Two evolutionary articles

Darwin in Open Access It is now difficult to determine who originally coined the phrase “Darwin, like other little‑read authors…”, but the authorship does not change the essence of the matter. From a scientist who changed the course of science with his ideas, Charles Darwin has become a bronze figure whose actual views interest few. Even specialists most often become acquainted with Darwin’s ideas through texts dissected by “Darwinists” (see “KT” # 645‑646). Now English‑speaking readers with fast internet connections have the opportunity to correct this lamentable situation. Cambridge University has put online the largest archive of Darwin’s manuscripts (50 thousand text pages and 40 thousand images). Over the next two years this archive is expected to double in size. The materials are presented not only as text and PDF files but also as mp3 – download and listen! Imagine being able to visit the described resource’s website (darwin‑online.org.uk) without hassle, read Fleming Jenkin’s review of “On the Origin of Species” (see “KT” #637) and see that most sources describe the “Jenkin nightmare” in a distorted form... [IMG_1] The figure of Charles Darwin (1809–1882), creator of the theory of evolution by natural selection, has provoked, provokes and will provoke controversy But how many really need such an opportunity? Darwin is already known and revered. Staff of the Darwinism department of one of the oldest museums in the post‑Soviet space celebrate on 12 February the professional holiday: Darwin’s birthday. A large plaster bust of the classic is adorned with wreaths, clinked with glasses of various liquids and, at most, not surrounded by folk dances. The department’s employees (all women) claim that no man cares for them like Darwin does. The immortal patron gives them work and sends school groups for paid tours. Against this quasi‑idolatrous veneration, the attacks on Darwin from scientific opponents and ideological adversaries become clearer. Recall, for example, the “scientific creationists”, although even their self‑designation is an oxymoron (a witty nonsense, Greek, a combination of opposite‑meaning words). These witty… people, offering a creed of faith instead of scientific facts, have rallied against Darwin, equating him with all modern evolutionary biology. From their writings one can learn, for instance, that Darwin is responsible for the genocide of World War II. Whatever one says, to argue specifically about Darwin rather than about various interpreters’ conceptions of him, it is still useful to work with primary sources. Science historians also continue to debate Darwin. For example, they are interested in the ethical side of Darwin’s relationship with Alfred Wallace. Recall that the publication of Darwin’s ideas, which had been developing for many years, was accelerated by a letter from Wallace, who was working in the tropics and asked that his manuscript be printed. Darwin told Wallace that their views coincided and published Wallace’s manuscript simultaneously with his own communication… Unfortunately, recent archival research has confirmed that Darwin corrected his own notes, inserting a number of his competitor’s thoughts (later a collaborator and the author of the term “Darwinism”, and this despite Wallace, who held priority on some fundamental questions, having more than sufficient grounds for scientific jealousy). Now anyone can examine the autograph of the so‑called “Long Manuscript” of Darwin. Do you want to determine what is written in blue ink, which the classic used in 1857, and which thoughts were added in black ink in 1858 after seeing Wallace’s manuscript? Then read the notebooks of 1838, 1842, 1844, see how Darwin’s ideas matured, and do not overemphasize the borrowings from Wallace in 1858. [IMG_2] It seems Thomas Huxley (1825–1895) foresaw the creation of the present archive Could the Darwin archive interest anyone besides science historians? Discussing such topics exceeds the scope of a short note, but its author is convinced that Darwin’s ideas will have to be revisited repeatedly by theorists pulling evolutionary theory out of the dead‑end into which it fell in the mid‑20th century. The subject is the so‑called synthetic theory of evolution (STE), a reductionist attempt to marry evolutionary theory with population genetics and to describe all evolution as change in gene frequencies. Consider one terminological subtlety. Contrary to its title, Darwin’s “Origin of Species” is mainly devoted to the study of organismal variability. Darwin distinguished two forms of variability: determinate and indeterminate. Determinate variability develops predictably in response to environmental influence and often proves adaptive. Indeterminate variability is undirected. Open any textbook and you will see that these terms are mentioned only to be radically reinterpreted. Supposedly, determinate