Sister chromatid cohesion, mediated by cohesin and regulated by Sororin, is 
essential for chromosome segregation. In mammalian cells, cohesion establishment 
and Sororin recruitment to chromatin-bound cohesin depends on the 
acetyltransferases Esco1 and Esco2. Mutations in Esco2 cause Roberts syndrome, a 
developmental disease in which mitotic chromosomes have a 'railroad' track 
morphology. Here, we show that Esco2 deficiency leads to termination of mouse 
development at pre- and post-implantation stages, indicating that Esco2 
functions non-redundantly with Esco1. Esco2 is transiently expressed during 
S-phase when it localizes to pericentric heterochromatin (PCH). In interphase, 
Esco2 depletion leads to a reduction in cohesin acetylation and Sororin 
recruitment to chromatin. In early mitosis, Esco2 deficiency causes changes in 
the chromosomal localization of cohesin and its protector Sgo1. Our results 
suggest that Esco2 is needed for cohesin acetylation in PCH and that this 
modification is required for the proper distribution of cohesin on mitotic 
chromosomes and for centromeric cohesion.