The heat shock response (HSR) is a conserved cellular defence mechanism to ensure cell viability under thermal stress. Satellite-III (Sat3) transcripts, a class of long non-coding RNAs, are expressed during the HSR in a heat shock transcription factor 1 (HSF1)-dependent manner. They accumulate at the site of their transcription in response to heat shock together with transcriptional regulators to form nuclear stress bodies (nSBs). Now (p. 3541), Subramaniam Ganesh and colleagues show that nSBs sequester transcription factors in the presence of Sat3 transcripts. Specifically, CREB-binding proteins (CREBBPs) bind to nSBs, which, in turn, is dependent on the serine/arginine splicing factor 1 (SRSF1). The Sat3 transcripts sequester both CREBBP and SRSF1 to nSBs, implying a scaffolding role of Sat3.Consistent with a role for Sat3 transcripts in the recruitment of proteins to an inactive compartment during heat shock, Sat3 transcripts are required for full protection from heat-shock-induced cell death. Loss of Sat3 transcripts leads to partial relief of heat-shock-induced transcriptional repression. When Sat3-repeat-bearing transcripts are overexpressed, cells form nSBs and repression of transcription is observed – even in the absence of heat shock. This study provides new insight into the regulatory role of Sat3 transcripts at nSBSs, and how these nuclear bodies indirectly alter gene expression after heat shock through sequestration of SRSF1 and CREBBP.

• © 2016. Published by The Company of Biologists Ltd