Glycoside Hydrolase CaGH17-12 Contributes to Phytophthora Blight Resistance by Activating the Production of Reactive Oxygen Species and Jasmonic Acid Signalling in Pepper

糖苷水解酶 CaGH17-12 通过激活辣椒中活性氧的产生和茉莉酸信号通路,促进辣椒对疫霉病的抗性。

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Abstract

Glycoside hydrolase family 17 (GH17) plays a critical role in degrading pathogen cell walls and is involved in plant defence responses against biotic stress. However, the functional roles of GH17 members in pepper in response to Phytophthora capsici, the causal agent of Phytophthora blight, remain unexplored. In this study, a total of 55 CaGH17 genes were identified in the pepper genome and classified into three distinct subfamilies based on phylogenetic relationships. Transcriptome analysis of both the resistant cultivar 17-p63 and the susceptible cultivar 16-217 inoculated with P. capsici at multiple time points revealed that CaGH17-12 exhibited markedly increased expression in the resistant cultivar, while no significant changes were observed in the susceptible cultivar at 60 h post-inoculation. Yeast secretion trap and subcellular localisation assays indicated that CaGH17-12 is secreted into the apoplast. The purified CaGH17-12 protein, expressed in yeast, exhibited β-glucan hydrolase activity, confirming its enzymatic function. Virus-induced gene silencing of CaGH17-12 significantly increased susceptibility to P. capsici, confirming its role in mediating Phytophthora blight resistance. CaGH17-12-silenced pepper plants exhibited reduced expression of jasmonic acid (JA)-related and reactive oxygen species (ROS)-associated genes. Moreover, exogenous application of β-glucan oligosaccharides, the putative hydrolytic products of CaGH17-12, induced pepper resistance to P. capsici by enhancing the production of ROS and activating the expression of defence-related genes. Taken together, these findings identified and characterised the CaGH17 gene family in pepper, highlighting the potential role of CaGH17-12 in conferring resistance to P. capsici through modulation of ROS accumulation and JA signalling.

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