for the appearance of multicellular organisms to random mutations in the original bacteria.

But let us consider the essential conditions necessary for the formation of a true muticellular organism. Jellyfish, for instance, ranking amongst the simplest animals existing today, have eleven types of different cells (mammals have around 200). For tissue formation in jellyfish to take place during embryonic development, the action of an “embryonic program”, no matter how simple, is indispensable to co-ordinate the position and proliferation of the already complex constituent cells. Bearing this in mind, what genetic material and which sequences allowed the transition from simple, typical eukaryotic cells to specialized cells capable of generating different structures and tissues? And, above all, irrespectively of the time available, how could the co-ordinated embryonic-development regulation appear? Could it have been through random accumulation of “copy errors” in the eukaryotic cell? Considering the extreme stability of cellular process, this seems very unlikely. But if we return to the “strange” pathogenic organisms that, together with bacteria, have turned into one of humanity’s worst enemies, we might find an answer in their non-pathogenic aspect (the “dual-condition” which, funnily enough, they share with bacteria). Viral abilities of self-insertion in animal and plant genomes and of translation of their own genetic information inside the host might sound like familiar phenomena in the context of our discussion: they represent a way for two genetic units (two systems) to combine and integrate themselves in a higher unit.

And such a mechanism could account for the most surprising evolutionary phenomenon for which irrefutable proof exists: the “Cambrian explosion”. The sudden and simultaneous appearance (in a strict sense) of all the great current animal phyla in strata immediately above those containing the simple Ediacarian fauna, radically challenges conventional evolutionary theory1. Amongst the identified organisms we find sponges, echinoderms, molluscs, polychaets, onychophorans, arthropods, and even the possible ancestors of chordates, and subsequently, of vertebrates.

In an unprecedented episode, structures as complex as antennae, articulated legs, rigid covers, shells, claws, eyes, propulsion structures, mouths and digestive tracts appeared. How can such a sudden revolution be explained?

The superficial orthodox explanation is “adaptive radiation in an empty environment”, but it is evident that such a “dogma of faith” is unsustainable. Even after admitting that different niche colonisation (there are diggers, swimmers, burrowers, grazers, etc.) could be justified on the basis of time availability, and that all the time in the world had been available for such an event to take place, how could we explain the great genetic and embryonic changes responsible for the appearance of all the current types of organization?

The palaeontologist S. J. Gould (86) once more makes use of the “intelligent doubt” to analyse this phenomenon: “If evolution took place in the commonly admitted way, that is, as a result of environmental adaptations through gradual changes, what we would initially find would be a few general designs and great variability inside each of them. However, we find exactly the opposite”*

And this global contradiction with the orthodox theory can be found in the intermediate steps, as well as at the initial phase and final result of evolution: it would be logical to expect the present situation to be the inverse of what the initial one “should be”?a greater variety of organization groups and less variability within each type of design. However, we find the opposite situation again. The appearance of the great taxa (fish, amphibians, reptiles, birds, mammals) is equally sudden and equally hard to justify through gradual and individual changes, since the great remodelling of their organization, both morphologicalal and genetic, implies simultaneous changes in many interdependent characters (for a more detailed discussion, see “Lamarck y los Mensajeros”, Sandín, 95). It is not only the great organization changes, but also the variations within them, both in animals and plants, that display a similar pattern to the “punctuated equilibrium” of species. As cladistic systematics shows, these sudden appearances (incidentally, they reflect a great initial variability) tend to be associated with eras of great “geological disturbances”, and very frequently with previous periodic extinctions (Rampino and Stothers, 84). The consequences of these episodes have little to do with natural selection, unless it is understood as “the survival of those who survive”. Different-sized asteroids, falling to Earth in different quantities during the last 250 million years at least, are clearly implicated in these extinctions, which despite being massive have some curious selective characteristics that greatly surprise palaeontologists (for some unknown reason, some species survive). Consequently, Hoyle’s hypothesis cannot be honestly discarded. That is, be it through their possible action as new virus transporters, or because their effects over ecosystems activated previously existing viruses, viral “dual nature” influenced by asteroid impacts would justify both new biological characteristic emergence, and at least some of the strange selective extinctions.

Naturally, to render feasible such a mechanism it is necessary to admit that viral sequences, whether individually or through combinations of them, would translate proteins with “biological content”, that is, susceptible of forming part of normal biological processes. The scientific attitude towards this hypothesis, which we have reached following strictly rational arguments, should not be one of rejection before a viral condition of difficult explanation, but of trying to confirm the existence of objective proof supporting serious consideration of this possibility.

