Uncovering Proteomic Insights Into Cell Wall Thickening Genes for Phytophthora Blight Resistance in Pigeon Pea

Phytophthora blight is a destructive disease affecting pigeon pea, often leading to significant yield losses. Resistance to this disease is complex, quantitative, and controlled by multiple genes, although the molecular mechanisms involved remain poorly understood. Cell wall thickening is a crucial aspect of quantitative resistance, regulated by receptors, transcriptional networks, and phytohormones. In this study, we conducted a comparative proteomic analysis on two contrasting pigeon pea genotypes-ICPL99010 (resistant) and ICPL7119 (susceptible)-to explore plant-pathogen interactions at the molecular level. The analysis identified key differentially expressed proteins associated with receptors, transcription factors, phytohormones, and secondary biosynthetic pathways, all of which play roles in lignin and callose deposition. Higher accumulation of phenylpropanoids (phenylalanine ammonia-lyase and caffeoyl-CoA O-methyltransferase), ATP-Binding Cassette G (ABCG) transporters, 1,3-β-glucan synthase, and respiratory burst oxidase homologs (RBOHs) was observed in the resistant genotype. Lignin and callose were deposited as polymers and contribute to cell wall thickening to prevent pathogen establishment. Histochemical staining further confirmed secondary cell wall thickening through lignin and callose accumulation. Quantitative real-time PCR studies revealed higher expressions of caffeoyl-CoA O-methyltransferase, NAC72, cysteine-rich receptor-like kinase 29, phospholipase D, calcium-dependent protein kinase 1, abscisic-aldehyde oxidase, and phospholipid-transporting ATPase 1 in the pathogen-inoculated resistant genotype than in the susceptible genotype. This study is the first to use comparative proteomics to investigate the molecular mechanisms of resistance in the Phytophthora-Pigeonpea interaction, offering valuable insights into the plant's defense strategies.