ArticlePloS one2012
Pph3 dephosphorylation of Rad53 is required for cell recovery from MMS-induced DNA damage in Candida albicans.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- From Jekyll to Hyde: The Yeast-Hyphal Transition ofPathogens (Basel, Switzerland) · 2021Review
- DNA damage response of major fungal pathogen Candida glabrata offers clues to explain its genetic diversity.Current genetics · 2021Review
- Article
- Functional connections between cell cycle and proteostasis in the regulation of Candida albicans morphogenesis.Cell reports · 2021Review
- Article
- Characterization of a novel separase-interacting protein and candidate new securin, Eip1p, in the fungal pathogenMolecular biology of the cell · 2019Article
- Ser/Thr protein phosphatases in fungi: structure, regulation and function.Microbial cell (Graz, Austria) · 2019Review
- Dissecting Nucleosome Function with a Comprehensive Histone H2A and H2B Mutant Library.G3 (Bethesda, Md.) · 2017Article
- Phenotypic Consequences of a Spontaneous Loss of Heterozygosity in a Common Laboratory Strain of Candida albicans.Genetics · 2016Article
- Ppg1, a PP2A-type protein phosphatase, controls filament extension and virulence in Candida albicans.Eukaryotic cell · 2014Article
- Rfa2 is specifically dephosphorylated by Pph3 in Candida albicans.The Biochemical journal · 2013Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenic fungus Candida albicans switches from yeast growth to filamentous growth in response to genotoxic stresses, in which phosphoregulation of the checkpoint kinase Rad53 plays a crucial role. Here we report that the Pph3/Psy2 phosphatase complex, known to be involved in Rad53 dephosphorylation, is required for cellular responses to the DNA-damaging agent methyl methanesulfonate (MMS) but not the DNA replication inhibitor hydroxyurea (HU) in C. albicans. Deletion of either PPH3 or PSY2 resulted in enhanced filamentous growth during MMS treatment and continuous filamentous growth even after MMS removal. Moreover, during this growth, Rad53 remained hyperphosphorylated, MBF-regulated genes were downregulated, and hypha-specific genes were upregulated. We have also identified S461 and S545 on Rad53 as potential dephosphorylation sites of Pph3/Psy2 that are specifically involved in cellular responses to MMS. Therefore, our studies have identified a novel molecular mechanism mediating DNA damage response to MMS in C. albicans.
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