Mediator Acts Upstream of the Transcriptional Activator Gal4

Ang, Keven; Ee, Gary; Ang, Edwin; Koh, Elvin; Siew, Wee Leng; Chan, Yu Mun; Nur, Sabrina; Tan, Yee Sun; Lehming, Norbert

doi:10.1371/journal.pbio.1001290

Cited by 13 publications

(6 citation statements)

References 59 publications

(93 reference statements)

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“…Intriguingly, the recruitment of TBP and RNA polymerase II to the promoter during GAL sense transcription is facilitated by the proteasome (1,2,49,92). Such regulation has recently been attributed to occur via degradation of Gal80p (92), which specifically controls GAL1-GAL10 sense transcription (60,61,(68)(69)(70)(71). However, our RT-PCR analysis revealed that, unlike its sense transcription, GAL10 antisense transcription in dextrose-containing growth medium was not regulated by the proteasome (Fig.…”

Section: Fig 4 Rna Polymerase II Is Essential For Gal10 Antisense Tramentioning

confidence: 72%

“…Collectively, our data support the idea that TBP promotes the targeting of RNA polymerase II for antisense transcription. Intriguingly, the recruitment of TBP and RNA polymerase II to the promoter during GAL sense transcription is facilitated by the proteasome (1,2,49,92). Such regulation has recently been attributed to occur via degradation of Gal80p (92), which specifically controls GAL1-GAL10 sense transcription (60,61,(68)(69)(70)(71).…”

Section: Fig 4 Rna Polymerase II Is Essential For Gal10 Antisense Tramentioning

confidence: 99%

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Mechanisms of Antisense Transcription Initiation from the 3′ End of the GAL10 Coding Sequence In Vivo

Malik

Durairaj

Bhaumik

2013

Molecular and Cellular Biology

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In spite of the important regulatory functions of antisense transcripts in gene expression, it remains unknown how antisense transcription is initiated. Recent studies implicated RNA polymerase II in initiation of antisense transcription. However, how RNA polymerase II is targeted to initiate antisense transcription has not been elucidated. Here, we have analyzed the association of RNA polymerase II with the antisense initiation site at the 3= end of the GAL10 coding sequence in dextrose-containing growth medium that induces antisense transcription. We find that RNA polymerase II is targeted to the antisense initiation site at GAL10 by Reb1p activator as well as general transcription factors (e.g., TFIID, TFIIB, and Mediator) for antisense transcription initiation. Intriguingly, while GAL10 antisense transcription is dependent on TFIID, its sense transcription does not require TFIID. Further, the Gal4p activator that promotes GAL10 sense transcription is dispensable for antisense transcription. Moreover, the proteasome that facilitates GAL10 sense transcription does not control its antisense transcription. Taken together, our results reveal that GAL10 sense and antisense transcriptions are regulated differently and shed much light on the mechanisms of antisense transcription initiation.

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Section: Fig 4 Rna Polymerase II Is Essential For Gal10 Antisense Tramentioning

confidence: 72%

Section: Fig 4 Rna Polymerase II Is Essential For Gal10 Antisense Tramentioning

confidence: 99%

Mechanisms of Antisense Transcription Initiation from the 3′ End of the GAL10 Coding Sequence In Vivo

Malik

Durairaj

Bhaumik

2013

Molecular and Cellular Biology

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“…Transcriptional complexes such as the mediator are able to orchestrate their own recruitment to the GAL promoter and act upstream of their recruiter, Gal4, in response to Snf1-conveyed signals, by controlling the E3 ligase SCF Mdm30 -mediated ubiquitination and subsequent proteasomal degradation of Gal80 (Ang et al ., 2012 ). Gal4 monoubiquitination, initially thought to destabilize this transcription factor, seems to serve instead as protective mechanism against the promoter-stripping proteasome ATPases (Archer et al ., 2008 ).…”

Section: Specific Nutrient Signaling Pathways: Triggered By a Single mentioning

confidence: 99%

Nutrient sensing and signaling in the yeastSaccharomyces cerevisiae

et al. 2014

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The yeast Saccharomyces cerevisiae has been a favorite organism for pioneering studies on nutrient-sensing and signaling mechanisms. Many specific nutrient responses have been elucidated in great detail. This has led to important new concepts and insight into nutrient-controlled cellular regulation. Major highlights include the central role of the Snf1 protein kinase in the glucose repression pathway, galactose induction, the discovery of a G-protein-coupled receptor system, and role of Ras in glucose-induced cAMP signaling, the role of the protein synthesis initiation machinery in general control of nitrogen metabolism, the cyclin-controlled protein kinase Pho85 in phosphate regulation, nitrogen catabolite repression and the nitrogen-sensing target of rapamycin pathway, and the discovery of transporter-like proteins acting as nutrient sensors. In addition, a number of cellular targets, like carbohydrate stores, stress tolerance, and ribosomal gene expression, are controlled by the presence of multiple nutrients. The protein kinase A signaling pathway plays a major role in this general nutrient response. It has led to the discovery of nutrient transceptors (transporter receptors) as nutrient sensors. Major shortcomings in our knowledge are the relationship between rapid and steady-state nutrient signaling, the role of metabolic intermediates in intracellular nutrient sensing, and the identity of the nutrient sensors controlling cellular growth.

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“…This result contrasts with our report that Cdc48 stimulates the activity of the yeast activator Gal4 ( Bonizec et al ., 2014 ). To confirm that Gcn4 and Gal4 are affected differently by the cdc48-3 mutation, we examined Gal4 activity in the cdc48-3 mutant strain; we also examined the effect of GAL80 deletion in this context, which has been argued to be a point of Gal4 regulation by the UPS ( Ang et al ., 2012 ). Supporting our previous study ( Bonizec et al ., 2014 ), mutation of Cdc48 reduced activation of the GAL10 locus ( Figure 4H ), whereas the GAL80 deletion did not affect the sensitivity of GAL10 transcription to the cdc48 -3 mutation.…”

Section: Resultsmentioning

confidence: 99%

Interaction of Gcn4 with target gene chromatin is modulated by proteasome function

Howard

Tansey

2016

MBoC

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Mediator Acts Upstream of the Transcriptional Activator Gal4

Abstract: We show that Mediator, a protein originally isolated on the basis of its ability to respond to transcriptional activators, and thought to be regulated by an activator, can also be the master that controls the activator.

Cited by 13 publications

References 59 publications

Mechanisms of Antisense Transcription Initiation from the 3′ End of the GAL10 Coding Sequence In Vivo

Mechanisms of Antisense Transcription Initiation from the 3′ End of the GAL10 Coding Sequence In Vivo

Nutrient sensing and signaling in the yeastSaccharomyces cerevisiae

Interaction of Gcn4 with target gene chromatin is modulated by proteasome function

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