Viral function in nature

If viruses share with bacteria the double condition of pathogenic agents (destroyers) and basic units of life (creators), maybe we should not be asking ourselves which is the predominant condition, since from the previously explained perspective, both opposed conditions would be, at the same time, complementary. The question arising from such a dual nature should be: what conditions determine which of the two characters is expressed? As a starting point in the search for an answer, we must take into consideration that if bacteria have been proven to be at the origin of life as well as at the base for the functioning of life, their “negative” character could be the result of a certain factor upsetting the natural equilibrium of their activity. It does not seem necessary at this point to revise “why” bacteria that normally act in our digestive tract acquire pathogenic nature, or under what conditions bacterial epidemics break out in human populations.

Is it possible to find in viral dual nature a similar function to that of bacteria? In other words, are viruses a mysterious “special case” amongst the different possible manifestations of life, or are they a fundamental element of it? Let us see what the facts suggest.

Variable amounts of DNA known as “endogenous viruses” have been identified in animal and plant genomes. Different types exist, and most of them are considered to have evolved from exogenous viruses that “infected” different species in the past, becoming endogenous through their insertion in germ cells. Thousands of sequences of viral origin with active participation in vital functions of different tissues are being identified in growing numbers (Coffin, 94). Some of these sequences can be considered true “genetic fossils”; they are “ancient” proviruses that have undergone many mutations, although it is still possible to relate them to current retroviruses. Having lost their terminal zones (they are defective viral particles), they are no longer capable of escaping their insertion site. However, some of them maintain this capacity, existing in the form of mobile elements or transposable elements (TE). They are DNA sequences capable of movement and self-insertion as well as insertion of self-copies at different sites in the genome. These elements have been classified in two groups: Transposons, that re-insert themselves directly through DNA copies, and Retrotransposons, that in order to allow insertion need to transcribe their RNA copies to DNA with the reverse transcriptase. The implication of these elements in genome “repetitive sequence” formation (it is estimated that they make up 42% of the human genome) is obvious. And even though under the assumptions of population genetics’ calculations they have a “non-functional” nature (Charlesworth et al., 94) (thus enabling the selfish DNA hypothesis to be sustained), the fact is that sequences of this kind, such as LINE (long inserted elements), code for proteins with reverse transcriptase activity, needed for various types of retroelement mobility (Mathias et al., 91). Amongst them we can find some taking part in mammal eye crystalline formation and functioning (Brosius & Gould, 92).

In respect to the viral origin (and current condition) of these elements, it has been recently confirmed (Kim et al., 94) that Drosophila´s Gypsy element is in fact a retrovirus with the ability to rebuild its capsid and re-infect again. This might be the reason behind the existence of shared transposons between man and arthropods, nematodes, and planarians (Auxolabéhère, 92; García et al., 95; Oosumi, 95).

A very different condition to what was originally thought has recently been attributed to another constituent part of the genome: introns, considered to be noncoding genome segments located between coding genes or exons. In 1982, Thomas R. Cech and Sidney Altman discovered that “some” intron sequences belonging to “certain” RNA had enzyme properties allowing that same RNA to cut and splice itself during the transcription process, a discovery that was worth the Nobel Prize. Well, in the fungus Saccaromyces cerevisiae, the intron I2 is actually a retroelement (Moran et al., 95) (a special case?).

It can be said, therefore, that when we forget the “selfish” and “expansionist” DNA doctrines, the proportion of sequences of viral origin in the genome grows spectacularly, especially if we limit ourselves to the analysis of what these sequences do and how they originated (Indraccolo et al., 95). On the other hand, are these activities merely a way for the genome to “take advantage” of viral-origin sequences present in it (Charlesworth et al., 94)?, or, on the contrary, are they a fundamental part integrating the genome? In order to answer, we will examine some of the data regarding their functions.

Through localization changes and duplications, mobile elements are able to provoke chromosomal rearrangements, as well as changes in gene expression and regulation, with important evolutionary consequences (McDonald & Cuticciaba, 93).

A retrotransposon responsible for an expanded expression of amylase secretion genes has been identified (Robins and Samuelson, 93). In many mammals, the enzyme secretion is restricted to the pancreas, whereas in humans the retrotransposon-mediated modification allows salivary glands to secrete the amylase as well, widening the range of foods that can be ingested, and thus conferring humans a clear evolutionary advantage.

In the same way, more retrotransposons have been identified and shown to be involved in histocompatibility gene regulation (Robins and Samuelson, 93), in the expression of the various tetra-1-alfaglobulins in human tissues (Kim et al., 89), as well as in other mammals, invertebrates (Dnig and Lipstick, 94) and plants (McClintock, 94).

