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Avoiding unscheduled transcription in shared promoters: Saccharomyces cerevisiae Sum1p represses the divergent gene pair SPS18 ‐ SPS19 through a midsporulation element (MSE)
Author(s) -
Gurvitz Aner,
Suomi Fumi,
Rottensteiner Hanspeter,
Hiltunen J. Kalervo,
Dawes Ian W.
Publication year - 2009
Publication title -
fems yeast research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 92
eISSN - 1567-1364
pISSN - 1567-1356
DOI - 10.1111/j.1567-1364.2009.00527.x
Subject(s) - biology , repressor , promoter , transcription (linguistics) , gene , mutant , saccharomyces cerevisiae , oleic acid , transcription factor , reporter gene , microbiology and biotechnology , lac operon , gene expression , genetics , biochemistry , linguistics , philosophy
The sporulation‐specific gene SPS18 shares a common promoter region with the oleic acid‐inducible gene SPS19 . Both genes are transcribed in sporulating diploid cells, albeit unevenly in favour of SPS18 , whereas in haploid cells grown on fatty acids only SPS19 is highly activated. Here, SPS19 oleate‐response element (ORE) conferred activation on a basal CYC1‐lacZ reporter gene equally in both orientations, but promoter analysis using SPS18‐lacZ reporter constructs with deletions identified a repressing fragment containing a midsporulation element (MSE) that could be involved in imposing directionality towards SPS19 in oleic acid‐induced cells. In sporulating diploids, MSEs recruit the Ndt80p transcription factor for activation, whereas under vegetative conditions, certain MSEs are targeted by the Sum1p repressor in association with Hst1p and Rfm1p. Quantitative real‐time PCR demonstrated that in haploid sum1 Δ, hst1 Δ, or rfm1 Δ cells, oleic acid‐dependent expression of SPS18 was higher compared with the situation in wild‐type cells, but in the sum1 Δ mutant, this effect was diminished in the absence of Oaf1p or Pip2p. We conclude that SPS18 MSE is a functional element repressing the expression of both SPS18 and SPS19 , and is a component of a stricture mechanism shielding SPS18 from the dramatic increase in ORE‐dependent transcription of SPS19 in oleic acid‐grown cells.

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