Abstract: The classical view of information flow within a cell, encoded by the famous central dogma of molecular biology, states that the instructions for producing amino acid chains are read from specific segments of DNA, just as computer instructions are read from a tape, transcribed to informationally equivalent RNA molecules, and finally executed by the cellular machinery responsible for synthesizing proteins. While this has always been an oversimplified model that did not account for a multitude of other processes occurring inside the cell, its limitations are today more dramatically apparent than ever. Ironically, in the same years in which researchers accomplished the unprecedented feat of decoding the complete genomes of higher-level organisms, it has become clear that the information stored in DNA is only a small portion of the total, and that the overall picture is much more complex than the one outlined by the dogma.
The cell is, at its core, an information processing machine based on molecular technology, but the variety of types of information it handles, the ways in which they are represented, and the mechanisms that operate on them go far beyond the simple model provided by the dogma. In this chapter we provide an overview of the most important aspects of information processing that can be found in a cell, describing their specific characteristics, their role, and their interconnections. Our goal is to outline, in an intuitive and nontechnical way, several different views of the cell using the language of information theory.
Information Processing at the Cellular Level: Beyond the Dogma
Se a nova teoria geral da evolução que somente será anunciada em 2020 (???) - a SÍNTESE EVOLUTIVA AMPLIADA ou ESTENDIDA não incorporar aspectos da Teoria da Informação, afinal de contas a Biologia do Século 21 é uma ciência de informação, ela será uma teoria científica EPISTEMICAMENTE NATIMORTA.
A INFORMAÇÃO COMPLEXA ESPECIFICADA (ICE) faz parte da TDI.
Fui, nem sei por que, rindo da Nomenklatura científica e da Galera dos meninos e meninas de Darwin: a Biologia é uma ciência de informação. A TDI também! KKKKKK
Metabolite concentrations reflect the physiological states of tissues and cells. However, the role of metabolic changes in species evolution is currently unknown. Here, we present a study of metabolome evolution conducted in three brain regions and two non-neural tissues from humans, chimpanzees, macaque monkeys, and mice based on over 10,000 hydrophilic compounds. While chimpanzee, macaque, and mouse metabolomes diverge following the genetic distances among species, we detect remarkable acceleration of metabolome evolution in human prefrontal cortex and skeletal muscle affecting neural and energy metabolism pathways. These metabolic changes could not be attributed to environmental conditions and were confirmed against the expression of their corresponding enzymes. We further conducted muscle strength tests in humans, chimpanzees, and macaques. The results suggest that, while humans are characterized by superior cognition, their muscular performance might be markedly inferior to that of chimpanzees and macaque monkeys.
Physiological processes that maintain our tissues' functionality involve the generation of multiple products and intermediates known as metabolites—small molecules with a weight of less than 1,500 Daltons. Changes in concentrations of these metabolites are thought to be closely related to changes in phenotype. Here, we assessed concentrations of more than 10,000 metabolites in three brain regions and two non-neural tissues (skeletal muscle and kidney) of humans, chimpanzees, macaque monkeys, and mice using mass spectrometry-based approaches. We found that the evolution of the metabolome largely reflects genetic divergence between species and is not greatly affected by environmental factors. In the human lineage, however, we observed an exceptional acceleration of metabolome evolution in the prefrontal cortical region of the brain and in skeletal muscle. Based on additional behavioral tests, we further show that metabolic changes in human muscle seem to be paralleled by a drastic reduction in muscle strength. The observed rapid metabolic changes in brain and muscle, together with the unique human cognitive skills and low muscle performance, might reflect parallel mechanisms in human evolution.
I argue that Darwinian evolutionary theory has a rhetorical dimension and that rhetorical criticism plays a role in how evolutionary science acquires knowledge. I define what I mean by rhetoric by considering Darwin’s Origin. I use the Modern Evolutionary Synthesis to show how rhetoric conceived as situated and addressed argumentation enters into evolutionary theorizing. Finally, I argue that rhetorical criticism helps judge the success, limits, and failures of these theories.
Outro dia no Facebook troquei ideias com um teísta evolucionista. Ele me chamou de desonesto porque nomeei aqui Francis Collins como criacionista. Uai, Collins se diz teísta evolucionista, e quem advoga essa posição teísta não pode deixar de ser criacionista. Esclareci ao ofendido que não havia desonestidade da minha parte em nomear assim o Collins, pois a Nomenklatura científica o tem nessa categoria. Fui além, informei ao jovem teísta evolucionista que sua posição é considerada pela Nomenklatura científica como péssima teologia e péssima ciência.
