Drosophila Piwi functions in Hsp90-mediated suppression of phenotypic variation
Vamsi K Gangaraju, Hang Yin, Molly M Weiner, Jianquan Wang, Xiao A Huang & Haifan Lin
Nature Genetics (2010) doi:10.1038/ng.743
It’s somehow stupid the way this kind of papers are presented in press releases. I grabbed this references from physorg.com, where the heading goes like that:
For decades, biology textbooks have been clear – our traits are the product of our genes. But a new study by Yale University researchers published Dec. 26 in Nature Genetics suggests another mechanism can regulate variations of traits even in genetically identical individuals.
Somewhere in the text is hidden:
Genes do play a role in protecting against harmful variations but probably work through actions of the molecules piRNA and Hsp-90.
Yeah, right, that’s really news! Genes play a role through their encoded products…
If you go and read the whole stuff, and hopefully the paper, you aren’t really overwhelmed by new evidence that genes act through their products, but the paper is excellent: this is an original mechanism of genetic expression regulation and it’s fun to read about it. But, the way it’s presented call for IDiots to read it superficially and draw conclusions that are somehow IDiotic:
It’s getting more and more difficult for those who cling to evolution to escape the facts.
The whole DNA system and now even some extraneous factors are designed to PROTECT against harmful mutations. Just about any random, unspecified mutation is either useless or harmful. There are very few random mutations that are actually good. This is not to be confused with the switching on or off of already existing genes which would in most cases be the source for speciation.
Tiring, isn’t it?
Canalization, also known as developmental robustness, describes an organism’s ability to produce the same phenotype despite genotypic variations and environmental influences. In Drosophila, Hsp90, the trithorax-group proteins and transposon silencing have been previously implicated in canalization. Despite this, the molecular mechanism underlying canalization remains elusive. Here using a Drosophila eye-outgrowth assay sensitized by the dominant Krirregular facets-1(KrIf-1) allele3 we show that the Piwi-interacting RNA (piRNA) pathway, but not the short interfering RNA or micro RNA pathway, is involved in canalization. Furthermore, we isolated a protein complex composed of Hsp90, Piwi and Hop, the Hsp70/Hsp90 organizing protein homolog, and we demonstrated the function of this complex in canalization. Our data indicate that Hsp90 and Hop regulate the piRNA pathway through Piwi to mediate canalization. Moreover, they point to epigenetic silencing of the expression of existing genetic variants and the suppression of transposon-induced new genetic variation as two major mechanisms underlying piRNA pathway-mediated canalization.