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Chronological lifespan extension by Ecl1 family proteins depends on Prr1 response regulator in fission yeast
Author(s) -
Ohtsuka Hokuto,
Azuma Kenko,
Kubota Sachiko,
Murakami Hiroshi,
GigaHama Yuko,
Tohda Hideki,
Aiba Hirofumi
Publication year - 2012
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2011.01571.x
Subject(s) - biology , schizosaccharomyces pombe , genetics , phenotype , gene , schizosaccharomyces , transcription factor , mutant , gene family , dna binding protein , gene silencing , protein family , gene expression , microbiology and biotechnology
ecl1+ , ecl2 + and ecl3 + genes encode highly homologous small proteins, and their over‐expressions confer both H 2 O 2 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 H 2 O 2 . We showed that the H 2 O 2 ‐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 H 2 O 2 stress resistance and chronological lifespan extension in ctt1 + ‐ and prr1 + ‐dependent manner, respectively.