The recently discovered Wolbachia bacterium is a striking case that has passed unnoticed until now, since its small size allowed it to escape the filters usually employed in bacteria isolation. This bacterium was discovered in the common pill bug (Armadillium vulgaris), and was found to contain a transposon, named f factor, that in the face of certain adverse environmental conditions has the ability of raising the proportion of female pill bug offspring to 90%. To achieve this, the transposon enters germ cell nuclei where it can either integrate itself in a male chromosome turning it into a female one, or inhibit the male chromosome from the pill bug’s genome. Does this phenomenon have any evolutionary consequences? Perhaps it can be better evaluated bearing in mind that it is not an isolated case: according to Rousett et al. (92), from 10 to 15% of all insect populations in nature are “infected”. And these peculiar “diseases” are also an important adaptative mechanism for plants (Galitski & Roth, 95) regarding response to environmental conditions: in plants, mitochondrial DNA acts “on certain occasions” over its “host’s” reproduction. A “male sterility” gene turns up to 95% of individuals of thyme, for example, into females (Gouyón and Couvet, 85). In maize and petunia, these genes come from both mitochondria and chloroplasts (let us remember their origin) and have been found in very different plants with higher or lower frequency (Gouyón and Couvet, 87). The mechanism has been recently described (Brennicke et al., 93): firstly, a messenger RNA from the organelle enters the cytoplasm, where it is transcribed to DNA by the reverse transcriptase enzyme, thus allowing its insertion in the nuclear genome. Apparently, large fragments of organelle DNA have been transferred directly to the nucleus (it is not known how), so that between 3 and 7% of the nuclear genome would be made up of such sequences.

Since 1988 (Varmus et al.), lineage relationships between reretrotransposons and retroviruses are being studied. On top of their replication and insertion mechanisms, they have in common the quality of “oncogene activation” (Dombrouski et al., 91). In this way, similar sequences to mammal LINE retrotransposons have been found inside the c-myc oncogene in breast cancer.

Regarding the evolutionary importance of such sequences, it must be remembered that in Drosophila (which is not a special genome case, but the most studied), from 3000 to 5000 mobile sequences related to “certain phenomena of quick adaptation to environmental change” * exist, making up from 10 to 15% of its DNA (Biemont and Brookfield 96).

In addition, the activity of endogenous viruses does not seem to be without evolutionary importance: placenta emergence in mammals, an achievement as complex as momentous, has been shown to have elements of retroviral origin implicated in different parts of its functioning mechanism. In placental mammals, parental genes from the male and the female contribute in a different but complementary way to embryonic development. Without the mother’s imprinting, the embryo is abnormal; without the father’s, the placenta cannot develop. This mechanism must necessarily be at the very origin and evolution of placentation: on the one hand, so that the mother accepts the development of a strange body inside and in close contact with her; on the other, to limit its development preventing invasion of maternal tissues (Hall, 90). According to Neumann et al. (95), this phenomenon has been induced by the presence of defective retroviral particles of the IAP type. But in addition to participating in its functioning, they are also implicated in its formation. It has been demonstrated (Lyden et al., 95) that antigens of retroviral origin are expressed in normal trophoblast cells in the human placenta with a very significant role: they take part in the morphological differentiation of these cells.

Furthermore, these phenomena are no exception. More than 1% of the 10,500 perfectly known gene sequences have been identified (up to now) as corresponding to endogenous retroviruses, and are expressed in 37 human tissues as constituent parts of the brain, placenta, embryo, lung, etc. (Genome Directory, Sept. 95.)

This phenomenon has an evident evolutionary significance concerning the explanation of saltationist events (as well as of another, more concrete phenomenon: cellular proliferation control), which can be further clarified by data derived from Drosophila, an organism studied in depth by the genetics of development. In its embryo, 15 retroviral sequences have been found to be implicated in the space and time control of different tissue development.

The growing evidence indicating the action of viral sequences in essential vital processes supports the view that they are not exceptional events. And a convincing argument to endorse the possible importance of their activity is that both their “infective character” and their “biological content” would consistently explain evolutionary puzzles currently unsolved. It has been proven (Tristem et al., 95) that there is a considerable difference between endogenous retroviral “populations” in reptiles and in birds and mammals. Could this fact be explained from our perspective?

Let us take a look at the answer to the question regarding their activation conditions.

Coxackieviruses form part of a “family” divided into two types, A and B. Their infection in humans produces pathology “only” in 10% of all cases. Some of them have been studied experimentally. For example, in mice, the CVB3 induces myocarditis, the CVB4 induces pancreatitis, etc. In a study (Gauntt & Tracy, 95) in which mice were inoculated with a non-virulent strain of CVB3 (named CVB3/0), it was seen that a selenium-deficient diet (cellular and extra-cellular selenoproteins act as antioxidants) produced the emergence of a unique type of extremely virulent CVB3 in different mice 10 days after inoculation. Examination of their genomes demonstrated that they had suffered six nucleotide changes in the same six positions. Studies of different nucleotide changes in the CVB3 genome have confirmed the existence of a limited number of changes associated with the virulent character.

