ArticleCurrent genetics2014
The expression of PHO92 is regulated by Gcr1, and Pho92 is involved in glucose metabolism in Saccharomyces cerevisiae.
Article in Current genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Expression pattern and phenotypic characterization of the mutant strain reveals target genes and processes regulated by pka1 in the dimorphic fission yeast Schizosaccharomyces japonicus.Current genetics · 2017Article
- Reprogramming of nonfermentative metabolism by stress-responsive transcription factors in the yeast Saccharomyces cerevisiae.Current genetics · 2017Review
- Core regulatory components of the PHO pathway are conserved in the methylotrophic yeast Hansenula polymorpha.Current genetics · 2016Article
- Responses to phosphate deprivation in yeast cells.Current genetics · 2016Review
- Cracking the epitranscriptome.RNA (New York, N.Y.) · 2016Review
- Less is more: Nutrient limitation induces cross-talk of nutrient sensing pathways with NADFrontiers in biology · 2015Article
- Regulation of NAD+ metabolism, signaling and compartmentalization in the yeast Saccharomyces cerevisiae.DNA repair · 2014Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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Abstract
Ydr374c (Pho92) contains a YTH domain in its C-terminal region and is a human YTHDF2 homologue. Previously, we reported that Pho92 regulates phosphate metabolism by regulating PHO4 mRNA stability. In this study, we found that growth of the ∆pho92 strain on SG media was slower than that of the wild type and that PHO92 expression was up-regulated by non-fermentable carbon sources, such as ethanol and glycerol, but not by fermentable carbon sources. Furthermore, two conserved Gcr1-binding regions were identified in the upstream, untranslated region of PHO92. Gcr1 is an important factor involved in the coordinated regulation of glycolytic gene expression. Mutation of two Gcr1-binding sites of the PHO92 upstream region resulted in a growth defect on SD media. Finally, mutagenesis of the Gcr1-binding sites of the PHO92 upstream region and deletion of GCR1 resulted in up-regulation of PHO92, and this resulted from inhibition of PHO4 mRNA degradation. Based on these results, we suggest that Gcr1 regulates the expression of PHO92, and Pho92 is involved in glucose metabolism.
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