Unravelling the mechanism of Fusarium wilt resistance in chickpea seedlings using biochemical studies and expression analysis of NBS-LRR and WRKY genes

Abstract

The yield potential of chickpea is highly compromised because of Fusarium wilt stress. Plant employs a series of physiological, biochemical and molecular changes to restrict pathogen spread. To understand the biochemical basis of resistance in chickpea against Fusarium oxysporum f.sp. ciceri (Foc), the temporal changes in antioxidant enzyme activity profiles were investigated. We documented guaiacol peroxidase, catalase, ascorbate peroxidase, and superoxide dismutase enzyme activities in resistant (WR 315) and susceptible (JG 62) chickpea genotypes under control and wilt stress conditions at two time points, 2- and 10- days post inoculation. Biochemical studies suggest that early and rapid defense responses, against pathogen attack, restrict pathogen spread in resistant cultivar while a weak and slow response by susceptible genotype leads to aggressive colonization by the pathogen. We have identified a set of wilt stress responsive nucleotide binding site and leucine rich repeat (NBS-LRR) resistance (R) and WRKY genes, known to be involved in plant defense, based on their co-localization with previously reported major Foc resistance QTLs and expression profiles. Sixteen NBS-LRR and eleven WRKY genes were co-localized to previously reported ten major Foc-QTLs present in chromosome 2 and 6. Interestingly, majority of these genes were co-localized to chromosome 2 which is also considered as a hotspot for Fusarium wilt resistance. The gene expression analysis in contrasting chickpea genotypes in response to Foc infection identified fourteen NBS-LRR and nine WRKY genes that showed differential expression suggesting their involvement in Fusarium wilt resistance. Our study provides new insights into biochemical and molecular mechanisms underlying resistance and susceptibility in chickpea against Fusarium oxysporum infection.