Affiliation:
1. Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115
Abstract
ABSTRACT
Cell type control of meiotic gene regulation in the budding yeast
Saccharomyces cerevisiae
is mediated by a cascade of transcriptional repressors, a1-α2 and Rme1. Here, we investigate the analogous regulatory pathway in the fission yeast
Schizosaccharomyces pombe
by analyzing the promoter of
mei3
, the single gene whose expression is sufficient to trigger meiosis. The
mei3
promoter does not appear to contain a negative regulatory element that represses transcription in haploid cells. Instead, correct regulation of
mei3
transcription depends on a complex promoter that contains at least five positive elements upstream of the TATA sequence. These elements synergistically activate
mei3
transcription, thereby constituting an on-off switch for the meiosis pathway. Element C is a large region containing multiple sequences that resemble binding sites for M
c
, an HMG domain protein encoded by the mating-type locus. The function of element C is extremely sensitive to spacing changes but not to linker-scanning mutations, suggesting the possibility that M
c
functions as an architectural transcription factor. Altered-specificity experiments indicate that element D interacts with P
m
, a homeodomain protein encoded by the mating-type locus. This indicates that P
m
functions as a direct activator of the meiosis pathway, whereas the homologous mating-type protein in
S. cerevisiae
(α2) functions as a repressor. Thus, despite the strong similarities between the mating-type loci of
S. cerevisiae
and
S. pombe
, the regulatory logic that governs the tight control of the key meiosis-inducing genes in these organisms is completely different.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
35 articles.
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