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Functional analysis of NopM, a novel E3 ubiquitin ligase (NEL) domain effector of Rhizobium sp strain NGR234
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 1528757
Author(s) Xin, D. W.; Liao, S.; Xie, Z. P.; Hann, D. R.; Steinle, L.; Boller, T.; Staehelin, C.
Author(s) at UniBasel Boller, Thomas
Hann, Dagmar
Year 2012
Title Functional analysis of NopM, a novel E3 ubiquitin ligase (NEL) domain effector of Rhizobium sp strain NGR234
Journal PLoS Pathogens
Volume 8
Number 5
Pages / Article-Number e1002707
Abstract

Type 3 effector proteins secreted via the bacterial type 3 secretion system (T3SS) are not only virulence factors of pathogenic bacteria, but also influence symbiotic interactions between nitrogen-fixing nodule bacteria (rhizobia) and leguminous host plants. In this study, we characterized NopM (nodulation outer protein M) of Rhizobium sp. strain NGR234, which shows sequence similarities with novel E3 ubiquitin ligase (NEL) domain effectors from the human pathogens Shigella flexneri and Salomonella enterica. NopM expressed in Escherichia coli, but not the non-functional mutant protein NopM-C338A, showed E3 ubiquitin ligase activity in vitro. In vivo, NopM, but not inactive NopM-C338A, promoted nodulation of the host plant Lablab purpureus by NGR234. When NopM was expressed in yeast, it inhibited mating pheromone signaling, a mitogen-activated protein (MAP) kinase pathway. When expressed in the plant Nicotiana benthamiana, NopM inhibited one part of the plant's defense response, as shown by a reduced production of reactive oxygen species (ROS) in response to the flagellin peptide flg22, whereas it stimulated another part, namely the induction of defense genes. In summary, our data indicate the potential for NopM as a functional NEL domain E3 ubiquitin ligase. Our findings that NopM dampened the flg22-induced ROS burst in N. benthamiana but promoted defense gene induction are consistent with the concept that pattern-triggered immunity is split in two separate signaling branches, one leading to ROS production and the other to defense gene induction.

Publisher Public Library of Science
ISSN/ISBN 1553-7366 ; 1553-7374
edoc-URL http://edoc.unibas.ch/dok/A6070637
Full Text on edoc No
Digital Object Identifier DOI 10.1371/journal.ppat.1002707
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/22615567
ISI-Number WOS:000305322900040
Document type (ISI) Journal Article
 
   

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