Quanta falsidade. As razões eram outras e eu só descobri depois que fui fazer mestrado em História da Ciência justamente sobre Darwin e um dos seus críticos científicos: St. George Jackson Mivart.
A recomendação para ler a 1a. edição é evitar que se torne conhecido duas coisas: a oposição à teoria da evolução de Darwin se deu também no meio científico, e o pensamento de Darwin sobre a seleção natural 'evoluiu' tanto a ponto dele defender posições lamarckistas na 6a. edição.
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Inefficient Selection: New Evolutionary Mechanism Accounts For Some Of Human Biological Complexity
ScienceDaily (Nov. 3, 2009) — A painstaking analysis of thousands of genes and the proteins they encode shows that human beings are biologically complex, at least in part, because of the way humans evolved to cope with redundancies arising from duplicate genes.
"We have found a specific evolutionary mechanism to account for a portion of the intricate biological complexity of our species," said Ariel Fernandez, professor of bioengineering at Rice University. "It is a coping mechanism, a process that enables us to deal with the fitness consequences of inefficient selection. It enables some of our proteins to become more specialized over time, and in turn makes us more complex."
Genomic and proteomic analysis has found a new evolutionary mechanism that accounts for some of the biological complexity of human beings. (Credit: iStockphoto/Liang Zhang)
Fernandez is the lead author of a paper slated to appear in the December issue of the journal Genome Research. The research is available online now.
Fernandez said the study drew from previous findings by his own research group and from seminal work of Michael Lynch, Distinguished Professor of Biology at Indiana University and a recently elected a fellow of the National Academy of Science. Lynch's work has shown that natural selection is less efficient in humans as compared with simpler creatures like bacteria. This "selection inefficiency" arises from the smaller population size of humans as compared with unicellular organisms.
"In all organisms, genes get duplicated every so often, for reasons we don't fully understand," Fernandez said. "When working efficiently, natural selection eliminates many of these duplicates, which are called 'paralogs.' In our earlier work, we saw that an unusual number of gene duplicates had survived in the human genome, which makes sense given selection inefficiency in humans."
In prior research on protein structure, Fernandez's team found that some proteins are packaged more poorly than others. Moreover, they found that the least-efficiently packed proteins are structurally stable only when they bind with partner proteins to form complexes.
"These poorly packed proteins are potential troublemakers when gene duplication occurs," Fernandez said. "The paralog encodes more copies of the protein than the body needs. This is called a 'dosage imbalance,' and it can make us sick. For instance, dosage imbalance has been implicated in Alzheimer's and other diseases."
Given selection inefficiency, Fernandez knew that paralogs encoding poorly packed proteins could remain in the human genome for quite a while. So he and graduate student Jianpeng Chen decided to examine whether gene duplicates had remained in the genome long enough for random genetic mutations to affect the paralogs dissimilarly. Fernandez and Chen, now a senior researcher in Beijing, China, cross-analyzed databases on genomics, protein structure, microRNA regulation and protein expression in such troublesome paralogs.
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Read more here/Leia mais aqui.
Journal reference:
Ariel Fernández, Jianping Chen. Human capacitance to dosage imbalance: Coping with inefficient selection. Genome Research, 2009; DOI: 10.1101/gr.094441.109
Adapted from materials provided by Rice University.
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Human capacitance to dosage imbalance: Coping with inefficient selection
Ariel Fernández1 and Jianping Chen
+ Author Affiliations
Department of Bioengineering, Rice University, Houston, Texas 77005, USA
Abstract
Proteins rely on associations to improve packing quality and thus maintain structural integrity. This makes packing deficiency a likely determinant of dosage sensitivity, that is, of the fitness impact of concentration imbalances relative to the stoichiometry of the protein complexes. This hypothesis was validated by examining evolution-related dosage imbalances: Duplicates of genes encoding for deficiently packed proteins are less likely to be retained than genes coding for well-packed proteins. This selection pressure is apparent in unicellular organisms, but is mitigated in higher eukaryotes. In human, this effect reveals a capacitance toward dosage imbalance. This capacitance is not expected in organisms with larger population size, where evolutionary forces are more efficient at promoting adaptive functional innovation and purifying selection, thus curbing the concentration imbalance arising from gene duplication. By examining miRNA target dissimilarities within human gene families, we show that the capacitance is operative at a post-transcriptional regulatory level: The higher the packing deficiency of a protein, the more likely that its paralogs will be dissimilarly targeted by miRNA to mitigate dosage imbalance. For families with low capacitance, paralog sequence divergence and family size correlate tightly with packing deficiency, just like in unicellular eukaryotes. Thus, a major component of human tolerance toward dosage imbalances is rooted in the paralog-discriminating capacity of miRNA regulation. The results may clarify the evolutionary etiology of aggregation-related diseases, since aggregation is often promoted by overexpression (a dosage imbalance) and aggregation propensity is associated with extreme packing deficiency.
Footnotes
↵1 Corresponding author.
E-mail arifer@rice.edu; fax 713 348 3699.
[Supplemental material is available online at http://www.genome.org.]
Article published online before print. Article and publication date are at http://www.genome.org/cgi/doi/10.1101/gr.094441.109.
Received March 29, 2009.
Accepted September 30, 2009.
Copyright © 2009 by Cold Spring Harbor Laboratory Press
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Professores, pesquisadores e alunos de universidades públicas e privadas com acesso ao site CAPES/Periódicos podem ler gratuitamente este artigo da Genome Research e de outras publicações científicas.
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UM PARÁGRAFO INTERESSANTE:
"Even more specialized proteins are needed to maintain and regulate them. This complexity requires that the duplicates of the original jack-of-all-trades gene be retained, but this does not happen unless selection is inefficient. This is frequently a point of contention between proponents of evolution and intelligent design."
