ArticleRNA (New York, N.Y.)2015
RNA polymerase II CTD phospho-sites Ser5 and Ser7 govern phosphate homeostasis in fission yeast.
Article in RNA (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Genetic suppression of precocious transcription termination identifies mutations in essential subunits of the fission yeast cleavage and polyadenylation machinery.RNA (New York, N.Y.) · 2025Article
- Suppression of inositol pyrophosphate toxicosis and hyper-repression of the fission yeastmBio · 2024Article
- Ssu72: a versatile protein with functions in transcription and beyond.Frontiers in molecular biosciences · 2024Review
- Fission yeast poly(A) polymerase active site mutation Y86D alleviates theRNA (New York, N.Y.) · 2023Article
- Inositol pyrophosphate dynamics reveals control of the yeast phosphate starvation program through 1,5-IPeLife · 2023Article
- Duf89 abets lncRNA control of fission yeast phosphate homeostasis via its antagonism of precocious lncRNA transcription termination.RNA (New York, N.Y.) · 2023Article
- Genetic screen for suppression of transcriptional interference reveals fission yeast 14-3-3 protein Rad24 as an antagonist of precocious Pol2 transcription termination.Nucleic acids research · 2022Article
- Long RNA-Mediated Chromatin Regulation in Fission Yeast and Mammals.International journal of molecular sciences · 2022Review
- Genetic screen for suppression of transcriptional interference identifies a gain-of-function mutation in Pol2 termination factor Seb1.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Diverse and conserved roles of the protein Ssu72 in eukaryotes: from yeast to higher organisms.Current genetics · 2021Review
- Structure-function analysis of fission yeast cleavage and polyadenylation factor (CPF) subunit Ppn1 and its interactions with Dis2 and Swd22.PLoS genetics · 2021Article
- Article
- A genetic screen for suppressors of hyper-repression of the fission yeast PHO regulon by Pol2 CTD mutation T4A implicates inositol 1-pyrophosphates as agonists of precocious lncRNA transcription termination.Nucleic acids research · 2020Article
- A lncRNA-regulated gene expression system with rapid induction kinetics in the fission yeastRNA (New York, N.Y.) · 2020Article
- Inactivation of fission yeast Erh1 de-repressesRNA (New York, N.Y.) · 2020Article
- Genetic interactions and transcriptomics implicate fission yeast CTD prolyl isomerase Pin1 as an agent of RNA 3' processing and transcription termination that functions via its effects on CTD phosphatase Ssu72.Nucleic acids research · 2020Article
- Inositol pyrophosphates impact phosphate homeostasis via modulation of RNA 3' processing and transcription termination.Nucleic acids research · 2019Article
- Structure of Fission Yeast Transcription Factor Pho7 Bound toMolecular and cellular biology · 2019Article
- Distinctive structural basis for DNA recognition by the fission yeast Zn2Cys6 transcription factor Pho7 and its role in phosphate homeostasis.Nucleic acids research · 2018Article
- RNA polymerase II CTD interactome with 3' processing and termination factors in fission yeast and its impact on phosphate homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Phosphorylation of the tandem YSPTSPS repeats of the RNA polymerase II CTD inscribes an informational code that orchestrates eukaryal mRNA synthesis. Here we interrogate the role of the CTD in phosphate homeostasis in fission yeast. Expression of Pho1 acid phosphatase, which is repressed during growth in phosphate-rich medium and induced by phosphate starvation, is governed strongly by CTD phosphorylation status, but not by CTD repeat length. Inability to place a Ser7-PO4 mark (as in S7A) results in constitutive derepression of Pho1 expression in phosphate-replete medium. In contrast, indelible installation of a Ser7-PO4 mimetic (as in S7E) hyper-represses Pho1 in phosphate-replete cells and inhibits Pho1 induction during starvation. Pho1 phosphatase is derepressed by ablation of the CTD Ser5-PO4 mark, achieved either by mutating Ser5 in all consensus heptads to alanine, or replacing all Pro6 residues with alanine. We find that Ser5 status is a tunable determinant of Pho1 regulation, i.e., serial decrements in the number of consensus Ser5 heptads from seven to two elicits a progressive increase in Pho1 expression in phosphate-replete medium. Pho1 is also derepressed by hypomorphic mutations of the CTD kinase Cdk9. Inactivation of the CTD phosphatase Ssu72 attenuates Pho1 induction in wild-type cells and blocks Pho1 derepression in S7A cells. These experiments implicate Ser5, Pro6, and Ser7 as component letters of a CTD coding "word" that transduces a repressive transcriptional signal via serine phosphorylation.
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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.