Non-adaptive origins of interactome complexity
Ariel Fernández 1,2 & Michael Lynch 3
The boundaries between prokaryotes, unicellular eukaryotes and multicellular eukaryotes are accompanied by orders-of-magnitude reductions in effective population size, with concurrent amplifications of the effects of random genetic drift and mutation 1 . The resultant decline in the efficiency of selection seems to be sufficient to influence a wide range of attributes at the genomic level in a nonadaptive manner 2. A key remaining question concerns the extent to which variation in the power of random genetic drift is capable of influencing phylogenetic diversity at the subcellular and cellular levels 2–4. Should this be the case, population size would have to beconsidered as a potential determinant of the mechanistic pathways underlying long-term phenotypic evolution. Here we demonstrate a phylogenetically broad inverse relation between the power of drift and the structural integrity of protein subunits. This leads to the hypothesis that the accumulation of mildly deleterious mutations in populations of small size induces secondary selection for protein–protein interactions that stabilize key gene functions. By this means, the complex protein architectures and interactions essential to the genesis of phenotypic diversity may initially emerge by non-adaptive mechanisms.
+++++
FREE PDF GRATIS
+++++
+++++
NOTA CAUSTICANTE DESTE BLOGGER:
Aqui Fernández e Lynch demonstraram o que as proteínas podem fazer sem a seleção natural - elas podem conduzir a vida para um nível mais complexo. E cabe aqui fazer uma pergunta científica que não é feita e nem permitem fazer nos cursos de Biologia das universidades públicas e privadas:
E o que pode a seleção natural fazer sem as proteínas? NADA, NIHIL, ZERO, capice!!!
E o que pode a seleção natural fazer sem as proteínas? NADA, NIHIL, ZERO, capice!!!
Eita teoria científica mais furada do que queijo suíço!!!
