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Originally published In Press as doi:10.1074/jbc.M100248200 on March 9, 2001

J. Biol. Chem., Vol. 276, Issue 20, 17117-17124, May 18, 2001
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Two WD Repeat-containing TATA-binding Protein-associated Factors in Fission Yeast That Suppress Defects in the Anaphase-promoting Complex*

Hiroshi MitsuzawaDagger §, Hiroaki Seino, Fumiaki Yamao, and Akira IshihamaDagger

From the Divisions of Dagger  Molecular Genetics and  Mutagenesis, Department of Molecular Genetics, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan

The general transcription factor IID consists of the TATA-binding protein (TBP) and multiple TBP-associated factors (TAFs). Here we report the isolation of two related TAF genes from the fission yeast Schizosaccharomyces pombe as multicopy suppressors of a temperature-sensitive mutation in the ubiquitin-conjugating enzyme gene ubcP4+. The ubcP4ts mutation causes cell cycle arrest in mitosis, probably due to defects in ubiquitination mediated by the anaphase-promoting complex/cyclosome. One multicopy suppressor is the previously reported gene taf72+, whereas the other is a previously unidentified gene named taf73+. We show that the taf73+ gene, like taf72+, is essential for cell viability. The taf72+ and taf73+ genes encode proteins homologous to WD repeat-containing TAFs such as human TAF100, Drosophila TAF80/85, and Saccharomyces cerevisiae TAF90. We demonstrate that TAF72 and TAF73 proteins are present in the same complex with TBP and other TAFs and that TAF72, but not TAF73, is associated with the putative histone acetylase Gcn5. We also show that overexpression of TAF72 or TAF73 suppresses the cell cycle arrest in mitosis caused by a mutation in the anaphase-promoting complex/cyclosome subunit gene cut9+. These results suggest that TAF72 and TAF73 may regulate the expression of genes involved in ubiquitin-dependent proteolysis during mitosis. Our study thus provides evidence for a possible role of WD repeat-containing TAFs in the expression of genes involved in progression through the M phase of the cell cycle.


* This work was supported by grants from the Ministry of Education, Science, Sports, and Culture of Japan and the Japan Science and Technology Corp.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The nucleotide sequence reported in this paper has been submitted to the DDBJ/GenBankTM/EBI Data Bank under accession number AB039954.

§ To whom correspondence should be addressed. Tel.: 81-559-81-6744; Fax: 81-559-81-6746; E-mail: hmitsuza@lab.nig.ac.jp.


Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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