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A heat shock–responsive lncRNA <i>Heat</i> acts as a HSF1-directed transcriptional brake via m <sup>6</sup> A modification

Quanquan Ji, Xin Zong, Yuanhui Mao, Shu‐Bing Qian

2021Proceedings of the National Academy of Sciences37 citationsDOIOpen Access PDF

Abstract

Significance The heat shock response is a universal homeostatic mechanism for cells to cope with adverse environmental conditions. However, little is known about whether an active mechanism is needed to turn off stress genes during stress recovery. We report a heat shock–inducible long noncoding RNA, Heat , in mouse cells that acts as a transcriptional brake to restrain stress gene expression during the recovery phase. We show that Heat targets specific stress genes via HSF1 as a carrier. Unexpectedly, Heat relies on m 6 A modification and the m 6 A reader YTHDC1 to silence stress genes to attenuate heat shock response. These results demonstrate an intimate connection between nuclear epitranscriptome and transcriptional regulation of heat shock response.

Topics & Concepts

HSF1Heat shockBrakeHeat shock proteinShock (circulatory)PhysicsChemistryMaterials scienceHsp70Internal medicineMedicineBiochemistryGeneMetallurgyRNA modifications and cancerCancer-related molecular mechanisms researchRNA Research and Splicing