Transcriptomic Analysis of Fludioxonil Resistance Mechanisms in Botrytis cinerea

Abstract

Botrytis cinerea is a destructive plant pathogen that infects a wide range of economically important crops. Limiting pathogen infection during production and after harvest is largely dependent on fungicide applications; fungicide-resistant isolates of B. cinerea have been recovered from various hosts. Resistance of B. cinerea to fludioxonil has been associated with overexpression of transporter genes ( BcatrB and mfsM2) and mutations on histidine kinase proteins ( Bos1, Bchhk2, Bchhk17). To identify possible mechanisms associated with fludioxonil resistance, the genomic expression of three sensitive and three low-resistant isolates was studied. Overexpression of BcatrB was observed when comparing low-resistant and sensitive isolates but was not specific to the fludioxonil treatment. Seven amino acid substitutions and one deletion were identified in the transcription factor Bcmrr1 in low-resistant isolates, associated with overexpression of BcatrB. The L497 deletion, previously associated with highly resistant isolates (MDR1h), was observed in two low-resistant isolates. Other differentially expressed genes associated with transmembrane transport, oxidoreductase activity, and lipid metabolic processes could be key in understanding the fungicidal mechanism(s) of fludioxonil. Expression profiles were isolate-specific. Following fludioxonil exposure, two sensitive isolates of B. cinerea sensu stricto showed a change in gene expression levels associated with cell membrane and peroxidase activity. In one low-resistant isolate of B. cinerea group S, fludioxonil exposure resulted in the overexpression of stress response genes and MFS transporter Bcstl1; one sensitive and two low-resistant isolates showed no significant changes in gene expression profiles. This work provides insight into the effect of fludioxonil on B. cinerea and potential fungicide resistance mechanisms. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .