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- W2010400539 abstract "Cytokinesis partitions the cytoplasm of a parent cell into two daughter cells and is essential for the completion of cell division. The final step of cytokinesis in animal cells is abscission, which is a process leading to the physical separation of two daughter cells. Abscission requires membrane traffic and microtubule disassembly at a specific midbody region called the secondary ingression. Here, we report that WD repeat-containing protein 5 (WDR5), a core subunit of COMPASS/MLL family histone H3 lysine 4 methyltransferase (H3K4MT) complexes, resides at the midbody and associates with a subset of midbody regulatory proteins, including PRC1 and CYK4/MKLP1. Knockdown of WDR5 impairs abscission and increases the incidence of multinucleated cells. Further investigation revealed that the abscission delay is primarily due to slower formation of secondary ingressions in WDR5 knockdown cells. Consistent with these defects, midbody microtubules in WDR5 knockdown cells also display enhanced resistance to depolymerization by nocodazole. Recruitment of WDR5 to the midbody dark zone appears to require integrity of the WDR5 central arginine-binding cavity, as mutations that disrupt histone H3 and MLL1 binding to this pocket also abolish the midbody localization of WDR5. Taken together, these data suggest that WDR5 is specifically targeted to the midbody in the absence of chromatin and that it promotes abscission, perhaps by facilitating midbody microtubule disassembly. Cytokinesis partitions the cytoplasm of a parent cell into two daughter cells and is essential for the completion of cell division. The final step of cytokinesis in animal cells is abscission, which is a process leading to the physical separation of two daughter cells. Abscission requires membrane traffic and microtubule disassembly at a specific midbody region called the secondary ingression. Here, we report that WD repeat-containing protein 5 (WDR5), a core subunit of COMPASS/MLL family histone H3 lysine 4 methyltransferase (H3K4MT) complexes, resides at the midbody and associates with a subset of midbody regulatory proteins, including PRC1 and CYK4/MKLP1. Knockdown of WDR5 impairs abscission and increases the incidence of multinucleated cells. Further investigation revealed that the abscission delay is primarily due to slower formation of secondary ingressions in WDR5 knockdown cells. Consistent with these defects, midbody microtubules in WDR5 knockdown cells also display enhanced resistance to depolymerization by nocodazole. Recruitment of WDR5 to the midbody dark zone appears to require integrity of the WDR5 central arginine-binding cavity, as mutations that disrupt histone H3 and MLL1 binding to this pocket also abolish the midbody localization of WDR5. Taken together, these data suggest that WDR5 is specifically targeted to the midbody in the absence of chromatin and that it promotes abscission, perhaps by facilitating midbody microtubule disassembly. WD repeat-containing protein 5 (WDR5) localizes to the midbody and regulates abscission.Journal of Biological ChemistryVol. 290Issue 37PreviewVOLUME 290 (2015) PAGES 8987–9001 Full-Text PDF Open Access" @default.
- W2010400539 created "2016-06-24" @default.
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- W2010400539 creator A5047236710 @default.
- W2010400539 creator A5049888866 @default.
- W2010400539 creator A5054869714 @default.
- W2010400539 date "2015-04-01" @default.
- W2010400539 modified "2023-10-15" @default.
- W2010400539 title "WD Repeat-containing Protein 5 (WDR5) Localizes to the Midbody and Regulates Abscission" @default.
- W2010400539 cites W1597678601 @default.
- W2010400539 cites W1967308267 @default.
- W2010400539 cites W1968271510 @default.
- W2010400539 cites W1969465539 @default.
- W2010400539 cites W1970442105 @default.
- W2010400539 cites W1975282459 @default.
- W2010400539 cites W1977002958 @default.
- W2010400539 cites W1979398151 @default.
- W2010400539 cites W1979827504 @default.
- W2010400539 cites W1981388324 @default.
- W2010400539 cites W1985180051 @default.
- W2010400539 cites W1991103421 @default.
- W2010400539 cites W1991475922 @default.
- W2010400539 cites W1992662525 @default.
- W2010400539 cites W1993341911 @default.
- W2010400539 cites W1996358062 @default.
- W2010400539 cites W1997504014 @default.
- W2010400539 cites W1998069675 @default.
- W2010400539 cites W2006463246 @default.
- W2010400539 cites W2007684630 @default.
- W2010400539 cites W2009858080 @default.
- W2010400539 cites W2012346714 @default.
- W2010400539 cites W2016024994 @default.
- W2010400539 cites W2019494208 @default.
- W2010400539 cites W2022936129 @default.
- W2010400539 cites W2024584416 @default.
- W2010400539 cites W2025014803 @default.
- W2010400539 cites W2026432118 @default.
- W2010400539 cites W2031128646 @default.
- W2010400539 cites W2033373463 @default.
- W2010400539 cites W2038926092 @default.
- W2010400539 cites W2046808709 @default.
- W2010400539 cites W2048608623 @default.
- W2010400539 cites W2052564025 @default.
- W2010400539 cites W2053793005 @default.
- W2010400539 cites W2053964757 @default.
- W2010400539 cites W2055567028 @default.
- W2010400539 cites W2057582154 @default.
- W2010400539 cites W2059004178 @default.
- W2010400539 cites W2060309579 @default.
- W2010400539 cites W2062406929 @default.
- W2010400539 cites W2065696846 @default.
- W2010400539 cites W2066933603 @default.
- W2010400539 cites W2068030382 @default.
- W2010400539 cites W2072134835 @default.
- W2010400539 cites W2073108127 @default.
- W2010400539 cites W2074542371 @default.
- W2010400539 cites W2080386975 @default.
- W2010400539 cites W2085168202 @default.
- W2010400539 cites W2087126960 @default.
- W2010400539 cites W2087392654 @default.
- W2010400539 cites W2091983770 @default.
- W2010400539 cites W2096011465 @default.
- W2010400539 cites W2098529801 @default.
- W2010400539 cites W2100589600 @default.
- W2010400539 cites W2107885943 @default.
- W2010400539 cites W2109684788 @default.
- W2010400539 cites W2110214166 @default.
- W2010400539 cites W2112252835 @default.
- W2010400539 cites W2115708035 @default.
- W2010400539 cites W2115799591 @default.
- W2010400539 cites W2118127229 @default.
- W2010400539 cites W2121910267 @default.
- W2010400539 cites W2124418801 @default.
- W2010400539 cites W2125695802 @default.
- W2010400539 cites W2127976626 @default.
- W2010400539 cites W2130495913 @default.
- W2010400539 cites W2130724559 @default.
- W2010400539 cites W2131775349 @default.
- W2010400539 cites W2133437282 @default.
- W2010400539 cites W2133938268 @default.
- W2010400539 cites W2137001129 @default.
- W2010400539 cites W2145271586 @default.
- W2010400539 cites W2146501674 @default.
- W2010400539 cites W2154435482 @default.
- W2010400539 cites W2155445544 @default.
- W2010400539 cites W2163000142 @default.
- W2010400539 cites W2164230292 @default.
- W2010400539 cites W2166691146 @default.
- W2010400539 cites W2167815875 @default.
- W2010400539 doi "https://doi.org/10.1074/jbc.m114.623611" @default.
- W2010400539 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4566220" @default.
- W2010400539 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26362543" @default.
- W2010400539 hasPublicationYear "2015" @default.