Molecular Characterization Differential Expression of Proteins and Stress Responsive Metabolites for Fusarium wilt in Chickpea Cicer arietinum L

Abstract

Chickpea (Cicer arietinum L.) is a vital pulse crop grown globally, particularly in arid and semi-arid regions. However, its productivity is severely constrained by Fusarium wilt, caused by the fungal pathogen Fusarium oxysporum f. sp. ciceri (Foc). Present study investigated the molecular mechanisms underlying Fusarium wilt resistance in chickpea, focusing on identifying resistant genotypes, characterizing them using molecular markers, and analysing differential protein expression and metabolite accumulation in response to Fusarium wilt infection. A set of 117 chickpea genotypes were screened for Fusarium wilt resistance under greenhouse conditions. Among the 117 genotypes evaluated, three genotypes (K9, K16, and K17) exhibited high resistance, while 12 genotypes were categorized as resistant, and 15 were classified as moderately resistant. The remaining chickpea germplasm lines evaluated were found to be susceptible to Fusarium wilt. Fusarium wilt disease progression, measured by Percent Disease Index (PDI), increased from 773.50 at 35 days post-inoculation (dpi) to 1380.44 at 55 dpi, demonstrating a temporal increase in infection. However, the Area Under the Disease Progress Curve (AUDPC), a cumulative measure of disease, was highest (13536.25) at 35 dpi, suggesting a rapid initial disease development despite the continued increase in PDI. Subsequent SDS-PAGE analysis revealed differential root protein expression in chickpea genotypes 48 hours post-Fusarium oxysporum f. sp. ciceri inoculation. Resistant genotypes K9 and D42 showed distinct banding patterns compared to the susceptible D41, including the absence/presence of bands at approximately 11, 16, 18.5, and 25 kDa. These differentially expressed proteins represent potential targets for further functional characterization to elucidate their precise roles in wilt resistance. To further characterize the identified resistant genotypes, ten Simple Sequence Repeat (SSR) markers were employed. Six of these SSR markers exhibited polymorphism across a panel of twe