期刊
MOLECULAR CELL
卷 52, 期 5, 页码 746-757出版社
CELL PRESS
DOI: 10.1016/j.molcel.2013.10.015
关键词
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资金
- Instituto de Salud Carlos III (ISCIII) FIS/FEDER [PI12/01250, CP08/00223]
- MINECO [SAF2010-16089]
- Association for International Cancer Research (AICR)
- Grups de Recerca Consolidats de Catalunya [2009 SGR 867]
- Red Tematica de Investigacion Cooperative en Cancer (RTICC) [RD06/0020/0040]
- Fundacion Cientifica de la Asociacion Espanola contra el Cancer (AECC)
- AECC Catalunya
- ISCIII/FIS
- Generalitat de Catalunya
- AICR
- Max Planck Society
- Medical Research Council [MC_U120085810] Funding Source: researchfish
- Worldwide Cancer Research [13-0094] Funding Source: researchfish
- MRC [MC_U120085810] Funding Source: UKRI
Although heterochromatin is enriched with repressive traits, it is also actively transcribed, giving rise to large amounts of noncoding RNAs. Although these RNAs are responsible for the formation and maintenance of heterochromatin, little is known about how their transcription is regulated. Here, we show that the Snail1 transcription factor represses mouse perk centromeric transcription, acting through the H3K4 deaminase LOXL2. Since Snail1 plays a key role in the epithelial-to-mesenchymal transition (EMT), we analyzed the regulation of heterochromatin transcription in this process. At the onset of EMT, one of the major structural heterochromatin proteins, HP1 alpha, is transiently released from heterochromatin foci in a Snail1/LOXL2-dependent manner, concomitantly with a downregulation of major satellite transcription. Moreover, preventing the downregulation of major satellite transcripts compromised the migratory and invasive behavior of mesenchymal cells. We propose that Snail1 regulates heterochromatin transcription through LOXL2, thus creating the favorable transcriptional state necessary for completing EMT.
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