Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 735-749 |
| Journal | Journal of Cell Biology |
| Volume | 206 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 2014 |
| MoE publication type | A1 Journal article-refereed |
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Expression of HSF2 decreases in mitosis to enable stress-inducible transcription and cell survival. / Elsing, Alexandra N.; Aspelin, Camilla; Björk, Johanna K.; Bergman, Heidi A.; Himanen, Samu V.; Kallio, Marko; Roos-Mattjus, Pia; Sistonen, Lea.
In: Journal of Cell Biology, Vol. 206, No. 6, 2014, p. 735-749.Research output: Contribution to journal › Article › Scientific › peer-review
TY - JOUR
T1 - Expression of HSF2 decreases in mitosis to enable stress-inducible transcription and cell survival
AU - Elsing, Alexandra N.
AU - Aspelin, Camilla
AU - Björk, Johanna K.
AU - Bergman, Heidi A.
AU - Himanen, Samu V.
AU - Kallio, Marko
AU - Roos-Mattjus, Pia
AU - Sistonen, Lea
PY - 2014
Y1 - 2014
N2 - Unless mitigated, external and physiological stresses are detrimental for cells, especially in mitosis, resulting in chromosomal missegregation, aneuploidy, or apoptosis. Heat shock proteins (Hsps) maintain protein homeostasis and promote cell survival. Hsps are transcriptionally regulated by heat shock factors (HSFs). Of these, HSF1 is the master regulator and HSF2 modulates Hsp expression by interacting with HSF1. Due to global inhibition of transcription in mitosis, including HSF1-mediated expression of Hsps, mitotic cells are highly vulnerable to stress. Here, we show that cells can counteract transcriptional silencing and protect themselves against proteotoxicity in mitosis. We found that the condensed chromatin of HSF2-deficient cells is accessible for HSF1 and RNA polymerase II, allowing stress-inducible Hsp expression. Consequently, HSF2-deficient cells exposed to acute stress display diminished mitotic errors and have a survival advantage. We also show that HSF2 expression declines during mitosis in several but not all human cell lines, which corresponds to the Hsp70 induction and protection against stress-induced mitotic abnormalities and apoptosis
AB - Unless mitigated, external and physiological stresses are detrimental for cells, especially in mitosis, resulting in chromosomal missegregation, aneuploidy, or apoptosis. Heat shock proteins (Hsps) maintain protein homeostasis and promote cell survival. Hsps are transcriptionally regulated by heat shock factors (HSFs). Of these, HSF1 is the master regulator and HSF2 modulates Hsp expression by interacting with HSF1. Due to global inhibition of transcription in mitosis, including HSF1-mediated expression of Hsps, mitotic cells are highly vulnerable to stress. Here, we show that cells can counteract transcriptional silencing and protect themselves against proteotoxicity in mitosis. We found that the condensed chromatin of HSF2-deficient cells is accessible for HSF1 and RNA polymerase II, allowing stress-inducible Hsp expression. Consequently, HSF2-deficient cells exposed to acute stress display diminished mitotic errors and have a survival advantage. We also show that HSF2 expression declines during mitosis in several but not all human cell lines, which corresponds to the Hsp70 induction and protection against stress-induced mitotic abnormalities and apoptosis
U2 - 10.1083/jcb.201402002
DO - 10.1083/jcb.201402002
M3 - Article
VL - 206
SP - 735
EP - 749
JO - Journal of Cell Biology
JF - Journal of Cell Biology
SN - 0021-9525
IS - 6
ER -