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A B‐Myb complex containing clathrin and filamin is required for mitotic spindle function
Author(s) -
Yamauchi Tomohiro,
Ishidao Takefumi,
Nomura Teruaki,
Shinagawa Toshie,
Tanaka Yasunori,
Yonemura Shigenobu,
Ishii Shunsuke
Publication year - 2008
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2008.118
Subject(s) - biology , myb , filamin , clathrin , microbiology and biotechnology , mitosis , cell cycle , genetics , spindle apparatus , transcription factor , cell division , gene , cytoskeleton , cell , endocytosis
B‐Myb is one member of the vertebrate Myb family of transcription factors and is ubiquitously expressed. B‐Myb activates transcription of a group of genes required for the G2/M cell cycle transition by forming the dREAM/Myb–MuvB‐like complex, which was originally identified in Drosophila . Mutants of zebrafish B‐ myb and Drosophila myb exhibit defects in cell cycle progression and genome instability. Although the genome instability caused by a loss of B‐Myb has been speculated to be due to abnormal cell cycle progression, the precise mechanism remains unknown. Here, we have purified a B‐Myb complex containing clathrin and filamin (Myb–Clafi complex). This complex is required for normal localization of clathrin at the mitotic spindle, which was previously reported to stabilize kinetochore fibres. The Myb–Clafi complex is not tightly associated with the mitotic spindles, suggesting that this complex ferries clathrin to the mitotic spindles. Thus, identification of the Myb–Clafi complex reveals a previously unrecognized function of B‐Myb that may contribute to its role in chromosome stability, possibly, tumour suppression.