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Identification and expression of uvi31 + , a UV‐inducible gene from Schizosaccharomyces pombe
Author(s) -
Kim SeungHwan,
Kim Minkyu,
Lee Joon Kyu,
Kim Min Ji,
Jin Yong Hwan,
Seong Rho Hyun,
Hong Seung Hwan,
Joe Cheol O,
Park Sang Dai
Publication year - 1997
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/(sici)1098-2280(1997)30:1<72::aid-em10>3.0.co;2-n
Subject(s) - cell cycle , biology , gene , gene expression , schizosaccharomyces pombe , cell cycle checkpoint , microbiology and biotechnology , dna damage , cell growth , dna repair , cell division , genetics , dna , cell , saccharomyces cerevisiae
The Schizosaccharomyces pombe uvi31 + gene has been previously isolated as a UV‐inducible gene [Lee JK et al. (1994) Biochem Biophys Res Commun 202:1113–1119]. This gene encodes a protein of about 12 kDa with 57% amino acid sequence similarity to Escherichia coli BolA protein which is known to be involved in switching between the cell elongation and septation systems during the cell division cycle. The putative Mlu l cell cycle box (MCB), SWI4/6‐dependent cell cycle box (SCB), and gear‐box elements are found in the upstream region of uvi31 + gene, suggesting that this gene shows the cell cycle‐regulated and growth phase‐dependent expression. Interestingly, the level of uvi31 − transcript varies throughout the cell cycle, peaking in G1 phase before septation, and also shows the growth phase‐dependent pattern during cellular growth, increasing maximally at the diauxic shift phase just before stationary phase. Furthermore, the transcript level of this gene is raised after S phase arrest, and is also increased maximally at 4 hr after UV irradiation of 240 J/m 2 . These results suggest that the delayed induction of uvi31 + gene after UV irradiation may be caused by cell cycle control of this gene after DNA replication checkpoint arrest. Thus, the uvi31 + gene may play a role in controlling the progress of the cell cycle after DNA damage (UV irradiation). Environ. Mol. Mutagen. 30:72–81, 1997 © 1997 Wiley‐Liss, Inc.