Although the interpretation for the phenomenon given in the study was that “multiple random mutations” had taken place, and that what was observed afterwards in the different mice was the result of natural selection driving the process to different viruses with exactly the same mutations (another example of Kuhn’s observations about scientists’ tendencies to see exactly what they have been trained to see), the fact is that the most reasonable interpretation seems to be a reaction to environmental stress.

A different but equally significant kind of response to environmental stress was observed by Ter-Grigorov et al. (97) in an experiment with the objective of studying the reaction to auto-immune stimuli in female mice. Females were crossed with males over a period of one year, reinforcing, after each crossing, the immune response of the female with male B6 immunoblasts. Of the 65 mice obtained, 13 developed acute leukaemia, and 50 a chronic “AIDS-like disease”, with the “appearance” of complete intra and extra-cellular C virions with horizontal and vertical transmission capability.

The meaning of these phenomena becomes clear if we add them to the previously mentioned viral activities. Just like bacteria, viral functional aspect in organisms is upset by environmental aggressions, whether intrinsic to the ecosystem or the result of human manipulation, triggering off a “response” in the shape of a pathogenic agent.

In short, it looks like there is enough experimental evidence answering the question about the causes (and consequences) of pathogen-character activation in viruses, which can be added to the already-known factors responsible for “provirus” activation. And we would possibly have many more if we could count those which, with all probability, have been discarded following orthodoxy’s failure at explaining them.

But if to these empirical data, which are increasingly hard to reject as exceptional or negligible in number, we add the effort to find the factor common to all the great (and small) evolutionary puzzles we have been discussing, it is possible to propose a new model totally modifying not only the fundamental mechanism of conventional evolutionary theory, but its very essence, the meaning of the evolutionary processes.

A new evolutionary model

Such a model can be synthesized in the following way: the origin and evolution of life would be a process of complex system integration, successively auto-organised in higher-level systems. Bacteria would be the basic units, equipped with all the basic processes and mechanisms needed for cellular life, with components that appear to have remained almost unchanged throughout the evolutionary process. Viruses, through their chromosome-integration mechanism, would be the agents that either individually, or in combinations of themselves, would introduce new sequences responsible for embryonic control of new tissue and organ appearance and functional regulation.

Viral and bacterial response capacity to environmental stimuli would justify the inevitably rapid and far-reaching changes shown in the fossil record, forcibly needed due to the complex interrelation between tissues and the whole organism. And their “infective” character would render these changes possible in a considerably large number of organisms simultaneously. On the other hand, this infective character could be implicated in mass and selective extinctions, often coinciding with episodes of environmental disruption, events that would therefore be part of the evolutionary process.

In this context, natural selection, whose lack of creative power has been previously discussed, would be relegated to a secondary plane in the evolutionary process, being occasional and void of meaning as a mechanism for evolution. Competition would no longer be the driving force behind evolution, since new species would arise and mature as a whole. And randomness, be it biological or statistical, would be further called into question by determinism, by the teleological content implied by the existence of “components of life”, whatever their origin. That is, whether these components have arisen on Earth, as a result of an “emergent property” of matter, or whether this, or any other phenomenon, implies that they exist and propagate in the universe.

But this new model not only leads us to a new view of the nature of biological processes. The relegation of the old concepts, with their deep cultural roots, to their rightful place implies the emergence of new ideas, of new values modelling the way reality is interpreted: in short, a new paradigm.

In the light of the above mentioned facts, this process would mean not only a substantial change in the interpretation of the general evolutionary process, but also a reinterpretation of many of the biological phenomena that are a part and consequence of it. This would be an enormous task, since it would imply, in some way or another, a “re-making of biology”, requiring a new integrated approach to the different research fields. In such an integrated model, it would be possible to fit those processes which are not only inconsistent with conventional theory, but in open contradiction with it.

In this way, in a Complex System Integration Model of Evolution the facts could be explained as follows:

Anti-stress proteins, employed by cells in environmental distress to repair injury, hold a close resemblance in all organisms, indicating extreme conservation. For example, the hsp10 and hsp60 have only been found in mitochondria and chlorplasts. The hsp60 and hsp70, denominated “chaperones”, re-nature proteins de-natured by heat. But, probably more significantly, the hsp70 has been associated with oncoviruses through the PP60 src enzyme implicated in cellular growth regulation (Langer et al., 92; Welch, 92).

Proteins involved in apoptosis (programmed cell death), basic in all living tissues, and with special importance in embryonic development, can work both to favour and to inhibit it. Now the Epstein-Barr virus produces substances “resembling” the Bcl-2 apoptosis inhibitor, or can alternatively manufacture molecules making the host cell increase its own Bcl-2 synthesis (Cohen et al., 92). Papilloma viruses disactivate or degrade the P53 apoptosis regulator, and this process has also been confirmed in various kinds of “viral origin” cancers, to which we will return later on (Korsmeyer, 95).

