Evidence map›Paper›PMID 25547512›Full record

ArticleCurrent genetics2015

Dissection of the PHO pathway in Schizosaccharomyces pombe using epistasis and the alternate repressor adenine.

Molly Estill, Christine L Kerwin-Iosue, Dennis D Wykoff

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Article in Current genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.6field-weighted citation impact, top 33% of its field
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 34 citations in OpenAlex.

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  11. Long RNA-Mediated Chromatin Regulation in Fission Yeast and Mammals.International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Molly EstillDepartment of Biology, Villanova University, Villanova, PA, 19085, USA.
Christine L Kerwin-Iosue
Dennis D Wykoff
Villanova University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Saccharomyces cerevisiae, intracellular phosphate levels are maintained by the PHO pathway, activation of which is assayed by increased phosphatase activity. The PHO pathway of Schizosaccharomyces pombe upregulates phosphatase activity (encoded by pho1 (+)) during low extracellular phosphate levels, but the underlying mechanism is poorly understood. We utilized an alternate repressor of pho1 (+) expression (adenine supplementation) along with epistasis analysis to develop a model of how S. pombe PHO pathway components interact. Analyzing Pho1 activity in S. pombe PHO pathway deletion mutants during adenine starvation, we observed most mutants with a phosphatase defect in phosphate starvation also had a defect in adenine starvation. Pho7, a transcription factor in the PHO pathway, is necessary for an adenine starvation-mediated increase in Pho1 activity. Comparing adenine starvation to phosphate starvation, there are differences in the degree to which individual mutants regulate the two responses. Through epistasis studies, we identified two positive regulatory arms and one repressive arm of the PHO pathway. PKA activation is a positive regulator of Pho1 activity under both environmental conditions and is critical for transducing adenine concentrations in the cell. The synthesis of IP7 also appears critical for the induction of Pho1 activity during adenine starvation, but IP7 is not critical during phosphate starvation, which differs from S. cerevisiae. Finally, Csk1 is critical for repression of pho1 (+) expression during phosphate starvation. We believe all of these regulatory arms converge to increase transcription of pho1 (+) and some of the regulation acts through pho7 (+).

Indexed as

Epistasis, GeneticAcid PhosphataseAdenineGene Expression Regulation, FungalPhosphatesProtein KinasesSchizosaccharomycesSchizosaccharomyces pombe ProteinsSequence DeletionSignal TransductionTranscription FactorsAcid Phosphataseacid phosphatase Pho1, S pombeAdenineCsk1 protein, S pombePhosphatesProtein KinasesSchizosaccharomyces pombe ProteinsTranscription Factors

Identifiers

PMID25547512
OpenAlexW2022580630

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.