Resistance to Turnip Crinkle Virus in Arabidopsis Is Regulated by Two Host Genes and Is Salicylic Acid Dependent but NPR1, Ethylene, and Jasmonate Independent

Kachroo, Pradeep; Yoshioka, Keiko; Shah, Jyoti; Dooner, Hugo K.; Klessig, Daniel F.

doi:10.2307/3870994

Cited by 81 publications

(151 citation statements)

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“…All genotypes were initially screened in the F 2 generation and confirmed further in F 3 and F 4 generations. The genotypes at various loci were determined by conducting cleaved amplified polymorphic sequence analysis (CAPS) or derived CAPS (d-CAPS), as described before (10)(11)(12)(15)(16)(17). Inoculations with TCV and P. syringae were conducted as described before (10,17).…”

Section: Methodsmentioning

confidence: 99%

“…HRT-mediated resistance is also dependent on PAD4, EDS5, and SID2, but is independent of RAR1 and SGT1 (10). In addition to HRT, resistance to TCV also requires the recessive locus rrt (11). However, this requirement for rrt can be overcome by increasing the levels of HRT transcript via exogenous application of SA (10).…”

mentioning

confidence: 98%

“…Although molecular mechanisms responsible for constitutive defense in cpr5 are not clear, characterization of ssi2 and its suppressors has implicated low levels of oleic acid (18:1) in altering defense signaling (15)(16)(17). The diverse biology of ssi2 and cpr5 mutants suggests that high levels of endogenous SA may be responsible for the up-regulation of HRT in HRT ssi2 and HRT cpr5 plants (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21).…”

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confidence: 99%

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Plastidial fatty acid levels regulate resistance gene-dependent defense signaling in Arabidopsis

Chandra-Shekara

Venugopal

Barman

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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In Arabidopsis, resistance to Turnip Crinkle Virus (TCV) depends on the resistance (R) gene, HRT, and the recessive locus rrt. Resistance also depends on salicylic acid (SA), EDS1, and PAD4. Exogenous application of SA confers resistance in RRT-containing plants by increasing HRT transcript levels in a PAD4-dependent manner. Here we report that reduction of oleic acid (18:1) can also induce HRT gene expression and confer resistance to TCV. However, the 18:1-regulated pathway is independent of SA, rrt, EDS1, and PAD4. Reducing the levels of 18:1, via a mutation in the SSI2-encoded stearoyl-acyl carrier protein-desaturase, or by exogenous application of glycerol, increased transcript levels of HRT as well as several other R genes. Second-site mutations in the ACT1-encoded glycerol-3-phosphate acyltransferase or GLY1-encoded glycerol-3-phosphate dehydrogenase restored 18:1 levels in HRT ssi2 plants and reestablished a dependence on rrt. Resistance to TCV and HRT gene expression in HRT act1 plants was inducible by SA but not by glycerol, whereas that in HRT pad4 plants was inducible by glycerol but not by SA. The low 18:1-mediated induction of R gene expression was also dependent on ACT1 but independent of EDS1, PAD4, and RAR1. Intriguingly, TCV inoculation did not activate this 18:1-regulated pathway in HRT plants, but instead resulted in the induction of several genes that encode 18:1-synthesizing isozymes. These results suggest that the 18:1-regulated pathway may be specifically targeted during pathogen infection and that altering 18:1 levels may serve as a unique strategy for promoting disease resistance.glycerol ͉ salicylic acid ͉ stearoyl-acyl carrier protein-desaturase ͉ Turnip Crinkle Virus ͉ ssi2 P lants respond to pathogen perception by triggering a cascade of responses. Perception involves strain-specific detection of a pathogen-encoded elicitor, through direct or indirect interaction, with the corresponding resistance (R) gene product. Such an interaction (also known as incompatible interaction) triggers one or more defense signaling pathways and is often associated with the induction of the hypersensitive response (HR) at the site of pathogen entry. HR is one of the first visible manifestations of the host-induced defense response and is thought to prevent development and movement of the pathogen by inducing deliberate death of the infected cells. R protein-mediated recognition of pathogen can also lead to the accumulation of various phytohormones including salicylic acid (SA), jasmonic acid, and/or ethylene, which in turn signal the activation of defense gene expression. Each hormone activates a specific pathway, and these act individually, synergistically, or antagonistically, depending on the pathogen involved, the ultimate effect of which confers disease resistance and prevents spread of the pathogen to uninoculated parts of the plant.Several components of the SA-mediated pathway have been identified, mutations in which lead to enhanced susceptibility to various pathogens [supporting information (SI...