These phenomena indicate an extreme conservation of fundamental processes, suggesting a kind of evolution not through changes of original sequences, but through the addition of new ones. This would explain, for example, why the study of hormone relationships among all biological groups indicates “lateral links, and not of descent” * (Barja de Quiroga, 93), or also why shark or human antibody molecules, for example, “have suffered relatively small changes for 450 million years” (Litman, 97). According to this author: “...what does seem surprising is that [...] apparently enigmatic evolutionary jumps take place in short periods, and in an uncommon magnitude, at least in humoral immunity” *.

Finally, and as exemplary of another fundamental process in Evolution, we will consider certain facts from the genetics of development, whose orthodox interpretation comes into head-on conflict with “official theory”, and which can provide an explanation as to how viral integration has operated upon morphological differentiation in the evolutionary processes. These facts concern homeosis, and are capable of truly explaining the mysterious (and inexplicable) cases of convergent adaptation produced at random. Homeotic genes control different tissue, organ and structure development. When situated at the same positions in chromosomes, they produce the same characteristics in organisms as phylogentically far apart as toads (Xenopus laevis), flies (Drosophila), fish, birds and mammals, affecting different level structures, from organs to global differentiations such as axis, segments, etc. “Homeoboxes” for eye, wing, globulin, gastrulation, etc. have been identified (Gilbert et al., 96). The layout and structure of their DNA suggests a formation through successive gene duplication. If to this duplication mechanism, in which transposons play an obvious part, we add the clear viral origin of sequences identified in embryonic differentiation of different tissues in different taxa, the origin of homeotic genes becomes clear. And their implication for our evolutionary model even more so, since they illustrate the possible working mechanism of viral sequences with specific biological content in new organ emergence.

A new paradigm

This new perspective offers new interpretations, and therefore possible answers to serious scientific problems resulting from an economicist approach in some cases, and in others from the lack of communication and exchange between different “specialists”, which prevents the incorporation of such problems into an evolutionary context. For the commercial use of pharmaceutical products, or of genetic engineering techniques, whose “spectacular” achievements have had great social repercussions through the media, is conditioning biological research to such a point that it is becoming an entrepreneurial activity. As a result, both the working rationale and the objectives of that work are being profoundly transformed.

In the first place, the need to render the results profitable gives rise to strong competition between different working groups (sometimes putting scientists in unedifying situations and attitudes) so that the fundamental practice of exchanging information and results, once a routine activity, is disappearing.

In the second place, research is increasingly being financed by private enterprises whose economic interests are far stronger than any other, leading to a rushed commercialisation of techniques and products (as patents) whose “side-effects” are only evaluated after their market release. This is the case of research that purports to manipulate “genes of commercial interest” * (Mackay et al., 92) such as those introduced in plants and animals using transgenic plasmid and retroviral vectors.

Nevertheless, given the special characteristics of these vectors, it would be more prudent to try to understand the phenomenon and put it in its right place in nature, before continuing with manipulations whose end-results might be unforeseeably dangerous, since the problems (already observed) of artificial character propagation to other species (such as the example of “transgenic” maize herbicide resistance) can be uncontrollable.

Another problem of similar consequences and origin is that raised by xenotransplants. The serious “side-effects” of animal organ use have finally been related to the activation of animal endogenous proviruses when introduced in another species. The danger of hybridisation and propagation of “new viruses” is evident.

This last phenomenon might lie behind the emergence of AIDS virus “variants”. Apparently, HIV-1 and HIV-2 are both closer to certain monkey viruses (chimpanzee and Macaca mulata) than between themselves (Huet, 90), a fact that supports the hypothesis of an origin brought about by human activities (possibly the preparation of vaccines with whole monkey blood). In other words, we would not be facing a “new” pathogenic virus, but the alteration of an endogenous virus that in normal conditions would have a specific function: immunodepression, a necessary phenomenon in mammals during pregnancy. And this would also explain the effects in AIDS patients treated with wide spectrum antiretrovirals, or with a combination of them. Failure in different organs would be the consequence of an alteration of viral sequences involved in normal activity.

Finally, the implication of viral-origin sequences in embryonic cell proliferation control, together with “proviral” activation factors, allows us to place “oncogenes” in an evolutionary context: “oncoviruses” would not be exceptional cases. With all probability, they would be viruses containing sequences responsible for embryonic development control of specific tissues, and their malignization would be the result of an activation at an inadequate time (Seifarth et al., 95).

In short, these answers might be able to shed some light at least on certain aspects of the problems that up to now have found no easy solution. In any case, they show that the procedures derived from the current paradigm (that is, of its scientific premises, but especially of its social component) not only distort the approach to these puzzles, but in some cases might be contributing to their creation.

