Mechanism of hsp70i gene bookmarking

被引:132
作者
Xing, HY
Wilkerson, DC
Mayhew, CN
Lubert, EJ
Skaggs, HS
Goodson, ML
Hong, YL
Park-Sarge, OK
Sarge, KD [1 ]
机构
[1] Univ Kentucky, Albert B Chandler Med Ctr, Dept Mol & Cellular Biochem, Lexington, KY 40536 USA
[2] Univ Kentucky, Albert B Chandler Med Ctr, Dept Physiol, Lexington, KY 40536 USA
[3] Univ Cincinnati, Dept Cell Biol Neurobiol & Anat, Cincinnati, OH 45267 USA
[4] Battelle Mem Inst, Columbus, OH 43201 USA
[5] Univ Calif Davis, Microbiol Sect, Davis, CA 95616 USA
关键词
D O I
10.1126/science.1106478
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
In contrast to most genomic DNA in mitotic cells, the promoter regions of some genes, such as the stress-inducible hsp70i gene that codes for a heat shock protein, remain uncompacted, a phenomenon called bookmarking. Here we show that hsp70i bookmarking is mediated by a transcription factor called HSF2, which binds this promoter in mitotic cells, recruits protein phosphatase 2A, and interacts with the CAP-G subunit of the condensin enzyme to promote efficient dephosphorylation and inactivation of condensin complexes in the vicinity, thereby preventing compaction at this site. Blocking HSF2-mediated bookmarking by HSF2 RNA interference decreases hsp70i induction and survival of stressed cells in the G, phase, which demonstrates the biological importance of gene bookmarking.
引用
收藏
页码:421 / 423
页数:3
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