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Abstract
Plants have evolved sophisticated genetic and epigenetic regulatory systems to respond quickly to unfavorable environmental conditions such as heat, cold, drought, and pathogen infections. In particular, heat greatly affects plant growth and development, immunity and circadian rhythm, and poses a serious threat to the global food supply. According to temperatures exposing, heat can be usually classified as warm ambient temperature (about 22–27°C), high temperature (27–30°C) and extremely high temperature (37–42°C, also known as heat stress) for the model plant Arabidopsis thaliana. The genetic mechanisms of plant responses to heat have been well studied, mainly focusing on elevated ambient temperature-mediated morphological acclimation and acceleration of flowering, modulation of circadian clock and plant immunity by high temperatures, and thermotolerance to heat stress. Recently, great progress has been achieved on epigenetic regulation of heat responses, including DNA methylation, histone modifications, histone variants, ATP-dependent chromatin remodeling, histone chaperones, small RNAs, long non-coding RNAs and other undefined epigenetic mechanisms. These epigenetic modifications regulate the expression of heat-responsive genes and function to prevent heat-related damages. This review focuses on recent progresses regarding the genetic and epigenetic control of heat responses in plants, and pays more attention to the role of the major epigenetic mechanisms in plant heat responses. Further research perspectives are also discussed.
Highlights
Owing to the global warming, the annual mean maximum and minimum temperatures have been reported to increase by 0.35 and 1.13◦C, respectively, for the period 1979–2003 (Peng et al, 2004)
This review briefly introduces the genetic mechanisms of plant responses to heat and highlights recent progresses regarding the underlying epigenetic regulations mainly in the Arabidopsis model, with aspects of some important physiological processes
In hac1-1 mutants, repetitively heat stress failed to induce enhanced resistance to bacteria, priming of pattern-triggered immunity (PTI), and enrichment of H3K9/14ac, H3K4me2 and H3K4me3. These findings reveal that HISTONE ACETYLTRANSFERASE1 (HAC1) is a necessary component for bacterial resistance, priming of PTI, and open chromatin configurations mediated by repetitive heat stress exposure
Summary
Reviewed by: Hongchang Cui, Florida State University, USA Clelia De-la-Peña, Centro de Investigación Científica de Yucatán, Mexico. The genetic mechanisms of plant responses to heat have been well studied, mainly focusing on elevated ambient temperature-mediated morphological acclimation and acceleration of flowering, modulation of circadian clock and plant immunity by high temperatures, and thermotolerance to heat stress. Great progress has been achieved on epigenetic regulation of heat responses, including DNA methylation, histone modifications, histone variants, ATP-dependent chromatin remodeling, histone chaperones, small RNAs, long non-coding RNAs and other undefined epigenetic mechanisms. These epigenetic modifications regulate the expression of heat-responsive genes and function to prevent heat-related damages.
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