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Cancer scientists determine mechanism of 1 of the most powerful tumor-suppressor proteins, Chd5
Date:1/10/2013

that help to "express" them. Broadly speaking, tightly bundled chromatin is inaccessible to the gene-expression machinery, causing genes located in a given bundle to be shut off. The reverse is true of loosely packed chromatin.

The CSHL team's new finding involves Chd5's role in another process through which chromatin can be shaped and modified. Namely, via reading molecular groups on chromatin that effectively flag parts of its structure, a process called epigenetic marking.

Mills explains: "Our new work demonstrates that the Chd5 protein can activate the tumor-suppressive network when a portion of its structure (called PHD domains) bind to histone H3, one of the five histone proteins that make up the main structure of chromatin. Importantly, we found that this binding occurs specifically when the tail-like portion of histone H3 is what we call 'naked' that is, free of any epigenetic marks."

The team showed in living mice that when the gene that expresses Chd5 is mutated, yielding a protein that cannot bind the H3 histone, Chd5's usual tumor-suppressive effects do not occur; it no longer inhibits proliferation, thereby setting the stage for cancer initiation. The cancer used as a model for this part of the work was human neuroblastoma.

The team reported other details of the mechanism behind Chd5's tumor suppression, revealing how the interaction of Chd5 and naked H3 histones orchestrates programs that prevent cancer, mainly by binding to genes and affecting their "on" vs. "off" state.

"It is likely that Chd5's multi-faceted ways of enforcing tumor suppression will prove useful for regulating diverse types of cancers, including cancers with many different combinations of genetic lesions," Mills says.


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Contact: Peter Tarr
tarr@cshl.edu
516-367-8455
Cold Spring Harbor Laboratory
Source:Eurekalert

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