期刊
EXPERIMENTAL CELL RESEARCH
卷 316, 期 11, 页码 1845-1855出版社
ELSEVIER INC
DOI: 10.1016/j.yexcr.2010.02.002
关键词
HSF1; Heat shock; Heterochromatin; Satellite sequences; Transcription
资金
- French Association pour la Recherche contre le Cancer [5113]
- Institut National du Cancer
- Canceropole Lyon Auvergne Rhone Alpes
- Region Rhone-Alpes (Emergence)
- Fondation pour la Recherche Medicale
Cells respond to stress by activating the synthesis of heat shock proteins (HSPs) which protect the cells against the deleterious effects of stress. This mechanism is controlled by the heat shock factor 1 (HSF1). In parallel to HSP gene transcription, in human cells, HSF1 also binds to and transcribes satellite III repeated sequences present in numerous copies in the 9q12 pericentromeric region of chromosome 9. These HSF1 accumulation sites are termed nuclear stress bodies (nSBs). In tumor cells, however, the number of nSBs is higher than the number of 9q12 copies, suggesting the existence of other HSF1 targets. In this paper, we were interested in characterizing these other HSF1 binding sites. We show that HSF1 indeed binds to the pericentromeric region of 14 chromosomes, thereby directing the formation of 'secondary nSBs'. The appearance of secondary nSBs depends on the number of satellite sequences present in the target locus, and on the cellular amount of HSF1 protein. Moreover, secondary nSBs also correspond to transcription sites, thus demonstrating that heat shock induces a genome-wide transcription of satellite sequences. Finally, by analyzing published transcriptomic data, we show that the derepression of these large heterochromatic blocks does not significantly affect the transcription of neighboring genes. (C) 2010 Elsevier Inc. All rights reserved.
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