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Molecular and Cellular Biology, December 1998, p. 7317-7326, Vol. 18, No. 12
Department of Biological Chemistry and
Molecular Pharmacology, Harvard Medical School, Boston,
Massachusetts 02115
Received 22 July 1998/Returned for modification 19 August
1998/Accepted 28 August 1998
Cell type control of meiotic gene regulation in the budding yeast
Saccharomyces cerevisiae is mediated by a cascade of
transcriptional repressors, a1-
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
The Mating-Type Proteins of Fission Yeast Induce
Meiosis by Directly Activating mei3 Transcription
2 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 Mc, 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 Mc functions as an architectural
transcription factor. Altered-specificity experiments indicate that
element D interacts with Pm, a homeodomain protein encoded
by the mating-type locus. This indicates that Pm functions
as a direct activator of the meiosis pathway, whereas the homologous
mating-type protein in S. cerevisiae (
2) 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.
*
Corresponding author. Mailing address: Department of
Biological Chemistry and Molecular Pharmacology, Harvard Medical
School, 240 Longwood Ave., Boston, MA 02115-5730. Phone: (617)
432-2104. Fax: (617) 432-2529. E-mail:
kevin{at}hms.harvard.edu.
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