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Journal Article

The non-redundant function of cohesin acetyltransferase Esco2: some answers and new questions.

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Whelan,  G.
Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society;

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Eichele,  G.
Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society;

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Citation

Whelan, G., Kreidl, E., Peters, J. M., & Eichele, G. (2012). The non-redundant function of cohesin acetyltransferase Esco2: some answers and new questions. Nucleus, 3(4), 1-5. doi:10.4161/nucl.20440.


Cite as: http://hdl.handle.net/11858/00-001M-0000-000F-9ADA-B
Abstract
Cohesin and cohesin regulatory proteins function in an essential pathway enabling proper cohesion and segregation of sister chromatids. Additionally, these proteins are involved in double-strand break (DSB) repair and transcriptional regulation. Mutations in establishment of cohesion 1 homolog 2 (Esco2), an evolutionary conserved cohesin acetyltransferase, are the cause of Roberts syndrome (RBS), a human congenital disorder. To explore the mechanism by which the deficiency in Esco2 affects cohesin’s functions, we generated a mouse harboring a conditional Esco2 allele. To our surprise and in marked contrast to RBS, mouse Esco2 turns out to be a cell viability factor, the absence of which results in severe chromosome segregation defects and apoptosis. We found that the acetylation of the cohesin subunit Smc3 is significantly reduced in Esco2-deficient cells resulting in a marked reduction of Sororin recruitment to several, but not all cohesin bound loci. Here, we provide evidence that Esco2 is also required for DSB repair, which is consistent with previous studies in RBS cells.