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 98%

mentioning

confidence: 99%

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Plastidial fatty acid levels regulate resistance gene-dependent defense signaling in Arabidopsis

Chandra-Shekara

Venugopal

Barman

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…SA is involved in the plant defence response to a broad spectrum of pathogens. The role of SA-mediated resistance was extensively studied in resistant hosts (Yalpani et al, 1991;Kachroo et al, 2000;Park et al, 2007). Apart from being implicated in incompatible interactions, SA also plays a role during infections in susceptible tobacco and A. thaliana plants (Chivasa et al, 1997;Wang et al, 2009).…”

Section: Rna Interference-mediated Resistancementioning

confidence: 99%

Modulation of host plant immunity by Tobamovirus proteins

Conti

Rodríguez

Venturuzzi

et al. 2016

Ann Bot

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Background To establish successful infection, plant viruses produce profound alterations of host physiology, disturbing unrelated endogenous processes and contributing to the development of disease. In tobamoviruses, emerging evidence suggests that viral-encoded proteins display a great variety of functions beyond the canonical roles required for virus structure and replication. Among these, their modulation of host immunity appears to be relevant in infection progression.Scope In this review, some recently described effects on host plant physiology of Tobacco mosaic virus (TMV)-encoded proteins, namely replicase, movement protein (MP) and coat protein (CP), are summarized. The discussion is focused on the effects of each viral component on the modulation of host defense responses, through mechanisms involving hormonal imbalance, innate immunity modulation and antiviral RNA silencing. These effects are described taking into consideration the differential spatial distribution and temporality of viral proteins during the dynamic process of replication and spread of the virus.Conclusion In discussion of these mechanisms, it is shown that both individual and combined effects of viralencoded proteins contribute to the development of the pathogenesis process, with the host plant's ability to control infection to some extent potentially advantageous to the invading virus.

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“…Dominant viral R genes characterized to date encode either TIR-NBS-LRR (TNL) (8) or CC-NBS-LRR (CNL)-type proteins (9)(10)(11)(12)(13). Studies of these genes have been focused primarily on members of the Solanaceae (e.g., tobacco, tomato, and potato) and Arabidopsis (7,14).…”

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confidence: 99%

A viral resistance gene from common bean functions across plant families and is up-regulated in a non-virus-specific manner

Seo

Rojas

Lee

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

103

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Genes involved in a viral resistance response in common bean (Phaseolus vulgaris cv. Othello) were identified by inoculating a geminivirus reporter (Bean dwarf mosaic virus expressing the green fluorescent protein), extracting RNA from tissue undergoing the defense response, and amplifying sequences with degenerate R gene primers. One such gene (a TIR-NBS-LRR gene, RT4-4) was selected for functional analysis in which transgenic Nicotiana benthamiana were generated and screened for resistance to a range of viruses. This analysis revealed that RT4-4 did not confer resistance to the reporter geminivirus; however, it did activate a resistance-related response (systemic necrosis) to seven strains of Cucumber mosaic virus (CMV) from pepper or tomato, but not to a CMV strain from common bean. Of these eight CMV strains, only the strain from common bean systemically infected common bean cv. Othello. Additional evidence that RT4-4 is a CMV R gene came from the detection of resistance response markers in CMV-challenged leaves of RT4-4 transgenic plants, and the identification of the CMV 2a gene product as the elicitor of the necrosis response. These findings indicate that RT4-4 functions across two plant families and is up-regulated in a non-virus-specific manner. This experimental approach holds promise for providing insights into the mechanisms by which plants activate resistance responses against pathogens.avirulence gene ͉ Cucumber mosaic virus ͉ geminivirus ͉ host defense response ͉ systemic necrosis

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Resistance to Turnip Crinkle Virus in Arabidopsis Is Regulated by Two Host Genes and Is Salicylic Acid Dependent but NPR1, Ethylene, and Jasmonate Independent

Cited by 81 publications

References 63 publications

Plastidial fatty acid levels regulate resistance gene-dependent defense signaling in Arabidopsis

Plastidial fatty acid levels regulate resistance gene-dependent defense signaling in Arabidopsis

Modulation of host plant immunity by Tobamovirus proteins

A viral resistance gene from common bean functions across plant families and is up-regulated in a non-virus-specific manner

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