東　剣虹
   Department   Research Institutes and Facilities, Research Institutes and Facilities
   Position   Assistant Professor
Article types Original article
Language English
Peer review Peer reviewed
Title Chronological lifespan extension by Ecl1 family proteins depends on Prr1 response regulator in fission yeast.
Journal Formal name：Genes to cells : devoted to molecular & cellular mechanisms
Abbreviation：Genes Cells
ISSN code：(1365-2443)1356-9597(Linking)
Domestic / ForeginForegin
Volume, Issue, Page 17(1),pp.39-52
Author and coauthor Ohtsuka Hokuto, Azuma Kenko, Kubota Sachiko, Murakami Hiroshi, Giga-Hama Yuko, Tohda Hideki, Aiba Hirofumi
Authorship 2nd author
Publication date 2012/01
Summary ecl1+, ecl2+ and ecl3+ genes encode highly homologous small proteins, and their over-expressions confer both H2O2 stress resistance and chronological lifespan extension on Schizosaccharomyces pombe. However, the mechanisms of how these Ecl1 family proteins function have not been elucidated. In this study, we conducted microarray analysis and identified that the expression of genes involved in sexual development and stress responses was affected by the over-expression of Ecl1 family proteins. In agreement with the mRNA expression profile, the cells over-expressing Ecl1 family proteins showed high mating efficiency and resistant phenotype to H2O2. We showed that the H2O2-resistant phenotype depends on catalase Ctt1, and over-expression of ctt1+ does not affect chronological lifespan. Furthermore, we showed that six genes, ste11+, spk1+, hsr1+, rsv2+, hsp9+ and lsd90+, whose expressions are increased in cells over-expressing Ecl1 family proteins are involved in chronological lifespan in fission yeast. Among these genes, the induction of ste11+ and hsr1+ was dependent on a transcription factor Prr1, and we showed that the extensions of chronological lifespan by Ecl1 family proteins are remarkably diminished in prr1 deletion mutant. From these results, we propose that Ecl1-family proteins conduct H2O2 stress resistance and chronological lifespan extension in ctt1+- and prr1+-dependent manner, respectively.
DOI 10.1111/j.1365-2443.2011.01571.x
PMID 22212525