To conclude, and taking up Kuhn’s arguments once more, the consequences of such a new approach would not only mean a theoretical model change. The bases of the new paradigm necessarily take us to a new way of interpreting the control mechanism of vital processes, and consequently, to a new perception of and attitude towards nature. If the
social (cultural) model determines to a great extent the way we see and relate to the world, it seems clear that the substitution of a paradigm based on competition and irresponsible chance for one of maturing as a whole and of essential unity and co-operation, and very especially of prudence and respect in the face of what we do not know or control, must come together with (or be preceded by) a substantial change in our social and cultural values.

It is true that no matter how benevolent the vision of nature and society may be, the existence of competitive behaviour cannot be ignored. However, in the same way as in the evolutionary process competition, whatever its connotations, is in no case a “creative force” but exactly the opposite, the social model based on “free competition” (which is no more than “big fish eats small fish”) is a rosy path for selfish and irresponsible attitudes that can only lead us to a cul-de-sac.

Acknowledgements

I should like to express my sincere gratitude to Lucía Serrano and María Bornemann for their effective collaboration, and above all for identifying with this work. I would also like to thank Juan Fernández Santarén for his lucid critical revision of the manuscript, and Carlos Sentís for his continuous contribution of information.

Notes
1. It has been recently suggested (Nature, 28th August 1997) that the origin of the main metazoan clades might be dated to the Ediacarian period. That is, their appearance would be even more sudden and inexplicable.

* Not original quotation. Re-translated into English from the Spanish version.

REFERENCES

* ALLAN, J. 1997. Silk purse or sow's ear. Nature Medicine, 3 (3): 275-276.

* AUXOLABEHERE, D. 1992. L'élément transposable P en Drosophila melanogaster: un transfer horizontal. C.R. Soc. Biol.186: 641.

* BARJA DE QUIROGA, G. 1993. Fisiología animal y evolución. Akal Universitaria. Madrid.

* BEATTY, J. 1994. Opportunities for genetics in the atomic age. Hellon Symposium, "Institutional and Disciplinary Contexts of the Life Sciences". M.T.I., Cambridge, M.A. (Citado por Gilbert et al., 96).

* BENOIT, D. 1997. La bacteria que convierte en hembra. Mundo Científico, 176: 124-127.

* BIEMONT, C. & BROOKFIELD, J.F. 1996. Los genes saltadores: Patrimonio manipulable. Mundo Científico, 170:642-647.

* BRENNICKE ET AL. 1993. The mitochondrial genome on its way to the nucleus-different stages of gene-transfer in higher-plants. FEBS LETTERS, 325 (1-2): 140-145.

* BROSIUS, J. & GOULD, S.J. 1992. On "genenomenclature": a comprehensive (and repectful) taxonomy for pseudogenes and other "Junk DNA". Proc. Nat. Acad. Sci., 89: 10706-10710.

* CAIRNS, J. & FOSTER, P.L. 1991. Adaptative reversion of a frameshift mutation in Escherichia coli. Genetics, 128: 695-701.

* COHEN, J.J.; DUKE, R.C.; FADOK, U.A. & SEELINS, K.S. 1992. Apoptosis and Programmed Cell Death in Inmunity. Annual Review of Inmunology, 10: 267-293.

* COFFIN, J. 1994. Sexta Conferencia Internacional sobre retrovirus humanos: HTLV. Absecon, New Jersey.

* CRICK, F. 1981. Life itself. Oxford University Press. Oxford.

* CHARLESWORTH, B.; SNIEGOWSKI, P. & STPAN, W. 1994. The evolutionary dynamics of repetitive DNA in eukaryots. Nature, 371: 215-220.

* CHILD, C.M. 1941. Patterns and Problems of Development. Univ. of Chicago Press. Chicago.

* DAWKINS, R. 1975. The selfish gene. Oxford University Press.

* DAWKINS, R. 1986. The blind watchmaker. Longmans. London.

* DEVILLERS, CH.; CHARLINE, J. & LAURIN, B. 1990. En defensa de una embriología evolutiva. Mundo Científico, 10 (105): 918.

* DNIG, D. & LIPSHITZ, H.D. 1994. Spatially regulated expression of retrovirus-like transposons during Drosophila melanogaster embryogenesis. Genetical Research, 64: 3.

* DOBZHANSKY, TH. 1951. Genetics and the origin of species. Columbia University Press. New York.

* DOMBROUSKI, B.A.; MATHIAS, S.L.; NANTHAKUMAR, E.J.; SCOTT, A.F. & KAZAZIAN, M.M.Jr. 1991.
Isolation of the L1 gene responsible for a retrotransposition event in man. Am. J. Hum. Genet., 49: 403.

* ELDREDGE, N. & GOULD, S.J. 1972. Models in Paleobiology. T.J.M. Schopf (ed.) W.M. Freeman.

