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Differential Expression Analysis of a Histidine phosphotransferase RNAi mutant in Magnaporthe oryzae

ABSTRACT: Differential Expression Analysis of a Histidine phosphotransferase RNAi mutant in Magnaporthe oryzae

PROVIDER: PRJNA793841 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17410087_1.fastq.gz	Fastqsanger.gz
	SRR17410087_2.fastq.gz	Fastqsanger.gz
	SRR17410088_1.fastq.gz	Fastqsanger.gz
	SRR17410088_2.fastq.gz	Fastqsanger.gz

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Differential Expression Analysis of a Histidine phosphotransferase RNAi mutant in Magnaporthe oryzae

Project description:Magnaporthe oryzae is notorious for its efficient evolution as a plant pathogen. Analysis of well organised fungal pathogenic mechanisms would enable the scientific understanding to fight against pathogens. Histidine phosphotransferase in fungal systems are good targets for antifungals since they are component of SAPK pathway, which is essential for survival of the fungus. The histidine Phosphotransferase YPD1 in M. oryzae is known to be light responsive and important for both asexual reproduction as well as pathogenicity. In this study, the knock-down (KD) mutant of YPD1 was highly sensitive to cell wall perturbing agents and were highly deficient in laccase expression and activity. A RNA-seq transcriptome screening of KD mutant compared to wild type revealed altered expression of about 146 genes important in biotrophic and necrotrophic phases of the pathogen. About 96 genes were found to be down regulated, of which several plant cell wall degrading genes vital for pathogenicity and fungal cell wall maintenance genes important for growth and fungal development were identified. Most of the genes identified are involved in biotrophic invasion and metabolism. Our results explain the reason for the deficiency of the KD mutant in asexual reproduction as well as pathogenicity. Analysis of differentially expressed genes in the KD YPD1 mutant suggests that YPD1 can be a good target for development of novel antifungal compounds, as YPD1 expression affects genes required for pathogenicity.

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