Dataset Information

Fludioxonil-induced differential gene expression in Aspergillus fumigatus and its DtcsC and Dskn7 mutants

ABSTRACT: The antifungal compound fludioxonil targets the fungal specific group III hybrid histidin kinaseTcsC of A. fumigatus, which in turn activate the High Osmolarity Glycerol (HOG) pathway and leads to drastic swelling of the fungal cells. We investigated the different responses of the AfS35 (wild type), the completely resistant mutant strain DtcsC and the partial resistant mutant strain Dskn7 to fludioxonil.

ORGANISM(S): Aspergillus fumigatus

PROVIDER: GSE224696 | GEO | 2023/11/16

REPOSITORIES: GEO

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Project description:Botrytis cinerea (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 protec-tion and is essential for controlling tomato gray mold. The emergence of fungicide-resistant strains has made the control of Botrytis cinerea more difficult. While the genome of Botrytis cinerea 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 flu-dioxonil resistance remain unclear. The present study prepared RNA-sequencing (RNA-seq) li-braries for three Botrytis cinerea strains [two highly resistant (LR and FR) versus one highly sen-sitive (S) to fludioxonil], with and without fludioxonil treatment, to identify fludioxonil responsive genes that facilitate fungicide resistance. Functional enrichment analysis identified nine resistant related DEGs in the fludioxonil-induced LR and FR transcriptome that were simultaneously up regulated, and seven resistant related DEGs down regulated. These included adenosine tri-phosphate (ATP)-binding cassette (ABC) transporter-encoding genes, major facilitator super-family (MFS) transporter-encoding genes, and the high-osmolarity glycerol (HOG) pathway homologues or related genes. The expression patterns of twelve out of the sixteen fludioxo-nil-responsive genes, obtained from the RNA-sequence data sets were validated using quantita-tive real-time PCR (qRT-PCR). Based on RNA-sequence analysis it was found that fugal HHKs, like BOS1, BcHHK2, and Bchhk17, were in some way involved in the fludioxonil resistance of B. cinerea, in addition, a number of ABC and MFS transporter genes that were not reported before, such as BcATRO, BMR1, BMR3, BcNMT1, BcAMF1, BcTOP1, BcVBA2, and BcYHK8 were differen-tially expressed in the fludioxonil-resistant strains, indicating that overexpression of these efflux transporters located in the plasma membranes played a crucial role in the fludioxonil resistant mechanism of B. cinerea. These lines of evidence together allowed us to draw a general portrait of the anti-fludioxonil mechanisms for Botrytis cinerea, and the assembled and annotated transcrip-tome data provide valuable genomic resources for further study of the molecular mechanisms of B. cinerea resistance to fludioxonil.