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Transcriptional regulators of the Schizosaccharomyces pombe fbp1 gene include two redundant Tup1p-like corepressors and the CCAAT binding factor activation complex

Lookup NU author(s): Dr Simon Whitehall


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The Schizosaccharomyces pombe fbp1 gene, which encodes fructose-1,6-bis-phosphatase, is transcriptionally repressed by glucose through the activation of the cAMP-dependent protein kinase A (PKA) and transcriptionally activated by glucose starvation through the activation of a mitogen-activated protein kinase (MAPK). To identify transcriptional regulators acting downstream from or in parallel to PKA, we screened an adh-driven cDNA plasmid library for genes that increase fbp1 transcription in a strain with elevated PKA activity. Two such clones express amino-terminally truncated forms of the S. pombe tup12 protein that resembles the Saccharomyces cerevisiae Tup1p global corepressor. These clones appear to act as dominant negative alleles. Deletion of both tup12 and the closely related tup11 gene causes a 100-fold increase in fbp1-lacZ expression, indicating that tup11 and tup12 are redundant negative regulators of fbp1 transcription. In strains lacking tup11 and tup12, the atf1-pcr1 transcriptional activator continues to play a central role in fbp1-lacZ expression; however, spc1 MAPK phosphorylation of atf1 is no longer essential for its activation. We discuss possible models for the role of tup11- and tup12-mediated repression with respect to signaling from the MAPK and PKA pathways. A third clone identified in our screen expresses the php5 protein subunit of the CCAAT-binding factor (CBF). Deletion of php5 reduces fbp1 expression under both repressed and derepressed conditions. The CBF appears to act in parallel to atf1-pcr1, although it is unclear whether or not CBF activity, is regulated by PKA.

Publication metadata

Author(s): Whitehall SK; Janoo RTK; Neely LA; Braun BR; Hoffman CS

Publication type: Article

Publication status: Published

Journal: Genetics

Year: 2001

Volume: 157

Issue: 3

Pages: 1205-1215

ISSN (print): 0016-6731

ISSN (electronic):

Publisher: Genetics Society of America


PubMed id: 11238405


Funder referenceFunder name
R01 GM046226-09NIGMS NIH HHS
R01 GM046226-10A1NIGMS NIH HHS
R01 GM046226-11NIGMS NIH HHS
R01 GM046226-12NIGMS NIH HHS
R01 GM046226-13NIGMS NIH HHS
R01 GM046226-13S1NIGMS NIH HHS