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MBC in Press, published online ahead of print March 23, 2005
Mol. Biol. Cell 10.1091/mbc.E04-12-1062

A more recent version of this article appeared on June 1, 2005
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Submitted on December 10, 2004
Revised on March 7, 2005
Accepted on March 14, 2005

SUMO Modification Represses Transcriptional Activity of the Drosophila SoxNeuro and Human Sox3 Central Nervous System Specific Transcription Factors

Jean Savare, Nathalie Bonneaud, and Franck Girard

Institut de Génétique Humaine, Centre National de la Recherche Scientifique, 34396 Montpellier, France

Monitoring Editor: Marianne Bronner-Fraser

Sox transcription factors are involved in the development of CNS in all metazoans. Little is known on the molecular mechanisms that regulate their transcriptional activity. Covalent posttranslational modification by SUMO (small ubiquitin like modifier) regulates several nuclear events, including the transcriptional activity of transcription factors. Here we demonstrate that SoxNeuro, an HMG box containing transcription factor involved in neuroblast formation in Drosophila, is a substrate for SUMO modification. SUMOylation assays in Hela cells and Drosophila S2 cells reveal that Lysine 439 is the major SUMO acceptor site. The sequence in SoxNeuro targeted for SUMOylation, IKSE, is part of a small inhibitory domain, able to repress in cis the activity of two adjacent transcriptional activation domains. Our data show that SUMO modification represses SoxNeuro transcriptional activity in transfected cells. Overexpression in Drosophila embryos of a SoxN form that cannot be targeted for SUMOylation strongly impairs the development of the CNS, suggesting that SUMO modification of SoxN is crucial for regulating its activity in vivo. Finally, we present evidence that SUMO modification of group B1 Sox factors was conserved during evolution, as Sox3, the human counterpart of SoxN, is also negatively regulated through SUMO modification.

Address correspondence to: Franck Girard (fgirard{at}igh.cnrs.fr)




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