Research Projects

Climate change is causing a significant increase in the impact of fungal pathogens, such as Fusarium oxysporum, on global health and agriculture. F. oxysporum f. sp. ciceri mediated vascular wilt disease poses a significant threat to chickpea production, while in worms, it causes neuronal stress and intestinal disintegration. Both organisms defend against pathogen attacks through innate immune responses, which are regulated by pathogen associated molecular pattern (PAMP) triggered immunity (PTI) and effector triggered immunity (ETI). PAMPs contribute to microbial fitness, while effectors are species, race, or strain-specific factors contributing to pathogen virulence. Molecular switches between ETI and interrelated signaling hubs, regulated by transcriptional dynamics, synergestic and antagonistic regulation of post-translational modifications (PTMs) of effectors and targeted host proteins, converge into a disease/immune response against pathogens. However, the nature and role of fungal effectors and host transcriptional regulators and how PTMs affect their function against multi-host pathogens, particularly F. oxysporum, is less understood. A recent study identified 43 putative F. oxysporum effectors, with 4 being cytosolic and apoplastic and 39 being nuclear effectors associated with redox homeostasis, wall remodelling, transcriptional activity, protein turnover, metabolism, and unknown function. The study aims to determine the functionality of these identified effectors and mycotoxins, investigate their role in modulating trans-kingdom host susceptibility, and understand the cross-talk between PTM machinery, DAF-16, and sIR 2.1 in worm during ETI response against Fusarium disease.