ArticleAntimicrobial agents and chemotherapy2014
Transcription factor CCG-8 as a new regulator in the adaptation to antifungal azole stress.
Article in Antimicrobial agents and chemotherapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
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- The role of VdSti1 in Verticillium dahliae: insights into pathogenicity and stress responses.Frontiers in microbiology · 2024Article
- The expression pattern, subcellular localization and function of three sterol 14α-demethylases inFrontiers in genetics · 2023Article
- Assessing Differences between Clinical Isolates ofPathogens (Basel, Switzerland) · 2022Article
- Coordinated Regulation of Membrane Homeostasis and Drug Accumulation by Novel Kinase STK-17 in Response to Antifungal Azole Treatment.Microbiology spectrum · 2022Article
- Fungal Zn(II)Antimicrobial agents and chemotherapy · 2021Article
- Transcription factor CCG-8 plays a pivotal role in azole adaptive responses of Neurospora crassa by regulating intracellular azole accumulation.Current genetics · 2019Article
- A new mechanism for reduced sensitivity to demethylation-inhibitor fungicides in the fungal banana black Sigatoka pathogen Pseudocercospora fijiensis.Molecular plant pathology · 2018Article
- Biofilm Formation and Resistance to Fungicides in Clinically Relevant Members of the Fungal Genus Fusarium.Journal of fungi (Basel, Switzerland) · 2018Article
- Abnormal Ergosterol Biosynthesis Activates Transcriptional Responses to Antifungal Azoles.Frontiers in microbiology · 2018Article
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- Function of the genetic element 'Mona' associated with fungicide resistance in Monilinia fructicola.Molecular plant pathology · 2017Article
- A Novel Zn2-Cys6 Transcription Factor AtrR Plays a Key Role in an Azole Resistance Mechanism of Aspergillus fumigatus by Co-regulating cyp51A and cdr1B Expressions.PLoS pathogens · 2017Article
- Article
- De-repression of CSP-1 activates adaptive responses to antifungal azoles.Scientific reports · 2016Article
- The Hsp90 Co-chaperones Sti1, Aha1, and P23 Regulate Adaptive Responses to Antifungal Azoles.Frontiers in microbiology · 2016Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antifungal azoles are widely used for controlling fungal infections. Fungi are able to change the expression of many genes when they adapt to azole stress, and increased expression of some of these genes can elevate resistance to azoles. However, the regulatory mechanisms behind transcriptional adaption to azoles in filamentous fungi are poorly understood. In this study, we found that deletion of the transcription factor gene ccg-8, which is known to be a clock-controlled gene, made Neurospora crassa hypersensitive to azoles. A comparative genome-wide analysis of the responses to ketoconazole of the wild type and the ccg-8 mutant revealed that the transcriptional responses to ketoconazole of 78 of the 488 transcriptionally ketoconazole-upregulated genes and the 427 transcriptionally ketoconazole-downregulated genes in the wild type were regulated by CCG-8. Ketoconazole sensitivity testing of all available knockout mutants for CCG-8-regulated genes revealed that CCG-8 contributed to azole adaption by regulating the ketoconazole responses of many genes, including the target gene (erg11), an azole transporter gene (cdr4), a hexose transporter gene (hxt13), a stress response gene (locus number NCU06317, named kts-1), two transcription factor genes (NCU01386 [named kts-2] and fsd-1/ndt80), four enzyme-encoding genes, and six unknown-function genes. CCG-8 also regulated phospholipid synthesis in N. crassa in a manner similar to that of its homolog in Saccharomyces cerevisiae, Opi1p. However, there was no cross talk between phospholipid synthesis and azole resistance in N. crassa. CCG-8 homologs are conserved and are common in filamentous fungi. Deletion of the CCG-8 homolog-encoding gene in Fusarium verticillioides (Fvccg-8) also made this fungus hypersensitive to antifungal azoles.
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