Maintenance of the correct level and organisation of nucleosomes is crucial for genome function. Here, we uncover a role for a conserved bromodomain AAA-ATPase, Abo1, in the maintenance of nucleosome architecture in fission yeast. Cells lacking abo1(+) experience both a reduction and mis-positioning of nucleosomes at transcribed sequences in addition to increased intragenic transcription, phenotypes that are hallmarks of defective chromatin re-establishment behind RNA polymerase II. Abo1 is recruited to gene sequences and associates with histone H3 and the histone chaperone FACT. Furthermore, the distribution of Abo1 on chromatin is disturbed by impaired FACT function. The role of Abo1 extends to some promoters and also to silent heterochromatin. Abo1 is recruited to pericentromeric heterochromatin independently of the HP1 ortholog, Swi6, where it enforces proper nucleosome occupancy. Consequently, loss of Abo1 alleviates silencing and causes elevated chromosome mis-segregation. We suggest that Abo1 provides a histone chaperone function that maintains nucleosome architecture genome-wide.BBSRC (Doctoral Training Grants)
Medical Research Council
National Institute for Health Research (NIHR) Newcastle Biomedical Research Centre based at Newcastle Upon Tyne Hospitals NHS Foundation Trust and Newcastle University
Marie Curie International Incoming FellowshipIIF275280
EMBO Long Term FellowshipALTF 1491‐2010
The Wellcome Trust095021
Wellcome Trust core funding092076
NIA fellowshipNRSA F31‐AG038153
NIH R01GM084045
Cancer CenterCCSG 2 P30 CA21765; American Lebanese Syrian Associated Charities of St. Jude Children's Research Hospital; Wellcome Trust Senior Investigator Award; Wellcome Trust Institutional Strategic Support FundWT097835MF; Newcastle UniversityWT 097823/Z/11/