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Nucleic Acids Research Advance Access originally published online on January 10, 2008
Nucleic Acids Research 2008 36(4):1343-1357; doi:10.1093/nar/gkm1068
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Nucleic Acids Research, 2008, Vol. 36, No. 4 1343-1357
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Saccharomyces cerevisiae HMO1 interacts with TFIID and participates in start site selection by RNA polymerase II

Koji Kasahara, Sewon Ki, Kayo Aoyama, Hiroyuki Takahashi and Tetsuro Kokubo*

Division of Molecular and Cellular Biology, International Graduate School of Arts and Sciences, Yokohama City University, Yokohama, 230-0045, Japan

*To whom correspondence should be addressed. Tel: +045 508 7237; Fax: +045 508 7369; Email: kokubo{at}tsurumi.yokohama-cu.ac.jp

Received October 11, 2007. Revised November 11, 2007. Accepted November 12, 2007.

Saccharomyces cerevisiae HMO1, a high mobility group B (HMGB) protein, associates with the rRNA locus and with the promoters of many ribosomal protein genes (RPGs). Here, the Sos recruitment system was used to show that HMO1 interacts with TBP and the N-terminal domain (TAND) of TAF1, which are integral components of TFIID. Biochemical studies revealed that HMO1 copurifies with TFIID and directly interacts with TBP but not with TAND. Deletion of HMO1 ({Delta}hmo1) causes a severe cold-sensitive growth defect and decreases transcription of some TAND-dependent genes. {Delta}hmo1 also affects TFIID occupancy at some RPG promoters in a promoter-specific manner. Interestingly, over-expression of HMO1 delays colony formation of taf1 mutants lacking TAND (taf1{Delta}TAND), but not of the wild-type strain, indicating a functional link between HMO1 and TAND. Furthermore, {Delta}hmo1 exhibits synthetic growth defects in some spt15 (TBP) and toa1 (TFIIA) mutants while it rescues growth defects of some sua7 (TFIIB) mutants. Importantly, {Delta}hmo1 causes an upstream shift in transcriptional start sites of RPS5, RPS16A, RPL23B, RPL27B and RPL32, but not of RPS31, RPL10, TEF2 and ADH1, indicating that HMO1 may participate in start site selection of a subset of class II genes presumably via its interaction with TFIID.


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