The Role of the Mediator Complex in Modulating <i>CjXDR1</i> -Induced Multidrug Resistance and Virulence in <i>Clarireedia jacksonii</i>
The Mediator complex is a central regulator of gene expression in pathogenic fungi, however, its composition and functions remain uncharacterized in Clarireedia jacksonii, a major fungal pathogen in turfgrass. In this study, we systematically analyzed the Mediator complex in C. jacksonii and identified its key role in transcriptional activation. Functional characterization of ten knockout mutants revealed distinct roles for Mediator subunits in cell growth, fungicide resistance, pathogenicity, and stress responses. Notably, Med1, Med31, Med15, and Cdk8 were essential for pathogenicity, while subunits from Tail and Kinase modules were closely associated with fungicide resistance and exhibited altered expression upon CjXDR1 deletion. Deletion of Med5 increased sensitivity to propiconazole, whereas deletion of Cdk8 and CycC conferred fungicide resistance. Further analyses demonstrated that disruption of Mediator complex altered the expression of CjXDR1-induced downstream targets and impacted sterol biosynthesis. Together, these findings provide the first comprehensive insight into the Mediator complex in C. jacksonii, highlighting its critical role in multidrug resistance and its potential as a target for antifungal strategies.
Authors
- Yinglu Dong
- Peiyuan Jin
- Yi Zhou (ORCID: https://orcid.org/0000-0002-0273-007X)
- Jian Hu (ORCID: https://orcid.org/0000-0002-8349-6595)
- Xiaojing Shi (ORCID: https://orcid.org/0000-0001-6428-6130)
- Geunhwa Jung (ORCID: https://orcid.org/0000-0002-6504-3883)
- Chenchen Jia
- Z L Li
- Yixuan Kong
- Huangwei Zhang
- Zhimin Yang
- Qifan Jin
Institutions
- Nanjing Agricultural University (CN)
- University of Massachusetts Amherst (US)
- Institute of Botany (CN)
Publication Details
- Journal
- Phytopathology
- Published
- 2026-06-17
- DOI
- https://doi.org/10.1094/phyto-03-26-0083-r
- Primary Topic
- Fungal Plant Pathogen Control
- Type
- article
- Field-Weighted Citation Impact
- 0.00