ArticleMolecular biology of the cell2012
Characterizing the roles of Met31 and Met32 in coordinating Met4-activated transcription in the absence of Met30.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
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- The Swi-Snf chromatin remodeling complex mediates gene repression through metabolic control.Nucleic acids research · 2023Article
- Linking the dynamics of chromatin occupancy and transcription with predictive models.Genome research · 2021Article
- Cdc48 cofactor Shp1 regulates signal-induced SCFProceedings of the National Academy of Sciences of the United States of America · 2020Article
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- Three distinct mechanisms of long-distance modulation of gene expression in yeast.PLoS genetics · 2017Article
- TIF-IA: An oncogenic target of pre-ribosomal RNA synthesis.Biochimica et biophysica acta · 2016Review
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- Identifying genetic modulators of the connectivity between transcription factors and their transcriptional targets.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Leveraging transcription factors to speed cellobiose fermentation by Saccharomyces cerevisiae.Biotechnology for biofuels · 2014Article
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.