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      Plant NBS-LRR proteins: adaptable guards

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      Author(s): 1 , 1 , 1 , 1 ,
      Publication date (Electronic):
      Journal: Genome Biology
      Publisher: BioMed Central

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          Abstract

          Plant nucleotide-binding site leucine-rich repeat (NBS-LRR) proteins are a large family involved in disease resistance; they may monitor the status of proteins targeted by pathogens.

          Abstract

          The majority of disease resistance genes in plants encode nucleotide-binding site leucine-rich repeat (NBS-LRR) proteins. This large family is encoded by hundreds of diverse genes per genome and can be subdivided into the functionally distinct TIR-domain-containing (TNL) and CC-domain-containing (CNL) subfamilies. Their precise role in recognition is unknown; however, they are thought to monitor the status of plant proteins that are targeted by pathogen effectors.

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          Plant pathogens and integrated defence responses to infection.

          J L Dangl, J. Jones (2001)
          Plants cannot move to escape environmental challenges. Biotic stresses result from a battery of potential pathogens: fungi, bacteria, nematodes and insects intercept the photosynthate produced by plants, and viruses use replication machinery at the host's expense. Plants, in turn, have evolved sophisticated mechanisms to perceive such attacks, and to translate that perception into an adaptive response. Here, we review the current knowledge of recognition-dependent disease resistance in plants. We include a few crucial concepts to compare and contrast plant innate immunity with that more commonly associated with animals. There are appreciable differences, but also surprising parallels.
          Article 0 comments Cited 893 times – based on 0 reviews     Review now
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            Bacterial disease resistance in Arabidopsis through flagellin perception.

            Cyril Zipfel, Silke Robatzek, Lionel Navarro … (2004)
            Plants and animals recognize microbial invaders by detecting pathogen-associated molecular patterns (PAMPs) such as flagellin. However, the importance of flagellin perception for disease resistance has, until now, not been demonstrated. Here we show that treatment of plants with flg22, a peptide representing the elicitor-active epitope of flagellin, induces the expression of numerous defence-related genes and triggers resistance to pathogenic bacteria in wild-type plants, but not in plants carrying mutations in the flagellin receptor gene FLS2. This induced resistance seems to be independent of salicylic acid, jasmonic acid and ethylene signalling. Wild-type and fls2 mutants both display enhanced resistance when treated with crude bacterial extracts, even devoid of elicitor-active flagellin, indicating the existence of functional perception systems for PAMPs other than flagellin. Although fls2 mutant plants are as susceptible as the wild type when bacteria are infiltrated into leaves, they are more susceptible to the pathogen Pseudomonas syringae pv. tomato DC3000 when it is sprayed on the leaf surface. Thus, flagellin perception restricts bacterial invasion, probably at an early step, and contributes to the plant's disease resistance.
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              Cross talk between signaling pathways in pathogen defense.

              Barbara Kunkel, David M. Brooks (2002)
              Plant defense in response to microbial attack is regulated through a complex network of signaling pathways that involve three signaling molecules: salicylic acid (SA), jasmonic acid (JA) and ethylene. The SA and JA signaling pathways are mutually antagonistic. This regulatory cross talk may have evolved to allow plants to fine-tune the induction of their defenses in response to different plant pathogens.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Genome Biol
                Title: Genome Biology
                Publisher: BioMed Central (London )
                ISSN (Print): 1465-6906
                ISSN (Electronic): 1465-6914
                Publication date (Print): 2006
                Publication date (Electronic): 26 April 2006
                Volume: 7
                Issue: 4
                Page: 212
                Affiliations
                [1 ]The Genome Center, University of California, Davis, CA 95616, USA
                Article
                Publisher ID: gb-2006-7-4-212
                DOI: 10.1186/gb-2006-7-4-212
                PMC ID: 1557992
                PubMed ID: 16677430
                SO-VID: 4888b470-d623-4ddc-a7a2-e8f886f9bf47
                Copyright © Copyright © 2006 BioMed Central Ltd
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                Subject: Review

                ScienceOpen disciplines: Genetics
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                ScienceOpen disciplines: Genetics

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