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Mol Cell. 2014 Feb 20;53(4):549-61. doi: 10.1016/j.molcel.2014.01.006. Epub 2014 Feb 6.

Control of Cdc28 CDK1 by a stress-induced lncRNA.

Author information

1
Cell Signaling Unit, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra (UPF), 08003 Barcelona, Spain.
2
EMBL Heidelberg, Meyerhofstrasse 1, 69117 Heidelberg, Germany.
3
Cell Signaling Unit, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra (UPF), 08003 Barcelona, Spain. Electronic address: eulalia.nadal@upf.edu.
4
Cell Signaling Unit, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra (UPF), 08003 Barcelona, Spain. Electronic address: francesc.posas@upf.edu.

Abstract

Genomic analysis has revealed the existence of a large number of long noncoding RNAs (lncRNAs) with different functions in a variety of organisms, including yeast. Cells display dramatic changes of gene expression upon environmental changes. Upon osmostress, hundreds of stress-responsive genes are induced by the stress-activated protein kinase (SAPK) p38/Hog1. Using whole-genome tiling arrays, we found that Hog1 induces a set of lncRNAs upon stress. One of the genes expressing a Hog1-dependent lncRNA in antisense orientation is CDC28, the cyclin-dependent kinase 1 (CDK1) that controls the cell cycle in yeast. Cdc28 lncRNA mediates the establishment of gene looping and the relocalization of Hog1 and RSC from the 3' UTR to the +1 nucleosome to induce CDC28 expression. The increase in the levels of Cdc28 results in cells able to reenter the cell cycle more efficiently after stress. This may represent a general mechanism to prime expression of genes needed after stresses are alleviated.

PMID:
24508389
PMCID:
PMC4148690
DOI:
10.1016/j.molcel.2014.01.006
[Indexed for MEDLINE]
Free PMC Article
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