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February 6, 2026Plant Biotechnology Journal0 citationsOpen Access

Lily Transcription Factors LlPLATZ1 and LlMYB4 Orchestrate the Homeostasis of Heat Stress Responses via Antagonistic Regulation of LlHSF24

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XGXue GongJXJun XiangZLZiwei Liao

Key Points

  • To investigate the roles of the transcription factors LlPLATZ1 and LlMYB4 in regulating heat stress responses in lilies.
  • Identified LlPLATZ1 as a heat-inducible protein in Lilium longiflorum.
  • Examined LlPLATZ1's interaction with LlHSF24 and its effect on gene expression.
  • Analyzed the effects of overexpressing and silencing LlPLATZ1 on thermotolerance.
  • Studied LlMYB4's role in counterbalancing LlPLATZ1's function.
  • LlPLATZ1 was rapidly induced by heat and repressed LlHSF24 expression.
  • Stable overexpression of LlPLATZ1 improved thermotolerance in lilies, while silencing decreased it.
  • LlHSF24 was shown to repress heat-protective genes, weakening thermotolerance.
  • LlMYB4 interacts with LlPLATZ1 to limit its DNA-binding ability, affecting the heat stress response.

Abstract

ABSTRACT Heat stress significantly damages crop yield and quality. PLATZ (PLANT A/T‐RICH SEQUENCE‐AND ZINC‐BINDING PROTEIN) transcription factors play pivotal roles in plant growth, development, and environmental stress responses. While the functions of PLATZ members in response to drought and salt stress are well characterised, their roles in heat stress remain largely unexplored. Here, LlPLATZ1, a heat‐inducible member of the PLATZ family from lily ( Lilium longiflorum ), was identified. LlPLATZ1 was rapidly induced by high temperature, and its protein was localised to the nucleus, showing transcriptional repression activity. LlPLATZ1 bound to the promoter of a class B heat stress transcription factor gene, LlHSF24, to inhibit its expression. Stable overexpression of LlPLATZ1 in lily enhanced its thermotolerance, whereas silencing LlPLATZ1 had the opposite effect. Further analysis showed that LlHSF24 directly repressed the expression of heat‐protective genes LlHSP22.0 and LlHSP70 to weaken thermotolerance. In addition, LlPLATZ1 interacted with LlMYB4, a later heat‐inducible MYB transcription factor that bound to the LlHSF24 promoter to activate its expression. LlMYB4 limited the heat stress response by interacting with LlPLATZ1 to antagonise its DNA‐binding ability. In combination, these results indicate that the LlPLATZ1/LlMYB4‐LlHSF24 module may play a crucial role in maintaining a balanced heat stress response, enabling plants to adapt to complex environmental changes.

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Cite This Study

Gong et al. (2026) studied this question.

synapsesocial.com/papers/698585fe8f7c464f23009c98https://doi.org/10.1111/pbi.70572
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