Premium
The nuclear actin‐related protein Act3p/Arp4p of Saccharomyces cerevisiae is involved in transcription regulation of stress genes
Author(s) -
Görzer Irene,
Schüller Christoph,
Heidenreich Erich,
Krupanska Ludmila,
Kuchler Karl,
Wintersberger Ulrike
Publication year - 2003
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2003.03759.x
Subject(s) - biology , mutant , saccharomyces cerevisiae , gene , transcription (linguistics) , genetics , actin , psychological repression , transcription factor , dna repair , dna damage , dna , microbiology and biotechnology , gene expression , linguistics , philosophy
Summary A mutational analysis of the essential nuclear actin‐related protein of Saccharomyces cerevisiae , Act3p/Arp4p, was performed. The five residues chosen for substitution were amino acids conserved between actin and Act3p/Arp4p, the tertiary structure of which most probably resembles that of actin. Two thermosensitive (ts) mutants, a single and a double point mutant, and one lethal double point mutant were obtained. Both ts mutants were formamide‐sensitive which supports a structural relatedness of Act3p/Arp4p to actin; they were also hypersensitive against hydroxyurea and ultraviolet irradiation pointing to a possible role of Act3p/Arp4p in DNA replication and repair. Their ‘suppressor of Ty’ (SPT) phenotype, ob‐served with another ts mutant of Act3p/Arp4p before, suggested involvement of Act3p/Arp4p in transcription regulation. Accordingly, genome‐wide expression profiling revealed misregulated transcription in a ts mutant of a number of genes, among which increased expression of various stress‐responsive genes (many of them requiring Msn2p/Msn4p for induction) was the most salient result. This provides an explanation for the mutant's enhanced resistance to severe thermal and oxidative stress. Thus, Act3p/Arp4p takes an important part in the repression of stress‐induced genes under non‐stress conditions.