Chaperone control of the activity and specificity of the histone H3 acetyltransferase Rtt109

被引：149

作者：

Fillingham, Jeffrey ^{[1
]}

Recht, Judith ^{[2
]}

Silva, Andrea C. ^{[3
]}

Suter, Bernhard ^{[1
,4
]}

Emili, Andrew ^{[1
,5
]}

Stagljar, Igor ^{[4
]}

Krogan, Nevan J. ^{[6
]}

Allis, C. David ^{[2
]}

Keogh, Michael-Christopher ^{[3
]}

Greenblatt, Jack F. ^{[1
,5
]}

机构：

[1] Univ Toronto, Banting & Best Dept Med Res, Terrence Donnelly Ctr Cellular & Biomol Res CCBR, Toronto, ON M5S 3E1, Canada

[2] Rockefeller Univ, Lab Chromatin Biol, New York, NY 10065 USA

[3] Albert Einstein Coll Med, Dept Cell Biol, Bronx, NY 10461 USA

[4] Univ Toronto, Dept Biochem, Toronto, ON M5S 3E1, Canada

[5] Univ Toronto, Dept Mol Genet, Toronto, ON M5S 3E1, Canada

[6] Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA

来源：

MOLECULAR AND CELLULAR BIOLOGY | 2008年 / 28卷 / 13期

关键词：

D O I：

10.1128/MCB.00182-08

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Acetylation of Saccharomyces cerevisiae histone H3 on K56 by the histone acetyltransferase (HAT) Rtt109 is important for repairing replication-associated lesions. Rtt109 purifies from yeast in complex with the histone chaperone Vps75, which stabilizes the HAT in vivo. A whole-genome screen to identify genes whose deletions have synthetic genetic interactions with rtt109 Delta suggests Rtt109 has functions in addition to DNA repair. We show that in addition to its known H3-K56 acetylation activity, Rtt109 is also an H3-K9 HAT, and we show that Rtt109 and Gcn5 are the only H3-K9 HATs in vivo. Rtt109's H3-K9 acetylation activity in vitro is enhanced strongly by Vps75. Another histone chaperone, Asf1, and Vps75 are both required for acetylation of lysine 9 on H3 (H3-K9ac) in vivo by Rtt109, whereas H3-K56ac in vivo requires only Asf1. Asf1 also physically interacts with the nuclear Hat1/Hat2/Hif1 complex that acetylates H4-K5 and H4-K12. We suggest Asf1 is capable of assembling into chromatin H3-H4 dimers diacetylated on both H4-K5/12 and H3-K9/56.

引用

页码：4342 / 4353

页数：12

共 55 条

[31] Activation of Rad53 kinase in response to DNA damage and its effect in modulating phosphorylation of the lagging strand DNA polymerase [J].