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Date:2/4/2013

er is placed across the genome. Changes in such signals are likely to play a role in the generation of disease, including cancers.

Next, the researchers sought to determine how the 5hmc signal is read. "We must understand what 5hmC is doing in normal cells," says Kriaucionis. "Understanding that will help us trace the process by which genes are incorrectly expressed in disease." The researchers discovered that a molecule known as methyl-CpG-binding protein (MeCP2), which binds 5mC, also binds 5hmC in the cells they studied. Mutations in this protein are known to contribute to Rett Syndrome, a developmental disorder that varies in severity depending on how precisely MeCP2 has been altered. Most importantly one of those mutant MeCP2 proteins was capable of binding 5mC, but not 5hmC. That mutant is known to cause relatively less severe cognitive and speech deficits in Rett patients.

Finally, investigators show in their paper that MeCP2 binding to 5hmC drives gene expression by making DNA more accessible to the molecular machinery that decodes genetic informationwhile its association with 5mC has the opposite effect. Though the current study focused on healthy mouse neural tissue, the unraveling of 5hmC's tangled role in genome expression is likely to be of value to cancer research. Other researchers have shown that 5hmC is highly depleted in several cancers, including the blood cancer acute myeloid leukemia and the blood disorder myelodysplastic syndrome, which can progress to cancer. This depletion is accompanied by the disruption of a tumor suppressor gene named TET2, which encodes a protein that creates the 5hmC signal on DNA.

Kriaucionis's lab is now assessing what role 5hmC plays in the development of different types of blood cells, with the aim of deciphering how its loss contributes to the generation of blood cancers.


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Contact: Rachel Steinhardt
rsteinhardt@licr.org
212-450-1582
Ludwig Institute for Cancer Research
Source:Eurekalert

Page: 1 2 3

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