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EMBO J. 2008 Jul 9;27(13):1852-62. doi: 10.1038/emboj.2008.118. Epub 2008 Jun 12.

A B-Myb complex containing clathrin and filamin is required for mitotic spindle function.

Author information

1
Laboratory of Molecular Genetics, RIKEN Tsukuba Institute, Tsukuba, Japan.

Abstract

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.

PMID:
18548008
PMCID:
PMC2486420
DOI:
10.1038/emboj.2008.118
[Indexed for MEDLINE]
Free PMC Article

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