Overexpression of a citrus NDR1 ortholog increases disease resistance in Arabidopsis

dc.contributor.authorLu, Hua
dc.contributor.authorZhang, Chong
dc.contributor.authorAlbrecht, Ute
dc.contributor.authorShimizu, Rena
dc.contributor.authorWang, Guanfeng
dc.contributor.authorBowman, Kim D.
dc.date.accessioned2023-07-19T20:41:59Z
dc.date.available2023-07-19T20:41:59Z
dc.date.issued2013-06-03
dc.description.abstractEmerging devastating diseases, such as Huanglongbing (HLB) and citrus canker, have caused tremendous losses to the citrus industry worldwide. Genetic engineering is a powerful approach that could allow us to increase citrus resistance against these diseases. The key to the success of this approach relies on a thorough understanding of defense mechanisms of citrus. Studies of Arabidopsis and other plants have provided a framework for us to better understand defense mechanisms of citrus. Salicylic acid (SA) is a key signaling molecule involved in basal defense and resistance (R) gene-mediated defense against broad-spectrum pathogens. The Arabidopsis gene NDR1 (NON-RACE-SPECIFIC DISEASE RESISTANCE 1) is a positive regulator of SA accumulation and is specifically required for signaling mediated by a subset of R genes upon recognition of their cognate pathogen effectors. Our bioinformatic analysis identified an ortholog of NDR1 from citrus, CsNDR1. Overexpression of CsNDR1 complemented susceptibility conferred by the Arabidopsis ndr1-1 mutant to Pseudomonas syringae strains and also led to enhanced resistance to an oomycete pathogen Hyaloperonospora arabidopsidis. Such heightened resistance is associated with increased SA production and expression of the defense marker gene PATHOGENESIS RELATED 1 (PR1). In addition, we found that expression of PR1 and accumulation of SA were induced to modest levels in citrus infected with Candidatus Liberibacter asiaticus, the bacterial pathogen associated with HLB disease. Thus, our data suggest that CsNDR1 is a functional ortholog of Arabidopsis NDR1. Since Ca. L. asiaticus infection only activates modest levels of defense responses in citrus, we propose that genetically increasing SA/NDR1-mediated pathways could potentially lead to enhanced resistance against HLB, citrus canker, and other destructive diseases challenging global citrus production.en_US
dc.description.sponsorshipWe thank members in the Lu laboratory for assistance with this work. We thank Dr. Kevin Omland for assistance in phylogenetic analysis, Dr. William LaCourse for sharing his HPLC instrument, and Mr. Tim Ford for taking pictures for this publication. This work was supported by a grant from Citrus Research and Development Foundation to Hua Lu and a scholarship from China Scholarship Council to Chong Zhang.en_US
dc.description.urihttps://www.frontiersin.org/articles/10.3389/fpls.2013.00157/fullen_US
dc.format.extent10 pagesen_US
dc.genrejournal articlesen_US
dc.identifierdoi:10.13016/m2p767-ie3v
dc.identifier.citationLu H, Zhang C, Albrecht U, Shimizu R, Wang G and Bowman KD (2013) Overexpression of a citrus NDR1 ortholog increases disease resistance in Arabidopsis. Front. Plant Sci. 4:157. doi: 10.3389/fpls.2013.00157en_US
dc.identifier.urihttps://doi.org/10.3389/fpls.2013.00157
dc.identifier.urihttp://hdl.handle.net/11603/28798
dc.language.isoen_USen_US
dc.publisherFrontiersen_US
dc.relation.isAvailableAtThe University of Maryland, Baltimore County (UMBC)
dc.relation.ispartofUMBC Biological Sciences Department Collection
dc.relation.ispartofUMBC Faculty Collection
dc.relation.ispartofUMBC Student Collection
dc.rightsThis work was written as part of one of the author's official duties as an Employee of the United States Government and is therefore a work of the United States Government. In accordance with 17 U.S.C. 105, no copyright protection is available for such works under U.S. Law.en_US
dc.rightsPublic Domain Mark 1.0*
dc.rights.urihttp://creativecommons.org/publicdomain/mark/1.0/*
dc.titleOverexpression of a citrus NDR1 ortholog increases disease resistance in Arabidopsisen_US
dc.typeTexten_US
dcterms.creatorhttps://orcid.org/0000-0002-7496-3200en_US

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