* GALITSKI, T. & ROTH, J.R. 1995. Evidence that F plasmid transfer replication underlies apparent adaptative mutation. Science, 268: 421-423.

* GARCIA, J.; BAYASCAS, J.R.; MARFANY, G.; MUÑOZ, A.; CASALI, A.; BAGUNA, J. & SALO, E. 1995. High copy number of highly similar mariner-like transposons in planarian (Platyhelminthe): evidence for a trans-phyla horizontal transfer. Molecular Biology and Evolution, 12: 3.

* GAUNT, Ch. & TRACY, S., 1995. Deficient diet evokes nasty heart virus. Nature Medicine, 1 (5): 405-406.

* GESTELAND, R.F. & ATKINS, J.F. 1993. The RNA World. Cold Spring Harbor Laboratory Press.

* GILBERT, S.F.; OPITZ, J.M. & RAFFS R.A. 1996. Resynthesizing Evolutionary and Developmental Biology.
Developmental Biology, 173: 357-372.

* GOLDSCHMIDT, E. 1940. The material basis of evolution. Yale University Press.

* GOULD, S.J. 1986. El pulgar del panda. H. Blume Editores. Madrid.

* GOULD, S.J. 1987. Is a New and General Theory of Evolution Emerging? F.E. Yats (ed): Selft Organizing Systems. The Emergence of Order, Plenum Press, London, New York.

* GOULD, S.J. 1987. La sonrisa del flamenco. H. Blume Editores. Madrid.

* GOULD, S.J. 1994. La evolución de la vida en la Tierra. Investigación y Ciencia, 219: 55.

* GOUYON, P.M. & COUVERT, D. 1985. Selfish cytoplasm and adaptation: variation in the reproductive system of thyme. Im. J. Haeck, J. W. Woldendorp (eds). Structure and functioning of plant population, 2: 299. North Holland Publ. Comp. New York.

* GOUYON, P.M. & COUVERT, D. 1987. A conflict betwen two sexes, females and hermaphrodites. En S. Steam ed. "The Evolution of sexes and its consequences". Birkhanser Verlag, Berlin.

* GRASSÉ, P. 1977. La evolución de lo viviente. H. Blume Ediciones. Madrid. (Traducción de "L'Evolution du vivant", 1975).

* HALDANE, J.B.S. 1957. The estimation of viability. J. Genetics, 54: 294.

* HALL, S.G. 1990. Genetic imprinting: Review and relevance to human diseases. Am. J. Hum. Genet, 46: 857-873.

* HARRISON, R.G. 1937. Embriology and its relations. Science, 85: 369-374.

* HOYLE, A. 1982. Evolution from space. University College Cardiff Press.

* HUET, T. 1990. Genetic organization of a chimpanzee lentivirus related to HIV-1. Nature, 345: 356.

* INDRACCOLO, S.; GUNZBURG, W.M.; LEIBMOSCH, C.; ERFLE, U. & SALMONS, B. 1995. Identification of three human sequences with viral superantigen-specific primers. Mammaliamn Genome, 6: 5.

* KIM, A.; TERZIAN, C.; SANTAMARIA, P.; PELISSON, A.; PURD'HOMME, N. & BUCHETON, A. 1994.
Retroviruses in invertebrates: The Gypsy retrotransposon is apparently an infectious retrovirus of Drosophila melanogaster . Proc. Natl. Acad. Sci. USA., 91 (4): 1285-1289.

* KIM, J.; YU, C.; BAILEY, A.; HARDISON, R. & SHEN, C. 1989. Unique sequence organization and erythroid
cell-specific nuclear factor-binding of mammalian theta-1 globin promoters. Nucleic Acids Res, 17 (14): 5687-5700.

* KORSMEYER, S.J. 1995. Regulators of Cell Death. Trends in Genetics, 11 (3): 101-105.

* KUHN, T. S. 1962. The Structure of Scientific Revolutions. University of Chicago Press.

* LANGER, T.; LU, C.; ECHOLS, H.; FLANAGAN, J.; HAYER, M.K. & ULRICH, F. 1992. Sucessive Action of
DNAK, DNAJ and GroEl Along the Pathway of Chaperone-Mediated Protein Folding. Nature, 356 (6371): 683-689.

* LITMAN, G.W. 1997. Origen de la inmunidad en los vertebrados. Investigación y Ciencia, 244.

* LYDEN, T.W.; JOHNSON, P.M.; MWENDA, J.M.; ROTE, N.S. 1995. Expresion of endogenous HIV-1 crossreactive antigens within normal extravillous trophoblast cells. Journal of Reproductive Inmunology, 28: 3.

* MACKAY, T.F.C. ET AL. 1992. Effects of P-element insertions on quantitative traits in Drosophila melanogaster. Genetics, 130 (2): 315-332.

* MARGULIS, L. & SAGAN, D. 1985. El origen de la célula eucariota. Mundo Científico, 5 (46).

