ArticleFrontiers in microbiology2015
Transcription factors Asg1p and Hal9p regulate pH homeostasis in Candida glabrata.
Article in Frontiers in microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
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- Med15B Regulates Acid Stress Response and Tolerance in Candida glabrata by Altering Membrane Lipid Composition.Applied and environmental microbiology · 2017Article
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- Crz1p Regulates pH Homeostasis in Candida glabrata by Altering Membrane Lipid Composition.Applied and environmental microbiology · 2016Article
- Membrane Proteomics Analysis of theFrontiers in microbiology · 2016Article
- A Network of Paralogous Stress Response Transcription Factors in the Human Pathogen Candida glabrata.Frontiers in microbiology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Candida glabrata is an important microorganism used in commercial fermentation to produce pyruvate, but very little is known about its mechanisms for surviving acid stress in culture. In this study, it was shown that transcription factors Asg1p and Hal9p play essential roles in C. glabrata in the tolerance of acid stress, as the deletion of CgASG1 or CgHAL9 resulted in the inability to survive in an acidic environment. Cgasg1Δ and Cghal9Δ mutant strains are unable to maintain pH homeostasis, as evidenced by a decrease in intracellular pH and an increase in reactive oxygen species production, which results in metabolic disorders. The results showed that intracellular acidification was partly due to the diminished activity of the plasma membrane proton pump, CgPma1p. In addition, transcriptome sequencing revealed that Cgasg1Δ and Cghal9Δ mutant strains displayed a variety of changes in gene expression under acidic conditions, including genes in the MAPK signaling pathway, plasma membrane, or cell wall organization, trehalose accumulation, and the RIM101 signaling pathway. Lastly, quantitative reverse-transcribed PCR and cellular localization showed that CgAsg1p and CgHal9p played independent roles in response to acid stress.
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