Overexpression of NDR1 leads to pathogen resistance at elevated temperatures

Samaradivakara, Saroopa; Chen, Huan; Lu, Yi-Ju; Li, Pai; Kim, Yongsig; Tsuda, Kazuhiko; Mine, Akira; Day, Brad

doi:10.1111/nph.18190

Cited by 11 publications

(7 citation statements)

References 83 publications

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“…1a). Furthermore, consistent with previous studies showing suppressed effector-triggered immunity (ETI) at elevated temperature [22][23][24][25] , we found that SA accumulation in Arabidopsis Col-0 plants is suppressed at 28 °C after infection with an ETI-activating P. syringae strain (Extended Data Fig. 1b).…”

supporting

confidence: 92%

Increasing the resilience of plant immunity to a warming climate

Kim

Castroverde

Huang

et al. 2022

Nature

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Extreme weather conditions associated with climate change affect many aspects of plant and animal life, including the response to infectious diseases. Production of salicylic acid (SA), a central plant defence hormone1–3, is particularly vulnerable to suppression by short periods of hot weather above the normal plant growth temperature range via an unknown mechanism4–7. Here we show that suppression of SA production in Arabidopsis thaliana at 28 °C is independent of PHYTOCHROME B8,9 (phyB) and EARLY FLOWERING 310 (ELF3), which regulate thermo-responsive plant growth and development. Instead, we found that formation of GUANYLATE BINDING PROTEIN-LIKE 3 (GBPL3) defence-activated biomolecular condensates11 (GDACs) was reduced at the higher growth temperature. The altered GDAC formation in vivo is linked to impaired recruitment of GBPL3 and SA-associated Mediator subunits to the promoters of CBP60g and SARD1, which encode master immune transcription factors. Unlike many other SA signalling components, including the SA receptor and biosynthetic genes, optimized CBP60g expression was sufficient to broadly restore SA production, basal immunity and effector-triggered immunity at the elevated growth temperature without significant growth trade-offs. CBP60g family transcription factors are widely conserved in plants12. These results have implications for safeguarding the plant immune system as well as understanding the concept of the plant–pathogen–environment disease triangle and the emergence of new disease epidemics in a warming climate.

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supporting

confidence: 92%

Increasing the resilience of plant immunity to a warming climate

Kim

Castroverde

Huang

et al. 2022

Nature

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“…However, and surprisingly, optimized CBP60g expression was sufficient to restore SA accumulation and plant immune responses at high temperature without growth or developmental penalty ( Kim et al., 2022 ). Another group unraveled the molecular mechanism explaining the temperature vulnerability of CNLs and SA defense signaling in Arabidopsis ( Samaradivakara et al., 2022 ). RESISTANCE TO P. SYRINGAE PV.…”

Section: The Effects Of Temperature On Eti and Sa-dependent Immunitymentioning

confidence: 99%

“…Samaradivakara et al. showed that overexpression of NDR1 rescues the transcript levels of RPS2 and SA-associated genes including those of ICS1 and CBP60g , which are repressed by high temperature, thus resulting in enhanced resistance to Pst DC3000 by maintaining ETI and SA defense signaling under elevated temperature (29°C) ( Samaradivakara et al., 2022 ). In wheat, CNLs such as TaRPM1 and TaRPS2 also positively regulate disease resistance to P. striiformis f. sp.…”

Section: The Effects Of Temperature On Eti and Sa-dependent Immunitymentioning

confidence: 99%

“…In Arabidopsis, the induction of CALMODULIN BINDING PROTEIN 60g (CBP60g) and NON-RACE SPECIFIC DISEASE RESISTANCE 1 (NDR1) is necessary for innate immunity against Pst DC3000. However, under high temperature, the formation of guanylate binding protein-like GTPase (GBPL) defense-activated condensate (GDAC), consisting of GBPL3, Mediator, and RNA polymerase II, at the CBP60g loci ( Kim et al, 2022 ) and the expression of NDR1 which can increase the transcript levels of RESISTANCE TO P. SYRINGAE 2 (RPS2) and SA-associated genes ( Samaradivakara et al, 2022 ) are repressed significantly, resulting in temperature vulnerability of SA-dependent immunity and ETI.…”

Section: The Effects Of Temperature On Eti and Sa-dependent Immunitymentioning

confidence: 99%

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Climate change impedes plant immunity mechanisms

Son

Park

2022

Front. Plant Sci.

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Rapid climate change caused by human activity is threatening global crop production and food security worldwide. In particular, the emergence of new infectious plant pathogens and the geographical expansion of plant disease incidence result in serious yield losses of major crops annually. Since climate change has accelerated recently and is expected to worsen in the future, we have reached an inflection point where comprehensive preparations to cope with the upcoming crisis can no longer be delayed. Development of new plant breeding technologies including site-directed nucleases offers the opportunity to mitigate the effects of the changing climate. Therefore, understanding the effects of climate change on plant innate immunity and identification of elite genes conferring disease resistance are crucial for the engineering of new crop cultivars and plant improvement strategies. Here, we summarize and discuss the effects of major environmental factors such as temperature, humidity, and carbon dioxide concentration on plant immunity systems. This review provides a strategy for securing crop-based nutrition against severe pathogen attacks in the era of climate change.

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“…For example, RIN4 also acts as a positive regulator of the jasmonate-signaling pathway downstream of the MPK4 protein, which promotes disease susceptibility [19]. The overexpression of non-race-specific disease resistance 1 (NDR1) gene would greatly improve the plant's pathogen resistance [27]. In Arabidopsis, the interaction between RIN4 and NDR1 was also identified [28].…”

Section: Introductionmentioning

confidence: 99%

The Upregulated Expression of the Citrus RIN4 Gene in HLB Diseased Citrus Aids Candidatus Liberibacter Asiaticus Infection

Cheng

Zhong

Wang

et al. 2022

IJMS

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The citrus industry has been threatened by Huanglongbing (HLB) for over a century. Here, an HLB-induced Arabidopsis RPM1-interacting protein 4 (RIN4) homologous gene was cloned from Citrus clementina, and its characteristics and function were analyzed to determine its role during citrus–Candidatus Liberibacter asiaticus (CLas) interactions. Quantitative real-time PCR showed that RIN4 was expressed in roots, stems, leaves and flowers, with the greatest expression level in leaves. Its expression was suppressed by gibberellic acid, indole-3-acetic acid, salicylic acid and jasmonic acid treatments, but was induced by abscisic acid and salt treatments, as well as wounding. The transient expression of a RIN4-GFP showed that RIN4 was localized in the cell membrane. RIN4-overexpressing transgenic C. maxima cv. ‘Shatianyou’ plants were obtained, and some transgenic plants showed greater sensitivity to CLas infection and earlier HLB symptoms appearance than non-transgenic controls. Results obtained in this study indicated that the upregulated expression of RIN4 in HLB diseased citrus may aid CLas infection.

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Overexpression of NDR1 leads to pathogen resistance at elevated temperatures

Cited by 11 publications

References 83 publications

Increasing the resilience of plant immunity to a warming climate

Increasing the resilience of plant immunity to a warming climate

Climate change impedes plant immunity mechanisms

The Upregulated Expression of the Citrus RIN4 Gene in HLB Diseased Citrus Aids Candidatus Liberibacter Asiaticus Infection

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