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The Journal of Neuroscience, August 11, 2004, 24(32):7186-7193; doi:10.1523/JNEUROSCI.0238-04.2004

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Development/Plasticity/Repair
A Conserved Role But Different Partners for the Transcriptional Corepressor CoREST in Fly and Mammalian Nervous System Formation

Julia E. Dallman,^1,2 Janet Allopenna,^1,2 Andrew Bassett,³ Andrew Travers,³ and Gail Mandel^1,2

¹Howard Hughes Medical Institute, ²Department of Neurobiology and Behavior, State University of New York, Stony Brook, Stony Brook, New York 11794, and ³Medical Research Council Laboratory of Molecular Biology, Cambridge CB2 2QH, United Kingdom

Identification of conserved proteins that act to establish the neuronal phenotype has relied predominantly on structural homologies of the underlying genes. In the case of the repressor element 1 silencing transcription factor (REST), a central player in blocking the neuronal phenotype in vertebrate non-neural tissue, the invertebrate homolog is absent, raising the possibility that distinct strategies are used to establish the CNS of invertebrates. Using a yeast two-hybrid screen designed specifically to identify functional analogs of REST, we show that Drosophila melanogaster uses a strategy that is functionally similar to, but appears to have evolved independently of, REST. The gene at the center of the strategy in flies encodes the repressor Tramtrack88 (Ttk88), a protein with no discernable homology to REST but that nonetheless is able to interact with the same transcriptional partners. Ttk88 uses the REST corepressor Drosophila CoREST to coordinately regulate a set of genes encoding the same neuronal hallmarks that are regulated by REST in vertebrates. Our findings indicate that repression is an important mechanism for regulating neuronal phenotype across phyla and suggest that co-option of a similar corepressor complex occurred to restrict expression of genes critical for neuronal function to a compartmentalized nervous system.

Key words: CoREST; Tramtrack; REST; repression; CNS; corepressor

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Received Jan 21, 2004; revised June 11, 2004; accepted June 29, 2004.

This article has been cited by other articles:

				P. K. Bajpe, J. A. van der Knaap, J. A. A. Demmers, K. Bezstarosti, A. Bassett, H. M. M. van Beusekom, A. A. Travers, and C. P. Verrijzer Deubiquitylating Enzyme UBP64 Controls Cell Fate through Stabilization of the Transcriptional Repressor Tramtrack Mol. Cell. Biol., March 1, 2008; 28(5): 1606 - 1615. [Abstract] [Full Text] [PDF]

				S. E. Cooper, C. M. Murawsky, N. Lowe, and A. A. Travers Two Modes of Degradation of the Tramtrack Transcription Factors by Siah Homologues J. Biol. Chem., January 11, 2008; 283(2): 1076 - 1083. [Abstract] [Full Text] [PDF]

				J. Visvanathan, S. Lee, B. Lee, J. W. Lee, and S.-K. Lee The microRNA miR-124 antagonizes the anti-neural REST/SCP1 pathway during embryonic CNS development Genes & Dev., April 1, 2007; 21(7): 744 - 749. [Abstract] [Full Text] [PDF]

				A. Mortazavi, E. C. L. Thompson, S. T. Garcia, R. M. Myers, and B. Wold Comparative genomics modeling of the NRSF/REST repressor network: From single conserved sites to genome-wide repertoire Genome Res., October 1, 2006; 16(10): 1208 - 1221. [Abstract] [Full Text] [PDF]

				C. Conaco, S. Otto, J.-J. Han, and G. Mandel Reciprocal actions of REST and a microRNA promote neuronal identity PNAS, February 14, 2006; 103(7): 2422 - 2427. [Abstract] [Full Text] [PDF]

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