* MARGULIS, L. & SAGAN, D. 1995. What is life?. Simon & Schuster. New York. London.

* MATHIAS, S.L.; SCOTT, A.F.; KAZAZIAN, H.H.; BOEKE, J.D. & GABRIEL, A. 1991. Reverse transcriptase
encoded by a human transponsable elements. Science, 254: 1808-1810.

* MAYR, E. 1966. Animal Species and Evolution. Harvard Univ. Press, Cambridge.

* MAYR, E. 1997. The establishment of evolutionary biology as a discrete biological discipline. BioEssays, 19 (3): 263-266.

* McCLINTOCK, B. 1951. Cold Spring Harbor Symp. Quant. Biol, 16: 13.

* McDONALD, J. & CUTICCHIABA, J. 1993. En "Transposable Elements and Evolution". McDonald, J. (ed). Kluwer.

* MITMAN, G. & FAUSTO-STERLING, A. 1989. Whatever happened to Planaria? C.M. Child and the physiology of inheritance. En "The Right Tool for the Right Job: At Work in Twentieth-Century Life Sciences" (A.E. Clarke & J.H. Fujimura, eds.). Princenton Univ. Press, Princenton.

* MORAN, J.V.; ESKES, R.; KENNELL, J.C.; LAMBOWITZ, A.M.; BUTOW, R.A. & PERLMAN, P.S. 1995. Mobil group II introns of yeast mitochondrial DNA are novel site-specific retroelements. Molecular and Cellular Biology, 15 (5): 2828.

* NEUMANN, B.; KUBICKA, P. & BARLOW, D.P. 1995. Characteristics of imprinted genes. Nature Genetics, 9: 12-13.

* OOSUMI, T.; BELKNAP, W.R. & GARLICK, B. 1995. Mariner transposons in humans. Nature, 378: 672.

* PAUL, D.B. 1988. The selection of survival of the fittest. J. Hist. Biol., 21: 411-424. (Citado por Gilbert et al., 96).

* PREVOSTI, P. 1984. Darwinismo y mendelismo. En "En el Centenario de Mendel: La Genética ayer y hoy." Ed. Alhambra, Madrid.

* RAMPINO, M.R. & STOTHERS, R.B. 1984. Terrestrial mass extinctions, cometary impacts and the sun's motion perpendicular tho the galactic plan. Nature, 308: 709.

* REBEK, J. 1994. A template for life. Chemistry in Britain, 30 (4).

* ROBINS, D. & SAMUELSON, L. 1993. En Transposable Elements and Evolution. McDonald, J. (ed). Kluwer.

* ROUSSET ET AL. 1992. Wolbachia endosymbionts responsible for various alterations of sexuality in arthropods. Proc. R. Soc. Lond. Series B-Biological Sciences, 250 (1328): 91-98.

* RÜBSAMEN-WAIGMANN, H. & DIETRICH, U. 1991. La genealogía de los virus. Mundo Científico, 11(117).

* SANDIN, M. 1995. Lamarck y los mensajeros. La función de los virus en la evolución. Ed. Istmo, Madrid.

* SEIFARTH, W.; SKLANDY, M.; KRIEGSCHNEIDER, F.; REICHERT, A.; MEHLMANN, R. & LEIBMOSCH, C. 1995. Retrovirus-like particles released from the human breast cancer line T47-D display tipe B- and C- related endogenous retroviral secuences. Journal of Virology, 69: 10.

* SEPKOSKI, J. 1993. Fundamentos de la vida en los océanos. En "El libro de la vida". S.J. Gould (ed.). Ed. Crítica, Madrid.

* STANLEY, S. M. 1981. The New Evolutionary Timetable. Simon & Schuster, New York.

* STOYE, J.P. 1997. Proviruses pose potential problems. Nature, 386: 126-127.

* TER-GRIGORIOV, V.S.; KRIFUKS, O.; LINBASHEVSKY, E.; NYSKA, A.; TRAININ, Z. & TODER, V. 1997. A
new transmissible AIDS-like disease in mice induced by alloimmune stimuli. Nature Medicine, 3 (1): 37-41.

* TRISTEM, M.; MYLES, T. & HILL, T. 1995. A highly divergent retroviral secuence in the tuatara (Sphenodon). Virology, 210: 1.

* VARMUS, M.E. 1988. Retroviruses. Science, 240: 1427-1435.

* WEISS, P. 1939. Principles of Development. Holt, New York.

* WELCH, W.J. 1992. Mammalian Stress Reponse: Cell Physiology, Structure/Function of Stress Proteins, and Implications for Medicine and Disease. Physiologycal Reviews, 72: 1063-1081.
viñeta WILKINS, A.S. 1996. Are there "Kuhnian" revolutions in Biology? BioEssays, 18 (9): 695-696.