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Heat Stress Responses and Thermotolerance in Maize

High temperatures causing heat stress disturb cellular homeostasis and impede growth and development in plants. Extensive agricultural losses are attributed to heat stress, often in combination with other stresses. Plants have evolved a variety of responses to heat stress to minimize damage and to protect themselves from further stress. A narrow temperature window separates growth from heat stress, and the range of temperatures conferring optimal growth often overlap with those producing heat stress.

Zhaoxia LiStephen H Howell

Int J Mol Sci.; 2021 Jan 19;22(2):948.  doi: 10.3390/ijms22020948.

Abstract

High temperatures causing heat stress disturb cellular homeostasis and impede growth and development in plants. Extensive agricultural losses are attributed to heat stress, often in combination with other stresses. Plants have evolved a variety of responses to heat stress to minimize damage and to protect themselves from further stress. A narrow temperature window separates growth from heat stress, and the range of temperatures conferring optimal growth often overlap with those producing heat stress. Heat stress induces a cytoplasmic heat stress response (HSR) in which heat shock transcription factors (HSFs) activate a constellation of genes encoding heat shock proteins (HSPs). Heat stress also induces the endoplasmic reticulum (ER)-localized unfolded protein response (UPR), which activates transcription factors that upregulate a different family of stress response genes. Heat stress also activates hormone responses and alternative RNA splicing, all of which may contribute to thermotolerance. Heat stress is often studied by subjecting plants to step increases in temperatures; however, more recent studies have demonstrated that heat shock responses occur under simulated field conditions in which temperatures are slowly ramped up to more moderate temperatures. Heat stress responses, assessed at a molecular level, could be used as traits for plant breeders to select for thermotolerance.

 

See: https://pubmed.ncbi.nlm.nih.gov/33477941/

 

Figure 2: Two systems involved in heat stress responses in plants. Heat stress triggers protective mechanisms collectively called heat stress responses (HSRs). Both HSR in the cytoplasm and unfolded protein responses (UPR) in the endoplasmic reticulum (ER) mitigate the damage from heat stress and protect plants from further stress. The UPR and HSR occur in different cellular compartments, but both responses are elicited by misfolded proteins that accumulate in the ER and cytoplasm, respectively. The HSP and UPR genes in plants are upregulated by the activation of stress-transducing transcription factors, such as bZIP60 (basic leucine zipper 60) in the UPR and HSFs in the HSR. IRE1, a key factor in the UPR, is a dual protein kinase and ribonuclease involved in the splicing of bZIP60 mRNA. HSR, heat stress response; UPR, unfolded protein response; ER, endoplasmic reticulum; bZIP60, basic leucine zipper 60; HSP, heat shock protein; HSF, heat shock transcription factor; HSP70, heat shock protein 70; BIP, binding immunoglobulin protein; and IRE1, inositol-requiring enzyme 1.

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