variability is phenotypic, non‑heritable variability that holds no value for evolution because it does not affect genes. By contrast, indeterminate, undirected changes are allegedly equivalent to genotypic, hereditary ones. According to STE supporters, these are what drive evolutionary progress. Unfortunately, such reasoning is merely sleight of hand. Determinate changes can substantially alter the nature of transmitted hereditary information. If an organism acquires a useful trait, the underlying basis is less important than the fact that it increases survival and reproductive chances. Predictably occurring, generation after generation, determinate (in Darwin’s sense) changes can preserve the lives of their bearers and steer evolution in a particular direction. What is needed for broad discussion and study of such phenomena? One condition is the elimination of misleading terminology, for which it is useful to become familiar with the history of the question. [IMG_3] Alfred Russel Wallace (1823–1913) managed to express almost the same ideas in a short article that Darwin had been developing for more than twenty years And yet, could anyone in the 21st century still find use for forgotten 19th‑century ideas? Another example. “KT” already wrote (Alexander Markov’s article #582) that the once‑ridiculed “temporal hypothesis of pangénesis” by Darwin suddenly found some confirmation more than a century after his death. Recall that the hypothesis suggested that body cells form special “messengers” that carry information to the germ cells. Recently it became clear that such a mechanism best explains certain aspects of immune information transfer. By the way, Darwin hesitated whether to publish the pangénesis hypothesis and consulted Thomas Huxley, a leading early Darwinist, about it. Huxley judged the hypothesis unsuccessful but advised publishing it: “I will persuade you to abandon it, and then our descendants will rummage through the archives, find our correspondence and say: ‘Look, Darwin anticipated current views, and that donkey Huxley persuaded him not to publish!’…” Will there be statistics on references to Darwin’s legacy? Whatever the outcome, it may disappoint the creators of the electronic archive. Unfortunately, reading Darwin and his contemporaries is often easier than shuffling through a deck of modern myths, biases and projections…   In Search of the Switch‑Operator As is known, context, entrenched stereotypes, and fashion are very important for the perception of new information. A classic example is that what medieval people took for angelic or demonic deeds later became called “intervention of an alien mind.” Scientific news are no exception – each stage of knowledge is characterized by messages that follow a certain template. Nowadays it is rarely heard that a complete genome sequencing of a given species will unlock all its secrets. The genotype is a system of such complexity that one cannot grasp it at a glance. What to do? – Choose an interesting point within it and “pull the thread” at that spot. This logic leads to the formation of a new template for scientific news. Here are some recent reports. Researchers at the University of Massachusetts Amherst found that the formation of sex differences in the mouse brain is linked to a single gene, Bax. Professor Jenny Graves of the Australian National University in Canberra expects that within the next ten million years the human genome will lose the SRY gene located on the Y chromosome. This is the only gene responsible for the development of male gonads and the production of male hormones. Biologists at Rockefeller University in New York discovered that the sense of smell in insects is determined by a single gene, Or83b, which governs the formation of olfactory receptors. Reduced activity of the sole gene BubR1 significantly accelerates mouse aging and shortens lifespan fivefold (results obtained by the Mayo Clinic). Researchers at the Cincinnati Children’s Hospital Medical Center identified the key gene Foxa2, responsible for fetal lung development during pregnancy and the first independent breath a newborn takes after birth. Changing just one gene (IGF‑1) increases muscle strength and endurance in rodents and could be used for genetic doping of athletes. In Australia, professional boxing will be banned for carriers of a single gene, APOE 4, which greatly raises the risk of brain injury. At the Garvan Institute in Sydney, scientists study the mouse gene c‑Cbl, which largely determines obesity and related diseases. Schizophrenia in mice, according to biochemists at the University of Texas Southwestern, is caused not by one but, oddly, by two genes, NPAS1 and NPAS3. To understand the “one‑gene” phenomenon, one must first grasp how development is regulated. The genome is an extremely complex system, and developmental regulation is no less