Research Article: The potato cyst nematode effector RHA1B is a ubiquitin ligase and uses two distinct mechanisms to suppress plant immune signaling

Date Published: April 12, 2019

Publisher: Public Library of Science

Author(s): Joanna Kud, Wenjie Wang, Rachel Gross, Youhong Fan, Li Huang, Yulin Yuan, Amanda Gray, Aida Duarte, Joseph C. Kuhl, Allan Caplan, Aska Goverse, Yongsheng Liu, Louise-Marie Dandurand, Fangming Xiao, Isgouhi Kaloshian.


Plant pathogens, such as bacteria, fungi, oomycetes and nematodes, rely on wide range of virulent effectors delivered into host cells to suppress plant immunity. Although phytobacterial effectors have been intensively investigated, little is known about the function of effectors of plant-parasitic nematodes, such as Globodera pallida, a cyst nematode responsible for vast losses in the potato and tomato industries. Here, we demonstrate using in vivo and in vitro ubiquitination assays the potato cyst nematode (Globodera pallida) effector RHA1B is an E3 ubiquitin ligase that employs multiple host plant E2 ubiquitin conjugation enzymes to catalyze ubiquitination. RHA1B was able to suppress effector-triggered immunity (ETI), as manifested by suppression of hypersensitive response (HR) mediated by a broad range of nucleotide-binding leucine-rich repeat (NB-LRR) immune receptors, presumably via E3-dependent degradation of the NB-LRR receptors. RHA1B also blocked the flg22-triggered expression of Acre31 and WRKY22, marker genes of pathogen‐associated molecular pattern (PAMP)‐triggered immunity (PTI), but this did not require the E3 activity of RHA1B. Moreover, transgenic potato overexpressing the RHA1B transgene exhibited enhanced susceptibility to G. pallida. Thus, our data suggest RHA1B facilitates nematode parasitism not only by triggering degradation of NB-LRR immune receptors to block ETI signaling but also by suppressing PTI signaling via an as yet unknown E3-independent mechanism.

Partial Text

Globodera pallida, a plant-parasitic cyst nematode, is a global threat to agronomically important crops such as potato and tomato. This sedentary plant endoparasite penetrates plant root systems to reach the inner cortex where it establishes a permanent feeding site, a multi-nucleate structure termed syncytium [1]. The transformation of plant root cells into syncytia by cyst nematodes is mediated by effectors produced in the nematode pharyngeal glands. It is generally believed that nematode effectors must manipulate various host physiological processes, particularly suppressing the plant defense responses, via largely unknown mechanisms, in order to facilitate the formation and maintenance of syncytia [1].




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