Então por que suportam ao Collins et al? Respondi - É porque eles descem o cacete nos criacionistas e na teoria do Design Inteligente. Fora disso, são apenas um incômodo suportado por razões pragmáticas: o seu inimigo é nosso inimigo e somos parceiros aqui.
Outra coisa que reclamou foi de minha retórica. Uai, a retórica faz parte do fazer ciência. Até na elaboração e críticas às teorias científicas. Naquela ocasião eu tinha este artigo em mente, mas não me lembrava onde tinha sido publicado. Como é bom ser vindicado pelos cientistas evolucionistas honestos e abalizados como Depew.
Pano rápido! Que Darwin-Rei está epistemicamente nu no contexto de justificação teórica desde 1859!!!
Lamarck was partially right—and that is good for corals
C. Mark Eakin
- Author Affiliations
Coral Reef Watch, National Oceanic and Atmospheric Administration (NOAA), Center for Satellite Applications and Research, College Park, MD 20740, USA.
Ocean warming is one of the most urgent threats to coral reefs (1–3). Some taxa may migrate in response to changing environmental conditions (4), but corals and other sessile organisms only migrate through larval movement (5). This is viable for coral species with planktonic larvae, but not for the many coral species with crawl-away larvae that cannot migrate far. Adult corals must therefore adapt evolutionarily or acclimate physiologically to survive warming. On page 895 of this issue, Palumbi et al. (6) show that tabletop corals (see the first photo) can both acclimate and adapt to elevated temperatures in American Samoan back-reef pools (see the second photo), where high-temperature extremes are common. If the result holds for other species and locations, it provides hope for coral reefs under global warming.
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NOTA DESTE BLOGGER:
Se Lamarck está 'parcialmente correto' isto significa que Darwin está 'parcialmente errado'. Hum, mas isso este blogger vem dizendo há anos - Darwin acertou no varejo e errou no atacado. É por essa e outras que as especulações transformistas de Darwin não são corroboradas no contexto de justificação teórica e isso demanda, URGENTEMENTE, a revisão ou o descarte de sua teoria da evolução. Ah, mas a Nomenklatura científica já está elaborando uma nova teoria geral da evolução que, para desespero de Darwin e discípulos, não será selecionista, mas incorporará aspectos neo-lamarckistas - a SÍNTESE EVOLUTIVA AMPLIADA ou ESTENDIDA. Todavia, contrariando o fato de que a ciência ABOMINA o vácuo epistemológico, esta nova teoria somente será anunciada em 2020.
Estamos fazendo biologia evolucionária como? Abracadabra? Perlimpimpim? Cartas de tarô? Entranhas de animais???
Pano rápido! Lamarck, você está 'parcialmente correto', e isso significa que Darwin está 'parcialmente errado'... Não resisti. Aliás, não resisto...
On Sexual Reproduction as a New Critique of the Theory of Natural Selection
Academisch Proefschrift ter verkrijging van de graad Doctor aan de Vrije Universiteit Amsterdam, op gezag van de rector magnificus prof. dr. L.M. Bouter, in het openbaar te verdedigen ten overstaan van de promotiecommissie van de Faculteit der Wijsbegeerte op dinsdag 11 december 2012 om 9.45 uur in de aula van de universiteit, De Boelelaan 1105 door JORIS PAUL VAN ROSSUM geboren te Nijmegen
II The Inability of the Theory of Natural Selection to Explain Sexual Reproduction
III An Analysis of Darwinian Attempts to Explain Sexual Reproduction and ‘The Queen of Evolutionary Problems’
Several groups are working to bring back long-dead species, but these efforts could undo some hard-learned lessons, argues Ben Minteer.
14 May 2014
The North American sky, according to historical accounts, was once black with passenger pigeons. Hunters, however, saw to it that the sky was clear of the birds by the second half of the nineteenth century. 'Martha', the last individual of the species, expired in the Cincinnati Zoo in 1914.
Writers have long elegized this vanished bird. The great conservationist-philosopher Aldo Leopold issued the most poignant tribute in his 1949 book A Sand County Almanac: “We grieve,” he wrote, “because no living man will see again the onrushing phalanx of victorious birds, sweeping a path for spring across the March skies, chasing the defeated winter from all the woods and prairies of Wisconsin.”
But what if we could once again see those victorious birds sweeping their path across the March skies?
