SlMAPK3 enhances tolerance to tomato yellow leaf curl virus (TYLCV) by regulating salicylic acid and jasmonic acid signaling in tomato (Solanum lycopersicum)

Li, Yunzhou; Qin, Lei; Zhao, Jingjing; Muhammad, Tayeb; Cao, He‐He; Li, Hailiang; Zhang, Yan; Liang, Yan

doi:10.1371/journal.pone.0172466

Cited by 68 publications

(51 citation statements)

References 101 publications

(128 reference statements)

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“…PR1a is SA‐responsive and considered a systemic acquired resistance (SAR) marker (López‐Ráez et al ., 2010; Martínez‐Medina et al ., 2013). PR1b is up‐regulated by both SAR and ISR activation (Harel et al ., 2014; Li et al ., 2017). Distinctions between ISR and SAR are not clear‐cut in tomato, and they can overlap (Liu et al ., 2016; Betsuyaku et al ., 2018).…”

Section: Resultsmentioning

confidence: 99%

Cytokinin response induces immunity and fungal pathogen resistance, and modulates trafficking of the PRR LeEIX2 in tomato

Gupta

Pizarro

Leibman‐Markus

et al. 2020

Molecular Plant Pathology

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Plant immunity is often defined by the immunity hormones: salicylic acid (SA), jasmonic acid (JA), and ethylene (ET). These hormones are well known for differentially regulating defence responses against pathogens. In recent years, the involvement of other plant growth hormones such as auxin, gibberellic acid, abscisic acid, and cytokinins (CKs) in biotic stresses has been recognized. Previous reports have indicated that endogenous and exogenous CK treatment can result in pathogen resistance. We show here that CK induces systemic immunity in tomato (Solanum lycopersicum), modulating cellular trafficking of the pattern recognition receptor (PRR) LeEIX2, which mediates immune responses to Xyn11 family xylanases, and promoting resistance to Botrytis cinerea and Oidium neolycopersici in an SA‐ and ET‐dependent mechanism. CK perception within the host underlies its protective effect. Our results support the notion that CK promotes pathogen resistance by inducing immunity in the host.

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Section: Resultsmentioning

confidence: 99%

Cytokinin response induces immunity and fungal pathogen resistance, and modulates trafficking of the PRR LeEIX2 in tomato

Gupta

Pizarro

Leibman‐Markus

et al. 2020

Molecular Plant Pathology

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“…Other kinases implicated in defense signal transduction pathways have also been manipulated to mitigate viral symptoms. Overexpression of SlMAPK3, a MAP kinase, showed enhanced expression of defense genes associated with SA- and JA-signaling, lower accumulation of reactive oxygen species, increased accumulation of antioxidant enzymes, and stronger tolerance to tomato yellow leaf curl virus infection as expressed by a 2-week delay in symptom induction which was sufficient to allow plant flowering ( Li et al, 2017 ). Similarly, overexpression of OsCIPK30, a kinase involved in calcium signaling, in rice provided enhance tolerance to rice stripe virus, that was associated with delayed and milder symptoms and enhanced expression of PR genes ( Liu et al, 2017 ).…”

Section: Engineering Tolerance To Virus Disease For Field Applicationmentioning

confidence: 99%

Exploring the Diversity of Mechanisms Associated With Plant Tolerance to Virus Infection

Paudel

Sanfaçon

2018

Front. Plant Sci.

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Tolerance is defined as an interaction in which viruses accumulate to some degree without causing significant loss of vigor or fitness to their hosts. Tolerance can be described as a stable equilibrium between the virus and its host, an interaction in which each partner not only accommodate trade-offs for survival but also receive some benefits (e.g., protection of the plant against super-infection by virulent viruses; virus invasion of meristem tissues allowing vertical transmission). This equilibrium, which would be associated with little selective pressure for the emergence of severe viral strains, is common in wild ecosystems and has important implications for the management of viral diseases in the field. Plant viruses are obligatory intracellular parasites that divert the host cellular machinery to complete their infection cycle. Highjacking/modification of plant factors can affect plant vigor and fitness. In addition, the toxic effects of viral proteins and the deployment of plant defense responses contribute to the induction of symptoms ranging in severity from tissue discoloration to malformation or tissue necrosis. The impact of viral infection is also influenced by the virulence of the specific virus strain (or strains for mixed infections), the host genotype and environmental conditions. Although plant resistance mechanisms that restrict virus accumulation or movement have received much attention, molecular mechanisms associated with tolerance are less well-understood. We review the experimental evidence that supports the concept that tolerance can be achieved by reaching the proper balance between plant defense responses and virus counter-defenses. We also discuss plant translation repression mechanisms, plant protein degradation or modification pathways and viral self-attenuation strategies that regulate the accumulation or activity of viral proteins to mitigate their impact on the host. Finally, we discuss current progress and future opportunities toward the application of various tolerance mechanisms in the field.

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“…Activation of SA also plays a role in tolerance of A. thaliana to P. syringae [ 115 ]. Analyses by Li et al [ 116 ] also suggested that SA and jasmonic acid could be involved in tolerance of tomato to TYLCV.…”

Section: Mechanistic Basis and Genetic Determinants Of Plant Tolermentioning

confidence: 99%

Tolerance to Plant Pathogens: Theory and Experimental Evidence

Pagán

García‐Arenal

2018

IJMS

105

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The two major mechanisms of plant defense against pathogens are resistance (the host’s ability to limit pathogen multiplication) and tolerance (the host’s ability to reduce the effect of infection on its fitness regardless of the level of pathogen multiplication). There is abundant literature on virtually every aspect of plant resistance to pathogens. Although tolerance to plant pathogens is comparatively less understood, studies on this plant defense strategy have led to major insights into its evolution, mechanistic basis and genetic determinants. This review aims at summarizing current theories and experimental evidence on the evolutionary causes and consequences of plant tolerance to pathogens, as well as the existing knowledge on the genetic determinants and mechanisms of tolerance. Our review reveals that (i) in plant-pathogen systems, resistance and tolerance generally coexist, i.e., are not mutually exclusive; (ii) evidence of tolerance polymorphisms is abundant regardless of the pathogen considered; (iii) tolerance is an efficient strategy to reduce the damage on the infected host; and (iv) there is no evidence that tolerance results in increased pathogen multiplication. Taken together, the work discussed in this review indicates that tolerance may be as important as resistance in determining the dynamics of plant-pathogen interactions. Several aspects of plant tolerance to pathogens that still remain unclear and which should be explored in the future, are also outlined.

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SlMAPK3 enhances tolerance to tomato yellow leaf curl virus (TYLCV) by regulating salicylic acid and jasmonic acid signaling in tomato (Solanum lycopersicum)

Cited by 68 publications

References 101 publications

Cytokinin response induces immunity and fungal pathogen resistance, and modulates trafficking of the PRR LeEIX2 in tomato

Cytokinin response induces immunity and fungal pathogen resistance, and modulates trafficking of the PRR LeEIX2 in tomato

Exploring the Diversity of Mechanisms Associated With Plant Tolerance to Virus Infection

Tolerance to Plant Pathogens: Theory and Experimental Evidence

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