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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)

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-...

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Autores principales: Gurvitz, Aner, Suomi, Fumi, Rottensteiner, Hanspeter, Hiltunen, J Kalervo, Dawes, Ian W
Formato: Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784042/
https://www.ncbi.nlm.nih.gov/pubmed/19583587
http://dx.doi.org/10.1111/j.1567-1364.2009.00527.x
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author Gurvitz, Aner
Suomi, Fumi
Rottensteiner, Hanspeter
Hiltunen, J Kalervo
Dawes, Ian W
author_facet Gurvitz, Aner
Suomi, Fumi
Rottensteiner, Hanspeter
Hiltunen, J Kalervo
Dawes, Ian W
author_sort Gurvitz, Aner
collection PubMed
description 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 sum1Δ, hst1Δ, or rfm1Δ cells, oleic acid-dependent expression of SPS18 was higher compared with the situation in wild-type cells, but in the sum1Δ 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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spelling pubmed-27840422009-11-28 Avoiding unscheduled transcription in shared promoters: Saccharomyces cerevisiae Sum1p represses the divergent gene pair SPS18-SPS19 through a midsporulation element (MSE) Gurvitz, Aner Suomi, Fumi Rottensteiner, Hanspeter Hiltunen, J Kalervo Dawes, Ian W FEMS Yeast Res Research Articles 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 sum1Δ, hst1Δ, or rfm1Δ cells, oleic acid-dependent expression of SPS18 was higher compared with the situation in wild-type cells, but in the sum1Δ 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. Blackwell Publishing Ltd 2009-09 2009-07-03 /pmc/articles/PMC2784042/ /pubmed/19583587 http://dx.doi.org/10.1111/j.1567-1364.2009.00527.x Text en © 2009 The Authors. Journal compilation © 2009 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. http://creativecommons.org/licenses/by/2.5/ Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.
spellingShingle Research Articles
Gurvitz, Aner
Suomi, Fumi
Rottensteiner, Hanspeter
Hiltunen, J Kalervo
Dawes, Ian W
Avoiding unscheduled transcription in shared promoters: Saccharomyces cerevisiae Sum1p represses the divergent gene pair SPS18-SPS19 through a midsporulation element (MSE)
title Avoiding unscheduled transcription in shared promoters: Saccharomyces cerevisiae Sum1p represses the divergent gene pair SPS18-SPS19 through a midsporulation element (MSE)
title_full Avoiding unscheduled transcription in shared promoters: Saccharomyces cerevisiae Sum1p represses the divergent gene pair SPS18-SPS19 through a midsporulation element (MSE)
title_fullStr Avoiding unscheduled transcription in shared promoters: Saccharomyces cerevisiae Sum1p represses the divergent gene pair SPS18-SPS19 through a midsporulation element (MSE)
title_full_unstemmed Avoiding unscheduled transcription in shared promoters: Saccharomyces cerevisiae Sum1p represses the divergent gene pair SPS18-SPS19 through a midsporulation element (MSE)
title_short Avoiding unscheduled transcription in shared promoters: Saccharomyces cerevisiae Sum1p represses the divergent gene pair SPS18-SPS19 through a midsporulation element (MSE)
title_sort avoiding unscheduled transcription in shared promoters: saccharomyces cerevisiae sum1p represses the divergent gene pair sps18-sps19 through a midsporulation element (mse)
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784042/
https://www.ncbi.nlm.nih.gov/pubmed/19583587
http://dx.doi.org/10.1111/j.1567-1364.2009.00527.x
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