Leopold could not have known that only a handful of decades after he wrote these words we would be on the verge of a scientific revolution in efforts to reverse the death of species. The 'de-extinction' movement — a prominent group of scientists, futurists and their allies — argues that we no longer have to accept the finality of extinction. By applying techniques such as cloning and genetic engineering, they believe that we can and should return lost species such as the passenger pigeon to the landscape. This is the goal of the San Francisco, California-based Long Now Foundation, which is actively supporting scientific efforts to recreate the lost bird within its 'Revive & Restore' project. But it does not stop there. Scientists in Spain say they are close to cloning the Pyrenean ibex, a mountain goat that took its last breath in 2000. Other species have also been targeted, including the Tasmanian tiger and even the woolly mammoth.
The de-extinction lobby makes persuasive arguments. The most powerful among them appeal to our sense of justice: de-extinction is our opportunity to right past wrongs and to atone for our moral failings. Advocates also point to the sense of wonder that the revival of extinct species could encourage among the public. Although we will always have passenger pigeons in museums and books, “book-pigeons,” Leopold lamented, “cannot dive out of a cloud to make the deer run for cover, nor clap their wings in thunderous applause of mast-laden woods.” De-extinctionists argue further that the revived species will restore lost ecological functions and enhance the diversity of ecosystems.
At the same time, the de-extinction proposal raises considerable concerns. Resuscitated species could create problems in contemporary environments and for native species that have evolved in the absence of the vanished biota. As with the introduction of any species into a new environment, there are risks of disease transmission and biological invasion. Some conservationists also express the fear that, given decades of ecological change and human development, the landscape won't be able to support the revived populations.
The Old and New Testaments of gene regulation: Evolution of multi-subunit RNA polymerases and co-evolution of eukaryote complexity with the RNAP II CTD
Zachary F Burton*
I relate a story of genesis told from the point of view of multi-subunit RNA polymerases (RNAPs) including an Old Testament (core RNAP motifs in all cellular life) and a New Testament (the RNAP II heptad repeat carboxy terminal domain (CTD) and CTD interactome in eukarya). The Old Testament: at their active site, one class of eukaryotic interfering RNAP and ubiquitous multi-subunit RNAPs each have two-double psi β barrel (DPBB) motifs (a distinct pattern for compact 6-β sheet barrels). Between β sheets 2 and 3 of the β subunit type DPBB of all multi-subunit RNAPs is a sandwich barrel hybrid motif (SBHM) that interacts with conserved initiation and elongation factors required to utilize a DNA template. Analysis of RNAP core protein motifs, therefore, indicates that RNAP evolution can be traced from the RNA-protein world to LUCA (the last universal common ancestor) branching to LECA (the last eukaryotic common ancestor) and to the present day, spanning about 4 billion years. The New Testament: in the eukaryotic lineage, I posit that splitting RNAP functions into RNAPs I, II and III and innovations developed around the CTD heptad repeat of RNAP II and the extensive CTD interactome helps to describe how greater structural, cell cycle, epigenetic and signaling complexity co-evolved in eukaryotes relative to eubacteria and archaea.
Por que a linguagem bíblica no título de uma publicação científica com revisão por pares??? Por que colocar a teoria do Design Inteligente - sinais de inteligência são empiricamente detectados na natureza todas as vezes que encontrarmos complexidade irredutível e informação complexa especificada - como criacionismo???
O que é bom em tudo isso? É que a Teoria do Design Inteligente, ainda que classificada erroneamente, aparece mencionada em uma publicação científica
REVIEW ARTICLE Front. Genet., 25 April 2014 | doi: 10.3389/fgene.2014.00087
Epigenetic control of mobile DNA as an interface between experience and genome change
James A. Shapiro*
Department of Biochemistry and Molecular Biology, University of Chicago, Chicago, IL, USA
Mobile DNA in the genome is subject to RNA-targeted epigenetic control. This control regulates the activity of transposons, retrotransposons and genomic proviruses. Many different life history experiences alter the activities of mobile DNA and the expression of genetic loci regulated by nearby insertions. The same experiences induce alterations in epigenetic formatting and lead to trans-generational modifications of genome expression and stability. These observations lead to the hypothesis that epigenetic formatting directed by non-coding RNA provides a molecular interface between life history events and genome alteration.
Biology has a dirty little secret. It's a well-known secret among those who deal with sequenced-genome data intensively, but I suspect many non-biologists are unaware of the problem, which is: Much of the existing genome data (for sequenced genomes, ranging from bacteria to human DNA) is either corrupt or misannotated.
