Sub-lethal dose exposure of cyflufenamid, flutianil, quinoxyfen, trifloxystrobin and metrafenone effects on conidial germination and gene expression in the grape powdery mildew pathogen
- 1Department of Plant Biology, Rutgers University, New Brunswick, NJ, United States
- 2Department of Plant, Soil and Microbial Sciences, Michigan State University, East Lansing, MI, United States
Abstract
Erysiphe necator is a destructive obligate plant pathogen that infects grapevines worldwide. Recently, specialized fungicides have been widely employed to control grape powdery mildew. However, for some fungicides their modes of action and the transcriptome changes caused in E. necator upon application remain unclear. In this study, a conidial germination assay was conducted on E. necator conidia to determine if cyflufenamid (FRAC U06), flutianil (FRAC U13), quinoxyfen (FRAC 13), trifloxystrobin (FRAC 11) and metrafenone (FRAC 50) inhibit conidial germination. Further a transcriptomic analyses of E. necator conidia treated with sub-lethal doses of flutianil, quinoxyfen, and trifloxystrobin were conducted at 3 and 6 h. The results showed that cyflufenamid and metrafenone did not consistently inhibit conidial germination, even at chemical concentrations as high as 100 ppm. In contrast, flutianil, trifloxystrobin and quinoxyfen effectively suppressed conidial germination. The differential gene expression analysis revealed limited overlap in differentially expressed genes compared to the control group at their respective time frames, though all fungicide applications resulted in upregulated genes involved in cellular respiration. Quinoxyfen exposure led to reduced expression of protein kinase genes, suggesting a disruption in signal transduction, while flutianil treatment showed increased expression of sugar transporters and chitinases, possibly reflecting enhanced energy demand and cell wall remodeling. Additionally, in samples treated with quinoxyfen and flutianil, there was an overexpression of major facilitator superfamily (MFS) and adenosine triphosphate-binding cassette (ABC) multidrug transporters. Overall, these findings highlight that while flutianil, trifloxystrobin and quinoxyfen effectively inhibit conidial germination, their mode of action may also trigger altered gene expression of various gene families. This knowledge is valuable for developing improved fungicide resistance management strategies for managing E. necator.
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BibTeX
@article{sharma2026sublethal,
title = {{Sub-lethal dose exposure of cyflufenamid, flutianil, quinoxyfen, trifloxystrobin and metrafenone effects on conidial germination and gene expression in the grape powdery mildew pathogen}},
author = {Nancy Sharma and Mohit Mahey and Rachel P. Naegele and Timothy D. Miles},
journal = {Frontiers in Microbiology},
year = {2026},
month = oct,
doi = {10.3389/fmicb.2026.1944688},
url = {https://doi.org/10.3389/fmicb.2026.1944688},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Sub-lethal dose exposure of cyflufenamid, flutianil, quinoxyfen, trifloxystrobin and metrafenone effects on conidial germination and gene expression in the grape powdery mildew pathogen
AU - Nancy Sharma
AU - Mohit Mahey
AU - Rachel P. Naegele
AU - Timothy D. Miles
PY - 2026
DA - 2026/10/12
JO - Frontiers in Microbiology
DO - 10.3389/fmicb.2026.1944688
UR - https://doi.org/10.3389/fmicb.2026.1944688
AB - Erysiphe necator is a destructive obligate plant pathogen that infects grapevines worldwide. Recently, specialized fungicides have been widely employed to control grape powdery mildew. However, for some fungicides their modes of action and the transcriptome changes caused in E. necator upon application remain unclear. In this study, a conidial germination assay was conducted on E. necator conidia to determine if cyflufenamid (FRAC U06), flutianil (FRAC U13), quinoxyfen (FRAC 13), trifloxystrobin (FRAC 11) and metrafenone (FRAC 50) inhibit conidial germination. Further a transcriptomic analyses of E. necator conidia treated with sub-lethal doses of flutianil, quinoxyfen, and trifloxystrobin were conducted at 3 and 6 h. The results showed that cyflufenamid and metrafenone did not consistently inhibit conidial germination, even at chemical concentrations as high as 100 ppm. In contrast, flutianil, trifloxystrobin and quinoxyfen effectively suppressed conidial germination. The differential gene expression analysis revealed limited overlap in differentially expressed genes compared to the control group at their respective time frames, though all fungicide applications resulted in upregulated genes involved in cellular respiration. Quinoxyfen exposure led to reduced expression of protein kinase genes, suggesting a disruption in signal transduction, while flutianil treatment showed increased expression of sugar transporters and chitinases, possibly reflecting enhanced energy demand and cell wall remodeling. Additionally, in samples treated with quinoxyfen and flutianil, there was an overexpression of major facilitator superfamily (MFS) and adenosine triphosphate-binding cassette (ABC) multidrug transporters. Overall, these findings highlight that while flutianil, trifloxystrobin and quinoxyfen effectively inhibit conidial germination, their mode of action may also trigger altered gene expression of various gene families. This knowledge is valuable for developing improved fungicide resistance management strategies for managing E. necator.
SN - 1664-302X
ER -