ArticleMolecular biology of the cell2007
Critical role of DNA checkpoints in mediating genotoxic-stress-induced filamentous growth in Candida albicans.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 124 citations in OpenAlex.
- Rad53 orchestrates divergent pathways governing genotoxic resistance, morphogenesis, and virulence inVirulence · 2025Article
- A CRISPR-Cas9-based system for the dose-dependent study of DNA double-strand break sensing and repair.The FEBS journal · 2025Article
- Yeast gene of unknown functionmicroPublication biology · 2025Article
- Genetic microevolution of clinicalEmerging microbes & infections · 2024Article
- Raman Spectroscopic Algorithms for Assessing Virulence in Oral Candidiasis: The Fight-or-Flight Response.International journal of molecular sciences · 2024Article
- Loss of Gst1 enhances resistance to MMS by reprogramming the transcription of DNA damage response genes in a Rad53-dependent manner in Candida albicans.Cell communication and signaling : CCS · 2024Article
- DNA Damage Checkpoints Govern Global Gene Transcription and Exhibit Species-Specific Regulation onJournal of fungi (Basel, Switzerland) · 2024Article
- Opi1-mediated transcriptional modulation orchestrates genotoxic stress response in budding yeast.Genetics · 2023Article
- Essential Roles of Ribonucleotide Reductases under DNA Damage and Replication Stresses in Cryptococcus neoformans.Microbiology spectrum · 2022Article
- Article
- The macrophage-derived protein PTMA induces filamentation of the human fungal pathogen Candida albicans.Cell reports · 2021Article
- From Jekyll to Hyde: The Yeast-Hyphal Transition ofPathogens (Basel, Switzerland) · 2021Review
- LncRNA DINOR is a virulence factor and global regulator of stress responses in Candida auris.Nature microbiology · 2021Article
- DNA damage response of major fungal pathogen Candida glabrata offers clues to explain its genetic diversity.Current genetics · 2021Review
- Factors that influence bidirectional long-tract homozygosis due to double-strand break repair in Candida albicans.Genetics · 2021Article
- Functional connections between cell cycle and proteostasis in the regulation of Candida albicans morphogenesis.Cell reports · 2021Review
- DNA damage checkpoint and repair: From the budding yeastComputational and structural biotechnology journal · 2021Review
- Pseudohyphal Growth of the Emerging Pathogen Candida auris Is Triggered by Genotoxic Stress through the S Phase Checkpoint.mSphere · 2020Article
- Hof1 plays a checkpoint-related role in MMS-induced DNA damage response inMolecular biology of the cell · 2020Article
- Nucleotide Excision Repair Protein Rad23 Regulates Cell Virulence Independent of Rad4 in Candida albicans.mSphere · 2020Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The polymorphic fungus Candida albicans switches from yeast to filamentous growth in response to a range of genotoxic insults, including inhibition of DNA synthesis by hydroxyurea (HU) or aphidicolin (AC), depletion of the ribonucleotide-reductase subunit Rnr2p, and DNA damage induced by methylmethane sulfonate (MMS) or UV light (UV). Deleting RAD53, which encodes a downstream effector kinase for both the DNA-replication and DNA-damage checkpoint pathways, completely abolished the filamentous growth caused by all the genotoxins tested. Deleting RAD9, which encodes a signal transducer of the DNA-damage checkpoint, specifically blocked the filamentous growth induced by MMS or UV but not that induced by HU or AC. Deleting MRC1, the counterpart of RAD9 in the DNA-replication checkpoint, impaired DNA synthesis and caused cell elongation even in the absence of external genotoxic insults. Together, the results indicate that the DNA-replication/damage checkpoints are critically required for the induction of filamentous growth by genotoxic stress. In addition, either of two mutations in the FHA1 domain of Rad53p, G65A, and N104A, nearly completely blocked the filamentous-growth response but had no significant deleterious effect on cell-cycle arrest. These results suggest that the FHA domain, known for its ability to bind phosphopeptides, has an important role in mediating genotoxic-stress-induced filamentous growth and that such growth is a specific, Rad53p-regulated cellular response in C. albicans.
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Registered trials
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.