"Junk DNA" probably doesn't exist in living cells. But it certainly exists in published genomes.
A substantial portion of published genome data is suspect, at this point, either because of contamination issues, technical problems surrounding DNA sequencing technology, or faulty gene annotation. An example is the Oryza sativa indica (rice) genome, which inexplicably contains at least 10% of the genome of the bacterium Acidovorax citrulli. There's also a Culex (mosquito) genome with a complete copy of Wolbachia embedded. The genome of Rothia mucilaginosa DY-18 contains over 300 genes incorrectly annotated in antisense orientation (as does the genome of Burkholderia pseudomallei strain 1710b, a truly execrable train-wreck of a genome).
Another example of a genome gone wrong (arguably) is that of the bacterium Ktedonobacter racemifer, which is filled with forward and backward copies of transposases. Incredibly, one in 13 Ktedonobacter genes is a transposase, integrase, or resolvase (and that's not counting the many "hypothetical proteins" with "transposase-like" mentioned in the gene ontology notes). Disregarding the 40% of that organism's genes that are marked as hypothetical proteins, one can say that in Ktedonobacter, one in four genes of known function is a transposase, integrase, or resolvase. (Some of the organism's 4000+ "hypothetical proteins" are actually transposases incorrectly annotated in an antisense orientation.) Common sense says something's amiss.
The "dark matter" problem in microbial genetics is widespread and openly acknowledged. At least 20% 28.3% (according to the Joint Genome Institute) of bacterial genes are annotated as "hypothetical protein," and most of these are so annotated because they have no sequence similarity match to any known protein. In many cases, there's no match because many of the sequences are in the wrong reading frame, or have an improperly located start codon (or other serious issues). When Ely and Scott (PLoS ONE, 2014) manually reannotated the genome of the bacterium Caulobacter crescentus, they identified 11 new genes, modified the start site of 113 genes, changed the reading frame of 38 genes, and found that 112 "hypothetical proteins" were actually non-coding DNA (not genes at all). A recent transcriptome analysis of the archaeon Sulfolobus solfataricus resulted in correction of 162 gene annotations and the addition of 80 new open reading frames. But these numbers barely hint at the extent of gene misannotation. In examining the Gene Ontology database (GOSeqLite), Jones et al. found:
Annotations made without use of sequence similarity based methods (non-ISS) had an estimated error rate of between 13% and 18%. Annotations made with the use of sequence similarity methodology (ISS) had an estimated error rate of 49%.
Surprisingly, the use of sequence similarity as a guide to function identification is less reliable than non-SS methods. This is no doubt partly a reflection of the fact that gene databases contain a great deal of aberrant data. Gene-annotation programs like the widely used Glimmer (Gene Locator and Interpolated Markov Modeler) have to be trained, using a training set. If the training set contains faulty data, it's a classic GIGO situation.
Published online Mar 18, 2014. doi: 10.3389/fpsyg.2014.00226
Conceptual and empirical problems with game theoretic approaches to language evolution
Jeffrey Watumull1,* and Marc D. Hauser2
The importance of game theoretic models to evolutionary theory has been in formulating elegant equations that specify the strategies to be played and the conditions to be satisfied for particular traits to evolve. These models, in conjunction with experimental tests of their predictions, have successfully described and explained the costs and benefits of varying strategies and the dynamics for establishing equilibria in a number of evolutionary scenarios, including especially cooperation, mating, and aggression. Over the past decade or so, game theory has been applied to model the evolution of language. In contrast to the aforementioned scenarios, however, we argue that these models are problematic due to conceptual confusions and empirical difficiences. In particular, these models conflate the comptutations and representations of our language faculty (mechanism) with its utility in communication (function); model languages as having different fitness functions for which there is no evidence; depend on assumptions for the starting state of the system, thereby begging the question of how these systems evolved; and to date, have generated no empirical studies at all. Game theoretic models of language evolution have therefore failed to advance how or why language evolved, or why it has the particular representations and computations that it does. We conclude with some brief suggestions for how this situation might be ameliorated, enabling this important theoretical tool to make substantive empirical contributions.
