Ralstonia solanacearum type III effector RipAF1 mediates plant resistance signaling by ADP-ribosylation of host FBN1

( ) causes destructive bacterial wilt across a broad range of host plants by delivering a repertoire of type III effectors. In the present study, we determined that the deletion of the type III effector RipAF1 resulted in increased virulence on , , and plants. RipAF1 showed ADP-ribosylation activity...

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Published inHorticulture research Vol. 11; no. 8; p. uhae162
Main Authors Wu, Wei, Zou, Huasong, Zheng, Huiying, Chen, Xinyu, Luo, Xuming, Fan, Xiaojing, Zhuo, Tao, Miao, Weiguo
Format Journal Article
LanguageEnglish
Published England Oxford University Press 01.08.2024
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Summary:( ) causes destructive bacterial wilt across a broad range of host plants by delivering a repertoire of type III effectors. In the present study, we determined that the deletion of the type III effector RipAF1 resulted in increased virulence on , , and plants. RipAF1 showed ADP-ribosylation activity and . Transient overexpression of RipAF1 suppressed jasmonic acid (JA) signaling and induced salicylic acid (SA) signaling. The ADP-ribosylation activity of RipAF1 was essential for JA and SA signaling mediation. Host fibrillin FBN1 was identified as a RipAF1-interactor that is ADP-ribosylated by RipAF1 directly. Most importantly, the ADP-ribosylation of conserved residues of FBN1 contributes to its localization to the plasma membrane and leads to the suppression of JA signaling and induction of SA signaling. We concluded that RipAF1 mediates antagonistic crosstalk between JA and SA signaling pathways by ADP-ribosylation of FBN1.
ISSN:2662-6810
2052-7276
2052-7276
DOI:10.1093/hr/uhae162