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<p>In mammals, prolonged heat stress induces an endoplasmic reticulum (ER) stress response that can damage internal organs. In <i>Drosophila</i>, larvae grow and develop into adults faster at warmer temperatures (e.g., 30°C) than at lower temperatures, but with reduced body size and fertility. In this study, we show that the neuropeptide gene <i>neuropeptide-like precursor 1</i> (<i>Nplp1</i>) alleviates temperature-induced ER stress in imaginal discs. Warm temperatures increase production of a specific Nplp1 splice variant that inhibits PKR-like endoplasmic reticulum kinase (PERK) activation and cell death. <i>Nplp1</i> inhibits <i>Dilp8</i> expression through the PERK/ATF4/Yki pathway, thereby enabling imaginal disc growth and ecdysone homeostasis under warm temperature conditions. These findings provide valuable insights into how animals cope with elevated temperatures.</p>

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Imaginal discs produce neuropeptide-like precursor 1 to alleviate ER stress in response to warm temperatures

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月16日

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  • Il-Ju Kim,
  • Do-Hyoung Kim,
  • Young-Joon Kim

摘要

In mammals, prolonged heat stress induces an endoplasmic reticulum (ER) stress response that can damage internal organs. In Drosophila, larvae grow and develop into adults faster at warmer temperatures (e.g., 30°C) than at lower temperatures, but with reduced body size and fertility. In this study, we show that the neuropeptide gene neuropeptide-like precursor 1 (Nplp1) alleviates temperature-induced ER stress in imaginal discs. Warm temperatures increase production of a specific Nplp1 splice variant that inhibits PKR-like endoplasmic reticulum kinase (PERK) activation and cell death. Nplp1 inhibits Dilp8 expression through the PERK/ATF4/Yki pathway, thereby enabling imaginal disc growth and ecdysone homeostasis under warm temperature conditions. These findings provide valuable insights into how animals cope with elevated temperatures.