Keywords: language evolution, evolutionary game theory, communication, universal grammar, models, theoretical
Marc D. Hauser1*, Charles Yang2, Robert C. Berwick3, Ian Tattersall4, Michael Ryan5, Jeffrey Watumull6, Noam Chomsky3 and Richard Lewontin7
1Risk-Eraser, LLC, USA
2University of Pennsylvania, USA
4American Museum of Natural History, USA
5University of Texas, Austin, USA
6Cambridge University, United Kingdom
7Harvard University, USA
Understanding the evolution of language requires evidence regarding origins and processes that led to change. In the last 40 years, there has been an explosion of research on this problem as well as a sense that considerable progress has been made. We argue instead that the richness of ideas is accompanied by a poverty of evidence, with essentially no explanation of how and why our linguistic computations and representations evolved. We show that, to date, 1) studies of nonhuman animals provide virtually no relevant parallels to human linguistic communication, and none to the underlying biological capacity; 2) the fossil and archaeological evidence does not inform our understanding of the computations and representations of our earliest ancestors, leaving details of origins and selective pressure unresolved; 3) our understanding of the genetics of language is so impoverished that there is little hope of connecting genes to linguistic processes any time soon; 4) all modeling attempts have made unfounded assumptions, and have provided no empirical tests, thus leaving any insights into language’s origins unverifiable. Based on the current state of evidence, we submit that the most fundamental questions about the origins and evolution of our linguistic capacity remain as mysterious as ever, with considerable uncertainty about the discovery of either relevant or conclusive evidence that can adjudicate among the many open hypotheses. We conclude by presenting some suggestions about possible paths forward.
Talk by the NIH Director - Francis S. Collins, MD, PHD
Genomics, Advanced Technology, and the Future of Medicine
The São Paulo Research Foundation, FAPESP, and National Institutes of Health - NIH, invite to
Talk by the NIH Director - Francis S. Collins, MD, PHD
Genomics, Advanced Technology, and the Future of Medicine
Dr. Collins is a physician-geneticist noted for his landmark discoveries of disease genes and his leadership of the international Human Genome Project, which culminated in April 2003 with the completion of a finished sequence of the human DNA instruction book. He served as director of the National Human Genome Research Institute at the NIH from 1993-2008.
Before coming to the NIH, Dr. Collins was a Howard Hughes Medical Institute investigator at the University of Michigan. He is an elected member of the Institute of Medicine and the National Academy of Sciences, was awarded the Presidential Medal of Freedom in November 2007, and received the National Medal of Science in 2009.
Venue: FAPESP - Rua Pio XI, 1500 - Lapa - São Paulo
Date: May, 22nd 2014
Time: 9:30 to 10:30
The conference will be given in English with simultaneous translation
Drawing on startling new evidence from the mapping of the genome, an explosive new account of the genetic basis of race and its role in the human story
Fewer ideas have been more toxic or harmful than the idea of the biological reality of race, and with it the idea that humans of different races are biologically different from one another. For this understandable reason, the idea has been banished from polite academic conversation. Arguing that race is more than just a social construct can get a scholar run out of town, or at least off campus, on a rail. Human evolution, the consensus view insists, ended in prehistory.
Inconveniently, as Nicholas Wade argues in A Troublesome Inheritance, the consensus view cannot be right. And in fact, we know that populations have changed in the past few thousand years—to be lactose tolerant, for example, and to survive at high altitudes. Race is not a bright-line distinction; by definition it means that the more human populations are kept apart, the more they evolve their own distinct traits under the selective pressure known as Darwinian evolution. For many thousands of years, most human populations stayed where they were and grew distinct, not just in outward appearance but in deeper senses as well.
Wade, the longtime journalist covering genetic advances for The New York Times, draws widely on the work of scientists who have made crucial breakthroughs in establishing the reality of recent human evolution. The most provocative claims in this book involve the genetic basis of human social habits. What we might call middle-class social traits—thrift, docility, nonviolence—have been slowly but surely inculcated genetically within agrarian societies, Wade argues. These “values” obviously had a strong cultural component, but Wade points to evidence that agrarian societies evolved away from hunter-gatherer societies in some crucial respects. Also controversial are his findings regarding the genetic basis of traits we associate with intelligence, such as literacy and numeracy, in certain ethnic populations, including the Chinese and Ashkenazi Jews.
Wade believes deeply in the fundamental equality of all human peoples. He also believes that science is best served by pursuing the truth without fear, and if his mission to arrive at a coherent summa of what the new genetic science does and does not tell us about race and human history leads straight into a minefield, then so be it. This will not be the last word on the subject, but it will begin a powerful and overdue conversation.
