The plant hypersensitive response: concepts, control and consequences

Balint‐Kurti, Peter

doi:10.1111/mpp.12821

Cited by 456 publications

(318 citation statements)

References 177 publications

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“…Interestingly, earlier studies demonstrated that loss of the chloroplast protein Les22, a uroporphyrinogen decarboxylase involved in chlorophyll biosynthesis, results in spontaneous lesions that resemble an HR [43]. This example with the Les22 protein is characteristic of the phenomenon observed in lesion mimic mutants of several plant species (e.g., rice, maize and the model plant Arabidopsis) in which spontaneous HR like symptoms, the hallmark of ETI, are observed without a pathogen being present [44]. Lesion mimic mutations have also been identified in the maize (ZmLls1) and wheat (TaLls1) genes encoding pheophorbide a oxygenase (PaO) for chlorophyll breakdown [45].…”

Section: Chloroplast Pigments and Carbohydrate Metabolismmentioning

confidence: 96%

Chloroplasts and Plant Immunity: Where Are the Fungal Effectors?

et al. 2019

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Chloroplasts play a central role in plant immunity through the synthesis of secondary metabolites and defense compounds, as well as phytohormones, such as jasmonic acid and salicylic acid. Additionally, chloroplast metabolism results in the production of reactive oxygen species and nitric oxide as defense molecules. The impact of viral and bacterial infections on plastids and chloroplasts has been well documented. In particular, bacterial pathogens are known to introduce effectors specifically into chloroplasts, and many viral proteins interact with chloroplast proteins to influence viral replication and movement, and plant defense. By contrast, clear examples are just now emerging for chloroplast-targeted effectors from fungal and oomycete pathogens. In this review, we first present a brief overview of chloroplast contributions to plant defense and then discuss examples of connections between fungal interactions with plants and chloroplast function. We then briefly consider well-characterized bacterial effectors that target chloroplasts as a prelude to discussing the evidence for fungal effectors that impact chloroplast activities.

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Section: Chloroplast Pigments and Carbohydrate Metabolismmentioning

confidence: 96%

Chloroplasts and Plant Immunity: Where Are the Fungal Effectors?

et al. 2019

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“…Cell death triggered by ETI is often considered as a part of the defence response resulting in suppression of disease progress (Balint-Kurti, 2019). In general, some other immune responses may precede this exhibition, including ROS accumulation, callose deposition, and changes in levels of phytohormones (Asai and Yoshioka, 2009;Deb et al, 2018;Bürger and Chory, 2019).…”

Section: Expression Of Plavh142 Activates Various Immune Responsesmentioning

confidence: 99%

An RXLR effector PlAvh142 from Peronophythora litchii triggers plant cell death and contributes to virulence

Situ

Jiang

Fan

et al. 2020

Molecular Plant Pathology

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Litchi downy blight, caused by the phytopathogenic oomycete Peronophythora litchii, results in tremendous economic loss in litchi production every year. To successfully colonize the host cell, Phytophthora species secret hundreds of RXLR effectors that interfere with plant immunity and facilitate the infection process. Previous work has already predicted 245 candidate RXLR effector‐encoding genes in P. litchii, 212 of which have been cloned and tested for plant cell death‐inducing activity in this study. We found three such RXLR effectors could trigger plant cell death through transient expression in Nicotiana benthamiana. Further experiments demonstrated that PlAvh142 could induce cell death and immune responses in several plants. We also found that PlAvh142 localized in both the cytoplasm and nucleus of plant cells. The cytoplasmic localization was critical for its cell death‐inducing activity. Moreover, deletion either of the two internal repeats in PlAvh142 abolished the cell death‐inducing activity. Virus‐induced gene silencing assays showed that cell death triggered by PlAvh142 was dependent on the plant transduction components RAR1 (require for Mla12 resistance), SGT1 (suppressor of the G2 allele of skp1) and HSP90 (heat shock protein 90). Finally, knockout of PlAvh142 resulted in significantly attenuated P. litchii virulence on litchi plants, whereas the PlAvh142‐overexpressed mutants were more aggressive. These data indicated that PlAvh142 could be recognized in plant cytoplasm and is an important virulence RXLR effector of P. litchii.

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“…One of the earliest hallmarks of HR is the rapid and intense production of reactive oxygen species (ROS) [57]. In Ny-1-mediated resistance of cv.…”

Section: Hypersensitive Response-mediated Resistance: Response At Thementioning

confidence: 99%

Plant Molecular Responses to Potato Virus Y: A Continuum of Outcomes from Sensitivity and Tolerance to Resistance

Baebler

Coll

Gruden

2020

Viruses

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Potato virus Y (PVY) is the most economically important virus affecting potato production. PVY manipulates the plant cell machinery in order to successfully complete the infecting cycle. On the other side, the plant activates a sophisticated multilayer immune defense response to combat viral infection. The balance between these mechanisms, depending on the plant genotype and environment, results in a specific outcome that can be resistance, sensitivity, or tolerance. In this review, we summarize and compare the current knowledge on molecular events, leading to different phenotypic outcomes in response to PVY and try to link them with the known molecular mechanisms.

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The plant hypersensitive response: concepts, control and consequences

Cited by 456 publications

References 177 publications

Chloroplasts and Plant Immunity: Where Are the Fungal Effectors?

Chloroplasts and Plant Immunity: Where Are the Fungal Effectors?

An RXLR effector PlAvh142 from Peronophythora litchii triggers plant cell death and contributes to virulence

Plant Molecular Responses to Potato Virus Y: A Continuum of Outcomes from Sensitivity and Tolerance to Resistance

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