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Mouse CAF1, a mouse homologue of the yeast POP2 gene, complements the yeast pop2 null mutation
Author(s) -
ShimizuYoshida Yuki,
Sasamoto Mariko,
Yoshida Akira,
Yoshioka Tohru,
Matsumoto Atsuko,
Sakai Akira
Publication year - 1999
Publication title -
yeast
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.923
H-Index - 102
eISSN - 1097-0061
pISSN - 0749-503X
DOI - 10.1002/(sici)1097-0061(19990930)15:13<1357::aid-yea465>3.0.co;2-y
Subject(s) - biology , gene , saccharomyces cerevisiae , mutant , genetics , yeast , gene expression , plasmid , null allele , transcription (linguistics) , microbiology and biotechnology , mutation , linguistics , philosophy
The yeast POP2 protein (Pop2p) is a component of a global transcription regulatory complex and is required for gene expression of many genes in Saccharomyces cerevisiae . We constructed POP2 deletion plasmids encoding various Pop2p regions under the native POP2 promoter and found that the minimum functional region was located in two‐thirds of the carboxyl terminal region. A mouse homologue of the POP2 gene (mCAF1), which corresponds to the Pop2p minimum region, partially rescued the growth defect of pop2 null mutant cells. Addition of the Pop2p amino terminal region to mCAF1 strengthened the suppression. mCAF1 also weakly suppressed the relatively high expression of the SUC2 gene of pop2 cells under glucose‐repressing conditions; however, it failed to suppress the defect of full expression of the SUC2 gene under glucose‐derepressing conditions. Our findings clearly demonstrate that a mammalian homologue can substitute for the yeast POP2 gene in some aspect. Copyright © 1999 John Wiley & Sons, Ltd.