FancJ regulates interstrand crosslinker induced centrosome amplification through the activation of polo-like kinase 1
Author(s) -
Jianqiu Zou,
Fen Tian,
Ji Li,
Wyatt J. Pickner,
Molly Long,
Khosrow Rezvani,
Hongmin Wang,
Dong Zhang
Publication year - 2013
Publication title -
biology open
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.936
H-Index - 41
ISSN - 2046-6390
DOI - 10.1242/bio.20135801
Subject(s) - centrosome , biology , kinase , polo like kinase , microbiology and biotechnology , genetics , gene , cell cycle
DNA damage response (DDR) and the centrosome cycle are two of the most critical processes for maintaining a stable genome in animals. Sporadic evidence suggests a connection between these two processes. Here, we report our findings that six Fanconi Anemia (FA) proteins, including FancI and FancJ, localize to the centrosome. Intriguingly, we found that the localization of FancJ to the mother centrosome is stimulated by a DNA interstrand crosslinker, Mitomycin C (MMC). We further show that, in addition to its role in interstrand crosslinking (ICL) repair, FancJ also regulates the normal centrosome cycle as well as ICL induced centrosome amplification by activating the polo-like kinase 1 (PLK1). We have uncovered a novel function of FancJ in centrosome biogenesis and established centrosome amplification as an integral part of the ICL response.
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