Polycomb getting its due at Keystone

I didn?t want to give the impression from my last two posts that it?s all RNAi all the time at this year?

By | January 23, 2006

I didn?t want to give the impression from my last two posts that it?s all RNAi all the time at this year?s Keystone Symposium on Epigenetics and Chromatin Remodeling in Development. Polycomb group complex (PgC) proteins, their binding sites, and/or how they set up silencing states in development has been a feature in practically every other talk or poster, here. Not simply a 60-year old vagary of __Drosophila__ development that gave rise to wacky phenotypes, PgCs deserve more respect says Renato Paro of the University of Heidelberg who first cloned the gene more than a decade ago. And with Paro as an organizer of the meeting, Polycomb certainly got it?s due here. Increasingly, research is finding PgCs at work in mammals, including humans, and the homeotic genes they control have a powerful effect on development, and maintenance of cellular state. Keji Zhao of the NHLBI presented a collection of putative human PgC response elements (PREs) uncovered using an algorithm developed for predicting fly PREs. The examples they tested indeed showed PcG-mediated repression, but some folks questioned the logic of using a fly sequencing predicting algorithm for human sequences. And Rudolf Jaenisch discussed the potential for polycomb related genes in maintaining embryonic stem cell pluripotency, along with the usual suspects Sox2, Oct4, and Nanog. He had opened by talking about the power of epigenetic programming to reverse the fate of a cell as in nuclear transplant. Although whether human nuclear transplant to derive stem cell lines is as inefficient as in mice or as efficient as in bovine species (as someone would have had us believe, he joked) is still unclear. With the power to reprogram genomes hidden within the depths of epigenetic programming, he proposed a new goal, to reprogram a skin cell to a neuron or a B cell without the use of an egg. He spoke of the ?controversial? literature on transdifferentiation and said, ?We might at some point be able to do this.? Later, he clarified for me. ?I?ve been very critical of any paper proposing transdifferentiation, and that hasn?t changed.? He says he?s seen no evidence of it to date. But that doesn?t mean it?s not possible. **Other notes:** I did talk to Giacomo Cavalli as per my linkurl:last post;http://www.the-scientist.com/blog/display/23001/ . He reminded me that there?s no direct evidence of RNAi dependent transcriptional silencing going on at his Fab7 PREs (shutting down RNAi genes could have myriad other effects on the cell, of course). But he doesn?t rule out the possibility that increasing the RNA pool could be assisting in silencing the reporter. Kevin Morris noted a bit of overzealousness on my part linkurl:in an earlier post;http://www.the-scientist.com/blog/display/23000/ . He wrote to me that he?s not sure whether dicer and slicer are at work in the silencing he?s observed. ?What we do know is that when you deliver an siRNA targeted to the promoter for either EF1a or HIV-1 that the gene gets silenced and this silencing exhibits a corresponding Histone methyl mark,i.e. H3K9 and H3K27 di and trimethylation, respectively. To date, nobody has published and/or shown to my knowledge that the dicer or slicer complexes are involved.?

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