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Background <p>High temperatures can substantially reduce plant survival and reproduction, and therefore decrease crop productivity. Plants activate several pathways in response to high temperatures, including the endoplasmic reticulum (ER) unfolded protein response (UPR), the cytoplasmic heat stress response (HSR), and autophagy, which together aid in stress tolerance by refolding or degrading misfolded and unfolded proteins. To assess the relationship between the distinct responses to heat stress in maize, we analyzed the effect of disruption of autophagy on the UPR and HSR, and the effect of disruption of the UPR on autophagy.</p> Results <p>We found that loss of autophagy, via mutants in <i>ATG10</i>, a core component of the autophagy machinery, led to increased activation of the UPR upon ER stress, and that autophagy is activated in a <i>bzip60</i> mutant, defective in the UPR, even in the absence of stress. By contrast, UPR activity was unaffected in <i>atg10</i> mutants in response to heat, whereas cytoplasmic heat stress components were increased.</p> Conclusions <p>Loss of autophagy differentially affects other heat stress response pathways, depending on the specific stress conditions leading to the activation of the pathways.</p>

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Interplay between autophagy, the unfolded protein response and the cytoplasmic heat stress response during heat stress in maize

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月29日

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  • Jie Tang,
  • Vishadinie Jayasinghe,
  • Zhaoxia Li,
  • Diane C. Bassham

摘要

Background

High temperatures can substantially reduce plant survival and reproduction, and therefore decrease crop productivity. Plants activate several pathways in response to high temperatures, including the endoplasmic reticulum (ER) unfolded protein response (UPR), the cytoplasmic heat stress response (HSR), and autophagy, which together aid in stress tolerance by refolding or degrading misfolded and unfolded proteins. To assess the relationship between the distinct responses to heat stress in maize, we analyzed the effect of disruption of autophagy on the UPR and HSR, and the effect of disruption of the UPR on autophagy.

Results

We found that loss of autophagy, via mutants in ATG10, a core component of the autophagy machinery, led to increased activation of the UPR upon ER stress, and that autophagy is activated in a bzip60 mutant, defective in the UPR, even in the absence of stress. By contrast, UPR activity was unaffected in atg10 mutants in response to heat, whereas cytoplasmic heat stress components were increased.

Conclusions

Loss of autophagy differentially affects other heat stress response pathways, depending on the specific stress conditions leading to the activation of the pathways.