( modifications in cancer cells contribu...)Researchers find protein that silences genes

modifications in cancer cells, contributing to tumor growth. And certain blood disorders resulting from defective genes expressed in adults might be alleviated if versions of those same genes that are only expressed very early in development, but are then silenced in adults, could only be turned on again. Though only dreams, at present, these sorts of ideas add to the excitement surrounding the field of epigenetics.

The Big Turn-Off

For many years biologists thought that gene silencing in nucleolar dominance was a result of one set of ribosomal RNA genes being selectively turned on. But in 1997, Pikaard and colleagues found that they could switch on the silent genes using chemicals that inhibit either DNA methylation or histone deacetylation, indicating that turning off one parental set of ribosomal genes was really the secret to nucleolar dominance. In other words, all the factors needed for expression of the genes were in place but somehow the silenced genes were denied access to them. Since that time, Pikaard and his colleagues have been on the hunt for the proteins responsible for keeping the silenced genes off.

In their current paper, published on-line on April 28, 2006, in Genes and Development, and the cover story for the print version of the journal due out May 15, Pikaard and his collaborators describe a systematic effort to examine the 16 predicted histone deacetylases in the genome to see if any play a role in nucleolar dominance. They made transgenic hybrids in which each of the deacetylases were knocked out one by one and then examined the plants to see if there were effects on nucleolar dominance. In this process they found that knocking down HDA6 eliminated nucleolar dominance, such that the normally silent genes were now turned on.

To find out where HDA6 is located in the cell, the group then genetically engineered the protein to include a fluorescent tag and found that much of the HDA6, seen as a glowin
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Source:Washington University in St. Louis

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