Nurit Ballas, Ph.D. Research Associate Professor Department of Biochemistry and Cell Biology Life Sciences Building Stony Brook University Stony Brook, NY 11794-5215 Office telephone: 631-632-1572 Fax: 631-632-8575 E-mail: nballas@notes.cc.sunysb.edu

Research description:

My lab is focused on two projects:

1. Identifying the roles of the transcriptional repressor REST and its corepressor CoREST throughout neural development. The RE1 silencing transcription factor, REST, is a master regulator of a large network of genes involved in acquisition of neural fate, including neuronal, proneural, and brain specific microRNA genes. Our recent studies show that REST, and its corepressor CoREST, play important roles in mediating repression and chromatin plasticity in stem cells. In addition, our data show that REST is regulated differentially during different stages of neural development, pointing to the significance of regulation of REST itself in maintaining and progressing to different lineages. Our research aims to identify the roles of REST and CoREST in maintaining stem cell identity and progressing into different neural lineages, using gain- and loss-of-function approaches, in vitro and in vivo.
2. The contribution of MeCP2-null glia to the neuropathology of Rett Syndrome. Patients afflicted with the neurodevelopmental disorder Rett Syndrome (RTT) have mutations in the gene encoding the methyl-CpG binding protein 2, MeCP2. Why mutations in MeCP2 cause RTT, and why the central nervous system preferentially is affected, is unknown. Previous studies have focused on MeCP2 function in neurons because of the prevailing view that glia do not express MeCP2. We found not only that glia express MeCP2, but cultured astroglia isolated from MeCP2-deficient (RTT) mice, or their conditioned medium, confer aberrant morphology on wild type (WT) neurons that is similar to that seen in human patients. We will continue to characterize the aberrant neuronal morphology caused by MeCP2-null glia and aim to identify the aberrantly secreted factors by the mutant glia.

Related publications:

• Ballas, N., Battaglioli, E., Atouf, F., Andres, M.E., Chenoweth, J., Anderson, M.E., Burger, C., Moniwa, M., Davie, J.R., Bowers, W.J., Federoff, H.J., Rose D., Rosenfeld M. G., Brehm P., and Mandel, G. (2001) Regulation of neuronal traits by a novel transcriptional complex. Neuron 31, 353-365.
• Ballas, N., Grunseich, C., Lu, D.D., Speh, J.C., and Mandel, G. (2005) REST and its corepressors mediate plasticity of neuronal gene chromatin throughout neurogenesis. Cell 121, 645-657.
• Ballas, N. and Mandel, G. (2005) The many faces of REST oversee epigenetic epigenetic programming of neuronal genes. Curr. Opin. Neurobiol. 15, 500-506.
• Ballas, N., Grunseich, C., Lioy, D., and Mandel, G. (2008) MeCP2-Dysfunction in Glia Contributes to the Neurodevelopmental Disorder Rett Syndrome. Nature Neuroscince  In submission.

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