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Heat shock transcription factor 3 regulates plant immune response through modulation of salicylic acid accumulation and signalling in cassava.

ABSTRACT: As the terminal components of signal transduction, heat stress transcription factors (Hsfs) mediate the activation of multiple genes responsive to various stresses. However, the information and functional analysis are very limited in non-model plants, especially in cassava (Manihot esculenta), one of the most important crops in tropical areas. In this study, 32 MeHsfs were identified from the cassava genome; the evolutionary tree, gene structures and motifs were also analysed. Gene expression analysis found that MeHsfs were commonly regulated by Xanthomonas axonopodis pv. manihotis (Xam). Amongst these MeHsfs, MeHsf3 was specifically located in the cell nucleus and showed transcriptionally activated activity on heat stress elements (HSEs). Through transient expression in Nicotiana benthamiana leaves and virus-induced gene silencing (VIGS) in cassava, we identified the essential role of MeHsf3 in plant disease resistance, by regulating the transcripts of Enhanced Disease Susceptibility 1 (EDS1) and pathogen-related gene 4 (PR4). Notably, as regulators of defence susceptibility, MeEDS1 and MePR4 were identified as direct targets of MeHsf3. Moreover, the disease sensitivity of MeHsf3- and MeEDS1-silenced plants could be restored by exogenous salicylic acid (SA) treatment. Taken together, this study highlights the involvement of MeHsf3 in defence resistance through the transcriptional activation of MeEDS1 and MePR4.

SUBMITTER: Wei Y

PROVIDER: S-EPMC6638013 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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Heat shock transcription factor 3 regulates plant immune response through modulation of salicylic acid accumulation and signalling in cassava.

Wei Yunxie Y Liu Guoyin G Chang Yanli Y He Chaozu C Shi Haitao H

Molecular plant pathology 20180719 10

As the terminal components of signal transduction, heat stress transcription factors (Hsfs) mediate the activation of multiple genes responsive to various stresses. However, the information and functional analysis are very limited in non-model plants, especially in cassava (Manihot esculenta), one of the most important crops in tropical areas. In this study, 32 MeHsfs were identified from the cassava genome; the evolutionary tree, gene structures and motifs were also analysed. Gene expression an ...[more]

PMID: 29660238

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Project description:BackgroundAbility to adapt to temperature changes trough the Heat Shock Response (HSR) pathways is one of the most fundamental and clinically relevant cellular response systems. Heat Shock (HS) affects the signalling and gene expression responses of the Nuclear Factor κB (NF-κB) transcription factor, a critical regulator of proliferation and inflammation, however, our quantitative understanding of how cells sense and adapt to temperature changes is limited.MethodsWe used live-cell time-lapse microscopy and mathematical modelling to understand the signalling of the NF-κB system in the human MCF7 breast adenocarcinoma cells in response to pro-inflammatory Interleukin 1β (IL1β) and Tumour Necrosis Factor α (TNFα) cytokines, following exposure to a 37-43 °C range of physiological and clinical temperatures.ResultsWe show that exposure to 43 °C 1 h HS inhibits the immediate NF-κB signalling response to TNFα and IL1β stimulation although uptake of cytokines is not impaired. Within 4 h after HS treatment IL1β-induced NF-κB responses return to normal levels, but the recovery of the TNFα-induced responses is still affected. Using siRNA knock-down of Heat Shock Factor 1 (HSF1) we show that this stimulus-specificity is conferred via the Inhibitory κB kinase (IKK) signalosome where HSF1-dependent feedback regulates TNFα, but not IL1β-mediated IKK recovery post HS. Furthermore, we demonstrate that through the temperature-dependent denaturation and recovery of IKK, TNFα and IL1β-mediated signalling exhibit different temperature sensitivity and adaptation to repeated HS when exposed to a 37-43 °C temperature range. Specifically, IL1β-mediated NF-κB responses are more robust to temperature changes in comparison to those induced by TNFα treatment.ConclusionsWe demonstrate that the kinetics of the NF-κB system following temperature stress is cytokine specific and exhibit differential adaptation to temperature changes. We propose that this differential temperature sensitivity is mediated via the IKK signalosome, which acts as a bona fide temperature sensor trough the HSR cross-talk. This novel quantitative understanding of NF-κB and HSR interactions is fundamentally important for the potential optimization of therapeutic hyperthermia protocols. Video Abstract.

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Heat shock transcription factor 3 regulates plant immune response through modulation of salicylic acid accumulation and signalling in cassava.

Publications

Heat shock transcription factor 3 regulates plant immune response through modulation of salicylic acid accumulation and signalling in cassava.

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