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First published online 11 February 2009
doi: 10.1242/dev.029363

Development 136, 943-953 (2009)
Published by The Company of Biologists 2009
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MIG-32 and SPAT-3A are PRC1 homologs that control neuronal migration in Caenorhabditis elegans

Ozgur Karakuzu, David P. Wang and Scott Cameron*

Departments of Pediatrics and Molecular Biology, Division of Pediatric Hematology-Oncology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.

* Author for correspondence (e-mail: scott.cameron{at}utsouthwestern.edu)

Accepted 9 January 2009

The Polycomb repression complex 2 (PRC2) methylates histone H3 lysine 27 at target genes to modify gene expression, and this mark is recognized by PRC1, which ubiquitylates histone H2A. In Caenorhabditis elegans, a complex of the MES-2, MES-3 and MES-6 proteins is functionally analogous to the PRC2 complex, but the functional analog of PRC1, and indeed whether C. elegans has such a complex, has been unclear. We describe here that MIG-32 and SPAT-3A are functional analogs of PRC1 in C. elegans, where they are required for neuronal migrations and during vulval development. mig-32 and spat-3 mutants are defective in H2A ubiquitylation, and have nervous system defects that partially overlap with those of mes mutants. However, unlike the mes mutants, mig-32 and spat-3 mutants are fertile, suggesting that PRC1 function is not absolutely required in the germline for essential functions of PRC2.

Key words: BMI-1, C. elegans, Histone modification, Polycomb, Neuronal migration, ring1B


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