intricate. When dealing with systems of such complexity, their holistic properties, also called emergent (from Latin emergi – to arise), come to the fore. An emergent property of a population of mortal organisms is potential immortality; an emergent property of a cell composed of non‑living molecules is life. An emergent property of the developmental control system is the presence of channeled (from “channel” – a directed path, not from sewage…) developmental trajectories – creodes. For their demonstration, the model proposed by Conrad Hall Waddington is convenient. The embodiment of developmental outcomes is compared in this model to a ball rolling down a complex surface – the epigenetic (epi – above, after) landscape. Creodes correspond to depressions on the epigenetic landscape (see Fig. 1). Any particular creode is virtually never the function of a single gene. A system with a very large number of degrees of freedom self‑organizes, dramatically reducing them at the output. Already in the 1920s Sergey Sergeevich Chetverikov showed that individuals with a normal phenotype are genetically highly diverse. For the overwhelming majority of traits there is no “gene of normality”; normality is defined by the entire genotype. When the formation of a normal phenotype becomes impossible, aberrations (deviations) appear. [IMG_4] 1. A typical genotype with well‑regulated development; the most stable path leads to a normal phenotype Here are some facts that fit the described model but are hard to explain from a gene‑determinist perspective, where genes are the immediate causes of traits. Individuals with identical developmental deviations are genetically diverse (as are normal individuals). Developmental outcomes are influenced not only by hereditary information encoded in nucleic acids but also by other factors: the folding of regulatory proteins, distribution of various substances in the egg, environmental influences, etc. Expression of mutations (genotype changes) in individuals with the same inheritance is highly unstable and ranges from full manifestation to complete absence. Even on opposite sides of a bilaterally symmetric organism, mutations often manifest differently because their development is poorly regulated. External influence on a developing organism can produce an effect equivalent to a mutation. External influence on a mutant organism can ensure the formation of a normal phenotype. [IMG_5] 2. Genotype restructuring made development along one of the aberrant paths probable But do these arguments contradict the link between important traits and a “single gene”? No! Imagine we want to identify which gene is the “cause” of an aberration (Fig. 2). We take relatively homogeneous material (typically a pure mouse line), study variation of different genes and find that none of them shows an effect on the trait of interest. Their involvement is tied to shaping the entire epigenetic landscape. If we manage to find a gene whose alteration shifts the system from state 1 to state 2, we call it the “cause” of the observed result. Yet this gene acted only as a switch, like a railway turnout. [IMG_6] 3. External influence can make development aberrant even with a normal genotype A reader may object. How can this be, when Mendel showed that pea colour (green or yellow) is determined by a single gene – what does all this have to do with it? In Mendel’s experiments stable pea varieties were used, in which the developmental creodes for green and yellow seeds had been fixed (paths were laid to both the “Green Pea” station and the “Yellow Pea” station). In such a situation one gene could act as a switch at the junction of these paths. [IMG_7] 4. External influence can make development normal even with an altered genotype In modern scientific fairy tales about the power of genetic engineering it is often assumed that to transfer a trait from one organism to another it suffices to move the corresponding gene. When dealing with simply determined traits (e.g., the composition of a particular protein), this sometimes works. When dealing with traits defined by the entire genotype (organs, functions), transferring genetic material from the outside contributes little. If you install a switch on the Moscow‑St Petersburg railway line that redirects traffic from Tokyo to Yokohama, passengers will reach neither Tokyo nor Yokohama: at best nothing changes, at worst the train derails. So what is the cause of a particular trait? Oh, we are far from being able to answer this exhaustively! D. Shabanov. Darwin in Open Access // Kompyuterrá, M., 2006. – No. 41 (661). – pp. 19‑20 D. Shabanov. In Search of the Switch‑Operator // Kompyuterrá, M., 2004. – No. 43 (567). – pp. 20‑21

D. Shabanov. Darwin in Open Access // Kompyuterrá, M., 2006. – No. 41 (661). – pp. 19‑20 D. Shabanov. In Search of the Switch‑Operator // Kompyuterrá, M., 2004. – No. 43 (567). – pp. 20‑21