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ARS Home » Midwest Area » East Lansing, Michigan » Sugarbeet and Bean Research » Research » Publications at this Location » Publication #410549
Research Project: Sugar Beet Genetics and Pathogen Interactions

Location: Sugarbeet and Bean Research

Title: Transcriptomic analysis of fludioxonil resistance mechanisms in Botrytis cinerea

Author
item Naegele, Rachel
item BUITRAGO ACOSTA, MARIA CAMILA - Michigan State University
item LUKASAKO, NICOLE - Michigan State University
item HAUSBECK, MARY - Michigan State University
item MILES, TIMOTHY - Michigan State University

Submitted to: PhytoFrontiers
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/20/2024
Publication Date: N/A
Citation: N/A

Interpretive Summary: Botrytis, a fungus that can cause disease on more than 500 species of plants, infects a wide range of important crops. Managing the disease is mainly achieved through the use of chemical-based fungicides, such as fludioxonil. Resistance to fungicides is common in this fungus, making it particularly challenging to manage. In this study we looked for gene changes associated with resistance to the fungicide fludioxonil. In contrast to previous work, few changes were associated with fludioxonil resistance and those that were identified were not the same as had been previously identified. In particular, the greatest number of changes were observed in response to the presence of acetone, used to dissolve the fludioxonil and included as a positive control treatment, compared to the negative control treatment.

Technical Abstract: Botrytis cinerea is a destructive plant pathogen that infects a wide range of economically important crops. Limiting pathogen infection during production and post-harvest is largely dependent on fungicide applications; B. cinerea isolates resistant to one or multiple fungicides have been recovered from various hosts. Resistance of B. cinerea to fludioxonil, a phenylpyrrole fungicide, 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, genomic expression of three sensitive and three low-resistant isolates were studied. Overexpression of BcatrB was observed when comparing low-resistant and sensitive isolates, but was not specific to the fludioxonil treatment. Based on the genomic sequence of the transcription factor Bcmrr1, seven amino acid substitutions and one deletion were identified in low-resistant isolates that were associated with overexpression of BcatrB. The L497 deletion, previously associated with highly resistance isolates (MDR1h), was observed in two low-resistant isolates of B. cinerea. 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.