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CSHL researchers map changing epigenetic modifications that enable transposons to run amok
Date:12/10/2008

hat in immortalized cells -- cells that are coaxed to grow endlessly in culture dishes -- the epigenetic changes resulting in a loss of heterochromatin and transposon "re-activation" are not due to a loss of the proteins that regulate heterochromatin. Instead, they find that the epigenetic modifications are due to a change in the population of siRNAs produced in the continuously dividing cells. When this occurs in the vicinity of genes, this epigenetic control can have important consequences for the organism. According to Martienssen, "our work implicates RNAi in epigenetic chromatin changes that occur in immortalized cells."

Epigenetic "restructuring" by siRNA

The CSHL researchers find that transposons that have lost heterochromatic marks are no longer associated with siRNA that are 24 nucleotides, or RNA "letters," in length. Rather, these re-activated transposons become associated with siRNAs that are 21nucleotides in length. In contrast, the transposons that retain their original heterochromatic marks and therefore remain silent continue to stay associated with 24-nucleotide siRNAs.

The team's eventual goal is to understand the mechanism responsible for the creation of epialleles epigenetic variations in gene expression patterns that stem from the creation of particular chromatin states. These predispose particular genes to become active when they shouldn't be and shut off the activity of genes that are essential. The team's epigenetic profiling study now implicates siRNA-driven heterochromatin restructuring as a mechanism that might lead to epiallele formation.


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Contact: Hema Bashyam
bashyam@cshl.edu
516-367-6822
Cold Spring Harbor Laboratory
Source:Eurekalert

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