A ribonuclease T2 protein FocRnt2 contributes to the virulence of Fusarium oxysporum f. sp. cubense tropical race 4

文献类型： 外文期刊

第一作者： He, Yanqiu

作者： He, Yanqiu;Li, Pengfei;Zhou, Xiaoshu;Ali, Shaukat;Zhu, Jie;Ma, Yini;Li, Jieling;Zhang, Nan;Li, Huaping;Li, Yunfeng;Nie, Yanfang;He, Yanqiu;Nie, Yanfang

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关键词： effector; Fusarium oxysporum f. sp. cubense; ribonucleases T2; transient expression; virulence

期刊名称：MOLECULAR PLANT PATHOLOGY （ 影响因子：4.8； 五年影响因子：6.0 ）

ISSN： 1464-6722

年卷期： 2024 年 25 卷 8 期

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收录情况： SCI

摘要： Banana Fusarium wilt, caused by Fusarium oxysporum f. sp. cubense tropical race 4 (Foc TR4), is a major disease of banana plants worldwide. Effector proteins play critical roles in banana-Foc TR4 interaction. Our previous studies highlighted a ribonuclease protein belonging to the T2 family (named as FocRnt2) in the Foc TR4 secretome, which was predicted to be an effector. However, its biological function in Foc TR4 infection is still unclear. Herein, we observed significant expression of FocRnt2 during the early stage of fungal infection in planta. A yeast signal sequence trap assay showed that FocRnt2 contained a functional signal peptide for secretion. FocRnt2 possessed ribonuclease activity that could degrade the banana total RNA in vitro. Subcellular localization showed that FocRnt2 was localized in the nucleus and cytoplasm of Nicotiana benthamiana leaves. Transient expression of FocRnt2 suppressed the expression of salicylic acid- and jasmonic acid-signalling marker genes, reactive oxygen species accumulation, and BAX-mediated cell death in N. benthamiana. FocRnt2 deletion limited fungal penetration, reduced fusaric acid biosynthesis in Foc TR4, and attenuated fungal virulence against banana plants, but had little effect on Foc TR4 growth and sensitivity to various stresses. Furthermore, FocRnt2 deletion mutants induced higher expression of the defence-related genes in banana plants. These results suggest that FocRnt2 plays an important role in full virulence of Foc TR4, further improving our understanding of effector-mediated Foc TR4 pathogenesis.

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