The great break in the organic chain between man and his nearest allies, which cannot be bridged over by any extinct or living species, has often been advanced as a grave objection to the belief that man is descended from some lower form; but this objection will not appear of much weight to those who, from general reasons, believe in the general principle of evolution. Breaks often occur in all parts of the series, some being wide, sharp and defined, others less so in various degrees; as between the orang and its nearest allies—between the Tarsius and the other Lemuridae between the elephant, and in a more striking manner between the Ornithorhynchus or Echidna, and all other mammals. But these breaks depend merely on the number of related forms which have become extinct. At some future period, not very distant as measured by centuries, the civilised races of man will almost certainly exterminate, and replace, the savage races throughout the world. At the same time the anthropomorphous apes, as Professor Schaaffhausen has remarked, will no doubt be exterminated. The break between man and his nearest allies will then be wider, for it will intervene between man in a more civilised state, as we may hope, even than the Caucasian, and some ape as low as a baboon, instead of as now between the negro or Australian and the gorilla.
Charles Darwin, in The Descent of Man, 24 fevereiro de 1871
"...Em algum futuro período, não muito distante sendo medido por séculos, as raças civilizadas de homem irão quase certamente exterminar, e substituir, as raças selvagens por todo o mundo. ...O rompimento entre o homem e os seus aliados mais próximos será então mais amplo, pois irá intervir entre o homem num estado mais civilizado, como nós podemos esperar, mesmo do que o Caucasiano, e algum macaco tão inferior quanto o babuíno, em vez de como agora entre o negro ou o Australiano e o gorila".
Today, DNA is central to modern biology, but scarcely a century ago biologists were debating whether or not genes actually existed. In his 1909 textbook on heredity, Danish botanist Wilhelm Johannsen coined the term gene to refer to that hereditary “something” that influences the traits of an organism, but without making a commitment to any hypothesis about what that “something” was. Just over a decade later, a prominent biologist could still note that some people viewed genes as “a convenient fiction or algebraic symbolism.”
As the century progressed, biologists came to see genes as real physical objects. They discovered that genes have a definite size, that they are linearly arrayed on chromosomes, that individual genes are responsible for specific chemical events in the cell, and that they are made of DNA and written in the language of the Genetic Code. By the time the Human Genome Project was initiated in 1988, researchers knew that a gene was a segment of DNA with a clear beginning and end and that it acted by directing the production of a particular enzyme or other molecule that did a specific job in the cell. As real things, genes are countable, and in 1999 biologists estimated that humans had “80,000 or so” of them.
Yet, when the dust from the Human Genome Project cleared, we didn’t havenearly as many genes as we thought. By the latest count, we have 20,805 conventional genes that encode enzymes and other proteins. Our inflated gene count, though, wasn’t the only casualty of the Human Genome Project. The very idea of a gene as a well-defined segment of DNA with a clear functional role has also taken a hit, and as a result, our understanding of our relationship with our genes is changing.
One major challenge to the concept of a gene is the growing evidence that many genes are shapeshifters. Instead of a well-defined segment of DNA that encodes a single protein with a clear function, we should view a gene as “a polyfunctional entity that assumes different forms under different cellular states,” according to University of Washington biologist John Stamatoyannopoulos. While researchers have long known that genes are made up of discrete subunits called “exons,” they hadn’t realized until recently the degree to which exons are assembled—like Legos—into sometimes thousands of different combinations. With new technologies, biologists are cataloging these various combinations, but in most cases they don’t know whether those combinations all serve the same function, different functions, or no function at all.
Por que sou ‘pós-darwinista’? Porque já fui evolucionista de carteirinha. Hoje, sou cético da teoria macroevolutiva como verdade científica. Contudo, meu ceticismo ao ‘dogma central’ darwinista não é baseado em relatos da criação de textos sagrados. Foi a séria e conflituosa consideração do debate que ocorre intramuros e nas publicações científicas há muitos anos sobre a insuficiência epistêmica da teoria geral da evolução. Eu fui ateu marxista-leninista. Hoje, não tenho mais fé cega no ateísmo. Não creio mais na interpretação literal dos dogmas de Darwin aceitos ‘a priori’ e defendidos ideologicamente com unhas e dentes pela Nomenklatura científica. A Ciência me deu esta convicção. Aprendi na universidade: quando uma teoria científica não é apoiada pelas evidências, ela deve ser revista ou simplesmente descartada. Sou pós-darwinista me antecipando à iminente e eminente ruptura paradigmática em biologia evolutiva. Chegou a hora de dizer adeus a Darwin. Mestre em História da Ciência – PUC-SP. CV Plataforma Lattes: http://lattes.cnpq.br/6602620537249723