Transcript profiling reveals potential regulators for oxidative stress response of a necrotrophic chickpea pathogen Ascochyta rabiei

3 Biotech. 2020 Mar;10(3):117. doi: 10.1007/s13205-020-2107-8. Epub 2020 Feb 15.

Abstract

Necrotrophic pathogens experience host-generated oxidative stress during pathogenesis. They overcome such hostile environment by intricate mechanisms which are largely understudied. In this article, reference-based transcriptome analysis of a devastating Ascochyta Blight (AB) disease causing chickpea pathogen Ascochyta rabiei was explored to get insights into survival mechanisms under oxidative stress. Here, expression profiling of mock-treated and menadione-treated fungus was carried out by RNA-Seq approach. A significant number of genes in response to oxidative stress were overrepresented, suggestive of a robust and coordinated defense system of A. rabiei. A total 73 differentially expressed genes were filtered out from both the transcriptomes, among them 64 were up-regulated and 9 were found down-regulated. The gene ontology and KEGG mapping were conducted to comprehend the possible regulatory roles of differentially expressed genes in metabolic networks and biosynthetic pathways. Transcript profiling, KEGG pathway and gene ontology-based enrichment analysis revealed 12 (16.43%) stress responsive factors, 25 (34.24%) virulence associated genes, 10 (13.69%) putative effectors and 28 (38.35%) important interacting proteins associated with various metabolic pathways. In addition, genes with differential expression were further explored for underlying putative pathogenicity factors. We identified five genes ST47_g10291, ST47_g9396, ST47_g10294, ST47_g4395, and ST47_g7191 that were common to stress and fungal pathogenicity. The factors recognized in this work can be used to establish molecular tools to explain the regulatory gene networks engaged in stress response of fungal pathogens and disease management.

Keywords: 454 Pyrosequencing; Differential expression profiles; Oxidative stress; Stress response; Transcriptome.