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Park, Jiyoung
Molecular Metabolism Laboratory (MML)
Research Interests
  • Obesity, diabetes, adipose tissue, cancer, cancer-associated adipocyte, dermal adipocyte, metabolic memory

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The stress-activated MAP kinase Sty1/Spc1 and a 3 '-regulatory element mediate UV-induced expression of the uvi15+ gene at the post-transcriptional level

Cited 7 times inthomson ciCited 7 times inthomson ci
Title
The stress-activated MAP kinase Sty1/Spc1 and a 3 '-regulatory element mediate UV-induced expression of the uvi15+ gene at the post-transcriptional level
Author
Kim, MLee, WPark, JiyoungKim, JBJang, YKSeong, RHChoe, SYPark, SD
Issue Date
2000-09
Publisher
OXFORD UNIV PRESS
Citation
NUCLEIC ACIDS RESEARCH, v.28, no.17, pp.3392 - 3402
Abstract
Exposure of Schizosaccharomyces pombe cells to UV light results in increased uvi15+ gene expression at both the mRNA and protein levels, leading to elevated cell survival. This UV-induced expression of the uvi15+ gene was reduced in Δsty1 and Δwis1 cells lacking the stress-activated protein kinase pathway, but not in DNA damage checkpoint mutants. To further understand the cellular mechanisms responsible for this UV-induced expression, the transcription rate and mRNA half-life were investigated. Transcription run-on assays revealed that the rate of uvi15+ transcription was increased 1.8-fold regardless of Sty1 when cells were UV irradiated. The half-life of uvi15+ mRNA was also increased 1.5-fold after UV irradiation, but it was decreased in the Δsty1 background for both basal and UV-induced mRNAs, indicating that the stress-activated MAPK cascade can mediate UV-induced gene expression by increasing mRNA half-life. Deletion analyses identified a 54 nt element downstream of the distal poly(A) site, which was involved in the increased half-life of uvi15+ mRNA. These results suggest that both Sty1 and the 3'-regulatory element regulate UV-induced expression of the uvi15+ gene at the post-transcriptional level.
URI
https://scholarworks.unist.ac.kr/handle/201301/7157
URL
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0034284362
DOI
10.1093/nar/28.17.3392
ISSN
0305-1048
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BIO_Journal Papers
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