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Transcriptomic Analysis of Resistant and Wild-Type Isolates Revealed Fludioxonil-Resistance Mechanisms. | LitMetric

Transcriptomic Analysis of Resistant and Wild-Type Isolates Revealed Fludioxonil-Resistance Mechanisms.

Int J Mol Sci

Engineering Research Center of Plant Growth Regulator, Ministry of Education/College of Agronomy, China Agricultural University, Beijing 100193, China.

Published: January 2023

, the causal agent of gray mold, is one of the most destructive pathogens of cherry tomatoes, causing fruit decay and economic loss. Fludioxonil is an effective fungicide widely used for crop protection and is effective against tomato gray mold. The emergence of fungicide-resistant strains has made the control of more difficult. While the genome of is available, there are few reports regarding the large-scale functional annotation of the genome using expressed genes derived from transcriptomes, and the mechanism(s) underlying such fludioxonil resistance remain unclear. The present study prepared RNA-sequencing (RNA-seq) libraries for three strains (two highly resistant (LR and FR) versus one highly sensitive (S) to fludioxonil), with and without fludioxonil treatment, to identify fludioxonil responsive genes that associated to fungicide resistance. Functional enrichment analysis identified nine resistance related DEGs in the fludioxonil-induced LR and FR transcriptome that were simultaneously up-regulated, and seven resistance related DEGs down-regulated. These included adenosine triphosphate (ATP)-binding cassette (ABC) transporter-encoding genes, major facilitator superfamily (MFS) transporter-encoding genes, and the high-osmolarity glycerol (HOG) pathway homologues or related genes. The expression patterns of twelve out of the sixteen fludioxonil-responsive genes, obtained from the RNA-sequence data sets, were validated using quantitative real-time PCR (qRT-PCR). Based on RNA-sequence analysis, it was found that hybrid histidine kinase, fungal HHKs, such as , , and probably involved in the fludioxonil resistance of , in addition, a number of ABC and MFS transporter genes that were not reported before, such as , , , , , , and were differentially expressed in the fludioxonil-resistant strains, indicating that overexpression of these efflux transporters located in the plasma membranes may associate with the fludioxonil resistance mechanism of All together, these lines of evidence allowed us to draw a general portrait of the anti-fludioxonil mechanisms for , and the assembled and annotated transcriptome data provide valuable genomic resources for further study of the molecular mechanisms of resistance to fludioxonil.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9861754PMC
http://dx.doi.org/10.3390/ijms24020988DOI Listing

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