Chromodomain mutation in S. pombe Kat5/Mst1 affects centromere dynamics and DNA repair.

Autor: Li T; Program in Molecular & Computational Biology, Department of Biological Sciences, University of Southern California, Los Angeles, CA, United States of America., Petreaca RC; Program in Molecular & Computational Biology, Department of Biological Sciences, University of Southern California, Los Angeles, CA, United States of America., Forsburg SL; Program in Molecular & Computational Biology, Department of Biological Sciences, University of Southern California, Los Angeles, CA, United States of America.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2024 Apr 25; Vol. 19 (4), pp. e0300732. Date of Electronic Publication: 2024 Apr 25 (Print Publication: 2024).
DOI: 10.1371/journal.pone.0300732
Abstrakt: KAT5 (S. pombe Mst1, human TIP60) is a MYST family histone acetyltransferase conserved from yeast to humans that is involved in multiple cellular activities. This family is characterized in part by containing a chromodomain, a motif associated with binding methylated histones. We show that a chromodomain mutation in the S. pombe Kat5, mst1-W66R, has defects in pericentromere silencing. mst1-W66R is sensitive to camptothecin (CPT) but only at an increased temperature of 36°C, although it is proficient for growth at this temperature. We also describe a de-silencing effect at the pericentromere by CPT that is independent of RNAi and methylation machinery. We also show that mst1-W66R disrupts recruitment of proteins to repair foci in response to camptothecin-induced DNA damage. Our data suggest a function of Mst1 chromodomain in centromere heterochromatin formation and a separate role in genome-wide damage repair in CPT.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2024 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
Databáze: MEDLINE
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