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


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.

SUBMITTER: Yamauchi T 

PROVIDER: S-EPMC2486420 | biostudies-other | 2008 Jul

REPOSITORIES: biostudies-other

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

Yamauchi Tomohiro T   Ishidao Takefumi T   Nomura Teruaki T   Shinagawa Toshie T   Tanaka Yasunori Y   Yonemura Shigenobu S   Ishii Shunsuke S  

The EMBO journal 20080612 13


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 abnorma  ...[more]

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