Isoforms from the Phytocyanin Gene Family Regulated Verticillium Wilt Resistance in Cotton.

Int J Mol Sci

State Key Laboratory of North China Crop Improvement and Regulation, Key Laboratory for Crop Germplasm Resources of Hebei, Hebei Agricultural University, Baoding 071001, China.

Published: March 2022

Verticillium wilt (VW), a fungal disease caused by , currently devastates cotton fiber yield and quality seriously, yet few resistance germplasm resources have been discovered in . The cotton variety Nongda601 with suitable VW resistance and high yield was developed in our lab, which supplied elite resources for discovering resistant genes. Early nodulin-like protein (ENODL) is mainly related to nodule formation, and its role in regulating defense response has been seldom studied. Here, 41 conserved ENODLs in were identified and characterized, which could divide into four subgroups. We found that was upregulated under stress and hormonal signal and displayed higher transcript levels in resistant cottons than the susceptible. The was proved to positively regulate VW resistance via overexpression and gene silencing experiments. Overexpression of significantly enhanced the expressions of salicylic acid (SA) hormone-related transcription factors and pathogenicity-related (PR) protein genes, as well as hydrogen peroxide (HO) and SA contents, resulting in improved VW resistance in transgenic . Correspondingly, in the silenced cotton, the expression levels of both phenylalanine ammonia lyase (PAL) and 4-coumarate-CoA ligase (4CL) genes significantly decreased, leading to the reduced SA content mediating by the phenylalanine ammonia lyase pathway. Taken together, played a crucial role in VW resistance by inducing SA signaling pathway and regulating the production of reactive oxygen species (ROS). These findings broaden our understanding of the biological roles of and the molecular mechanisms underlying cotton disease resistance.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8955391PMC
http://dx.doi.org/10.3390/ijms23062913DOI Listing

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