# Computational studies deciphered the role of key genes and associated networks regulating the defense mechanism in chickpea under Fusarium oxysporum f. sp. ciceris induced wilt condition

## TL;DR

This study identifies key genes and networks in chickpea that help defend against a fungal infection causing wilt, using transcriptomic data from infected roots.

## Contribution

The study reveals time-dependent gene expression patterns and hub genes involved in chickpea's defense against Fusarium wilt.

## Key findings

- A total of 894, 867, and 535 significant differentially expressed genes were identified at different time points.
- Hub genes related to reactive oxygen species scavenging and glycosyl hydrolase 28 were active during early infection.
- R-genes and specific transcription factors showed significant expression changes with infection progression.

## Abstract

Cicer arietinum, a nutritionally rich legume and a key Rabi crop, is severely impacted by vascular wilt caused by Fusarium oxysporum f. sp. ciceris, leading to substantial yield loss. To understand molecular reprogramming, a transcriptomic dataset of chickpea seedling roots exposed to fungal infection at 7 and 12 d post-inoculation (dpi) was analyzed. The comparison was made between the control and stressed at 7 and 12 dpi (C_7 vs S_7 and C_12 vs S_12) to be compared against stressed at 7 vs 12 dpi (S_7 vs S_12). The analyses included differentially expressed gene (DEGs) patterns, protein interaction networks, hub genes, carbohydrate-active enzymes (CAZymes), resistance genes (R-genes), and transcription factor (TF) identifications at two different time points. It revealed a total of 894, 867, and 535 significant DEGs respectively, which were associated mainly with cell-wall modification, membrane components, pectinesterase inhibitor activity, terpene synthase activity, and the biosynthesis of secondary metabolites. Further, the protein‒protein interaction network revealed that hub genes associated with chloroplast-localized reactive oxygen species scavenging activity and CAZyme, particularly glycosyl hydrolase 28 (GH28), to be involved during the early phase of infection. R-genes belonging to the classes of KIN (kinase domain), RLP (receptor-like protein), and RLK (receptor-like kinase) were significantly expressed while TFs, bHLH (basic helix–loop–helix), and GeBP (glabrous-enhancer-binding protein) were downregulated with prolonged infection. Hence, the overall study identified the key regulators, orchestrating the defense molecular mechanisms in relation to the time course of infection by the pathogen.