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Molecular and Cellular Biology, June 2000, p. 4340-4349, Vol. 20, No. 12
Department of Biological Chemistry and
Molecular Pharmacology, Harvard Medical School, Boston,
Massachusetts 02115
Received 20 January 2000/Returned for modification 13 March
2000/Accepted 21 March 2000
In Saccharomyces cerevisiae, the family of ATF/CREB
transcriptional regulators consists of a repressor, Acr1 (Sko1), and
two activators, Aca1 and Aca2. The AP-1 factor Gen4 does not activate transcription through ATF/CREB sites in vivo even though it binds these
sites in vitro. Unlike ATF/CREB activators in other species, Aca1- and
Aca2-dependent transcription is not affected by protein kinase A or by
stress, and Aca1 and Aca2 are not required for Hog1-dependent salt
induction of transcription through an optimal ATF/CREB site. Aca2 is
important for a variety of biological functions including growth on
nonoptimal carbon sources, and Aca2-dependent activation is modestly
regulated by carbon source. Strains lacking Aca1 are phenotypically
normal, but overexpression of Aca1 suppresses some defects associated
with the loss of Aca2, indicating a functional overlap between Aca1 and
Aca2. Acr1 represses transcription both by recruiting the Cyc8-Tup1
corepressor and by directly competing with Aca1 and Aca2 for target
sites. Acr1 does not fully account for osmotic regulation through
ATF/CREB sites, and a novel Hog1-dependent activator(s) that is not a
bZIP protein is required for ATF/CREB site activation in response to
high salt. In addition, Acr1 does not affect a number of phenotypes
that arise from loss of Aca2. Thus, members of the S. cerevisiae ATF/CREB family have overlapping, but distinct,
biological functions and target genes.
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Aca1 and Aca2, ATF/CREB Activators in Saccharomyces
cerevisiae, Are Important for Carbon Source Utilization but
Not the Response to Stress
*
Corresponding author. Mailing address: Department of
Biological Chemistry and Molecular Pharmacology, Harvard Medical
School, Boston, MA 02115. Phone: (617) 432-2104. Fax: (617) 432-2529. E-mail: kevin{at}hms.harvard.edu.
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