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Characterizing the roles of Met31 and Met32 in coordinating Met4-activated transcription in the absence of Met30
Year:
2012
Source of publication :
Molecular Biology of the Cell
Authors :
Ben-Ari, Giora
;
.
Volume :
23
Co-Authors:
Carrillo, E., Department of Biological Sciences, University of Wisconsin-Parkside, Kenosha, WI 53144, United States
Ben-Ari, G., Agricultural Research Organization, Bet-Dagan 50250, Israel
Wildenhain, J., Wellcome Trust Centre for Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom
Tyers, M., Wellcome Trust Centre for Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom
Grammentz, D., Department of Biological Sciences, University of Wisconsin-Parkside, Kenosha, WI 53144, United States
Lee, T.A., Department of Biological Sciences, University of Wisconsin-Parkside, Kenosha, WI 53144, United States
Facilitators :
From page:
1928
To page:
1942
(
Total pages:
15
)
Abstract:
Yeast sulfur metabolism is transcriptionally regulated by the activator Met4. Met4 lacks DNA-binding ability and relies on interactions with Met31 and Met32, paralogous proteins that bind the same cis-regulatory element, to activate its targets. Although Met31 and Met32 are redundant for growth in the absence of methionine, studies indicate that Met32 has a prominent role over Met31 when Met30, a negative regulator of Met4 and Met32, is inactive. To characterize different roles of Met31 and Met32 in coordinating Met4- activated transcription, we examined transcription in strains lacking either Met31 or Met32 upon Met4 induction in the absence of Met30. Microarray analysis revealed that transcripts involved in sulfate assimilation and sulfonate metabolism were dramatically decreased in met32Δ cells compared to its wild-type and met31Δ counterparts. Despite this difference, both met31Δ and met32Δ cells used inorganic sulfur compounds and sulfonates as sole sulfur sources in minimal media when Met30 was present. This discrepancy may be explained by differential binding of Met31 to Cbf1-dependent promoters between these two conditions. In the absence of Met30, genome-wide chromatin immunoprecipitation analyses found that Met32 bound all Met4-bound targets, supporting Met32 as the main platform for Met4 recruitment. Finally, Met31 and Met32 levels were differentially regulated, with Met32 levels mimicking the profile for active Met4. These different properties of Met32 likely contribute to its prominent role in Met4-activated transcription when Met30 is absent. © 2012 Carrillo et al.
Note:
Related Files :
metabolism
Microarray analysis
phenotype
sulfate
transcription factor Met14
transcription factor Met31
Show More
Related Content
More details
DOI :
10.1091/mbc.E11-06-0532
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
30346
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:53
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Scientific Publication
Characterizing the roles of Met31 and Met32 in coordinating Met4-activated transcription in the absence of Met30
23
Carrillo, E., Department of Biological Sciences, University of Wisconsin-Parkside, Kenosha, WI 53144, United States
Ben-Ari, G., Agricultural Research Organization, Bet-Dagan 50250, Israel
Wildenhain, J., Wellcome Trust Centre for Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom
Tyers, M., Wellcome Trust Centre for Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom
Grammentz, D., Department of Biological Sciences, University of Wisconsin-Parkside, Kenosha, WI 53144, United States
Lee, T.A., Department of Biological Sciences, University of Wisconsin-Parkside, Kenosha, WI 53144, United States
Characterizing the roles of Met31 and Met32 in coordinating Met4-activated transcription in the absence of Met30
Yeast sulfur metabolism is transcriptionally regulated by the activator Met4. Met4 lacks DNA-binding ability and relies on interactions with Met31 and Met32, paralogous proteins that bind the same cis-regulatory element, to activate its targets. Although Met31 and Met32 are redundant for growth in the absence of methionine, studies indicate that Met32 has a prominent role over Met31 when Met30, a negative regulator of Met4 and Met32, is inactive. To characterize different roles of Met31 and Met32 in coordinating Met4- activated transcription, we examined transcription in strains lacking either Met31 or Met32 upon Met4 induction in the absence of Met30. Microarray analysis revealed that transcripts involved in sulfate assimilation and sulfonate metabolism were dramatically decreased in met32Δ cells compared to its wild-type and met31Δ counterparts. Despite this difference, both met31Δ and met32Δ cells used inorganic sulfur compounds and sulfonates as sole sulfur sources in minimal media when Met30 was present. This discrepancy may be explained by differential binding of Met31 to Cbf1-dependent promoters between these two conditions. In the absence of Met30, genome-wide chromatin immunoprecipitation analyses found that Met32 bound all Met4-bound targets, supporting Met32 as the main platform for Met4 recruitment. Finally, Met31 and Met32 levels were differentially regulated, with Met32 levels mimicking the profile for active Met4. These different properties of Met32 likely contribute to its prominent role in Met4-activated transcription when Met30 is absent. © 2012 Carrillo et al.
Scientific Publication
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