| Literature DB >> 24565511 |
Hyun-Soo Kim1, Rituparna Mukhopadhyay1, Scott B Rothbart2, Andrea C Silva1, Vincent Vanoosthuyse3, Ernest Radovani4, Thomas Kislinger5, Assen Roguev6, Colm J Ryan7, Jiewei Xu6, Harlizawati Jahari8, Kevin G Hardwick3, Jack F Greenblatt9, Nevan J Krogan10, Jeffrey S Fillingham4, Brian D Strahl2, Eric E Bouhassira1, Winfried Edelmann1, Michael-Christopher Keogh11.
Abstract
Condensin is a central regulator of mitotic genome structure with mutants showing poorly condensed chromosomes and profound segregation defects. Here, we identify NCT, a complex comprising the Nrc1 BET-family tandem bromodomain protein (SPAC631.02), casein kinase II (CKII), and several TAFs, as a regulator of condensin function. We show that NCT and condensin bind similar genomic regions but only briefly colocalize during the periods of chromosome condensation and decondensation. This pattern of NCT binding at the core centromere, the region of maximal condensin enrichment, tracks the abundance of acetylated histone H4, as regulated by the Hat1-Mis16 acetyltransferase complex and recognized by the first Nrc1 bromodomain. Strikingly, mutants in NCT or Hat1-Mis16 restore the formation of segregation-competent chromosomes in cells containing defective condensin. These results are consistent with a model where NCT targets CKII to chromatin in a cell-cycle-directed manner in order to modulate the activity of condensin during chromosome condensation and decondensation.Entities:
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Year: 2014 PMID: 24565511 PMCID: PMC3969266 DOI: 10.1016/j.celrep.2014.01.029
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423