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  • Title: A Global Transcriptome and Co-expression Analysis Reveals Robust Host Defense Pathway Reprogramming and Identifies Key Regulators of Early Phases of Cicer-Ascochyta Interactions.
    Author: Singh R, Dwivedi A, Singh Y, Kumar K, Ranjan A, Verma PK.
    Journal: Mol Plant Microbe Interact; 2022 Nov; 35(11):1034-1047. PubMed ID: 35939621.
    Abstract:
    Ascochyta blight (AB) caused by the filamentous fungus Ascochyta rabiei is a major threat to global chickpea production. The mechanisms underlying chickpea response to A. rabiei remain elusive to date. Here, we investigated the comparative transcriptional dynamics of AB-resistant and -susceptible chickpea genotypes upon A. rabiei infection, to understand the early host defense response. Our findings revealed that AB-resistant plants underwent rapid and extensive transcriptional reprogramming compared with a susceptible host. At the early stage (24 h postinoculation [hpi]), mainly cell-wall remodeling and secondary metabolite pathways were highly activated, while differentially expressed genes related to signaling components, such as protein kinases, transcription factors, and hormonal pathways, show a remarkable upsurge at 72 hpi, especially in the resistant genotype. Notably, our data suggest an imperative role of jasmonic acid, ethylene, and abscisic acid signaling in providing immunity against A. rabiei. Furthermore, gene co-expression networks and modules corroborated the importance of cell-wall remodeling, signal transduction, and phytohormone pathways. Hub genes such as MYB14, PRE6, and MADS-SOC1 discovered in these modules might be the master regulators governing chickpea immunity. Overall, we not only provide novel insights for comprehensive understanding of immune signaling components mediating AB resistance and susceptibility at early Cicer-Ascochyta interactions but, also, offer a valuable resource for developing AB-resistant chickpea. [Formula: see text] Copyright © 2022 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
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