Abstract
Root-knot nematodes (RKNs) are obligate biotrophic parasites that invade plant roots and engage in prolonged and intimate relationships with their hosts. Nematode secretions, some of which have immunosuppressing activity, play essential roles in successful parasitism; however, their mechanisms of action remain largely unknown. Here, we show that the RKN-specific gene MiMsp40, cloned from Meloidogyne incognita, is expressed exclusively in subventral oesophageal gland cells and is strongly upregulated during early parasitic stages. Arabidopsis plants overexpressing MiMsp40 were more susceptible to nematode infection than were wild type plants. Conversely, the host-derived MiMsp40 RNAi suppressed nematode parasitism and/or reproduction. Moreover, overexpression of MiMsp40 in plants suppressed the deposition of callose and the expression of marker genes for bacterial elicitor elf18-triggered immunity. Transient expression of MiMsp40 prevented Bax-triggered defence-related programmed cell death. Co-agroinfiltration assays indicated that MiMsp40 also suppressed macroscopic cell death triggered by MAPK cascades or by the ETI cognate elicitors R3a/Avr3a. Together, these results demonstrate that MiMsp40 is a novel Meloidogyne-specific effector that is injected into plant cells by early parasitic stages of the nematode and that plays a role in suppressing PTI and/or ETI signals to facilitate RKN parasitism.
Highlights
Been postulated to play decisive roles because successful parasitism is heavily reliant on whether nematodes and feeding cells elude or survive attack by the plant immune system[15,16,17]
In Nicotiana benthamiana leaves, the transient expression of GrCEP12, an ubiquitin carboxyl extension protein secreted by G. rostochiensis dorsal gland cells, suppresses the production of reactive oxygen species (ROS) and the induction of PAMP-triggered immunity (PTI) marker genes triggered by the bacterial pathogen-associated molecular patterns (PAMPs) flg[22]
GrVAP1, a G. rostochiensis venom allergen protein expressed in the subventral gland cells, affects PCD mediated by surface-localized immune receptors, suppressing host defences activated by host detection of plant cell wall fragments released by migrating nematodes during the onset of parasitism[31]
Summary
Been postulated to play decisive roles because successful parasitism is heavily reliant on whether nematodes and feeding cells elude or survive attack by the plant immune system[15,16,17]. Heterodera schachtii and M. javanica infections activate Arabidopsis 13-lipoxygenase LOX4, whereas functionally deficient LOX4 plants have marked increases in the numbers of females and eggs or in the female/male ratio, accompanied by the accumulation of jasmonic acid and the increased expression of allene oxide synthase, allene oxide cyclase, and ethylene-responsive transcription factor 4 These results indicate that the nematode modifies LOX4-mediated plant defence[23]. In Nicotiana benthamiana leaves, the transient expression of GrCEP12, an ubiquitin carboxyl extension protein secreted by G. rostochiensis dorsal gland cells, suppresses the production of ROS and the induction of PTI marker genes triggered by the bacterial PAMP flg[22] These results provide direct evidence that GrCEP12 is involved in the suppression of PTI30. Considered together, our results suggest that MiMsp[40] represents a novel Meloidogyne immunomodulatory effector that suppresses the activation of plant cell death associated with PTI and/or ETI responses and thereby promotes nematode parasitism
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