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<p>Potassium is vital for life, yet how potassium homeostasis is maintained at the tissue or organismal level under dietary scarcity remains poorly understood. Stress-activated signaling pathway p38 MAPK is implicated in immune response and aging, but its specific role in low potassium response is unclear. Here we show that a specific p38 MAPK–ATF-7 pathway orchestrates cross-tissue potassium homeostasis in <i>Caenorhabditis elegans</i>. It drives transcriptional upregulation of a crucial P-type ATPase pump CATP-3 specifically in the hypodermis, a process that integrates cell-autonomous mechanisms with non-autonomous ASI neuronal signals, thereby enhancing organismal survival during potassium deficiency. Notably, this regulation is distinct from canonical osmotic stress responses, revealing a specialized and conserved survival strategy. Analogous p38-mediated control of P-type ATPases occurs in yeast and mammalian cells, suggesting broad relevance. Our findings redefine potassium regulation as a cross-tissue process linked to lifespan, stress signaling, and innate immunity with potential implications for aging and age-related diseases.</p>

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p38 MAPK orchestrates cross-tissue potassium homeostasis for survival

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月9日

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  • Rong Huang,
  • Fangchao Hu,
  • Yiyao Li,
  • Qifei Gao,
  • Jintao Huang,
  • Jiarui Wang,
  • Wei Lu,
  • Liping Wang,
  • Yapeng Fang,
  • T. Keith Blackwell,
  • Ziyun Wu

摘要

Potassium is vital for life, yet how potassium homeostasis is maintained at the tissue or organismal level under dietary scarcity remains poorly understood. Stress-activated signaling pathway p38 MAPK is implicated in immune response and aging, but its specific role in low potassium response is unclear. Here we show that a specific p38 MAPK–ATF-7 pathway orchestrates cross-tissue potassium homeostasis in Caenorhabditis elegans. It drives transcriptional upregulation of a crucial P-type ATPase pump CATP-3 specifically in the hypodermis, a process that integrates cell-autonomous mechanisms with non-autonomous ASI neuronal signals, thereby enhancing organismal survival during potassium deficiency. Notably, this regulation is distinct from canonical osmotic stress responses, revealing a specialized and conserved survival strategy. Analogous p38-mediated control of P-type ATPases occurs in yeast and mammalian cells, suggesting broad relevance. Our findings redefine potassium regulation as a cross-tissue process linked to lifespan, stress signaling, and innate immunity with potential implications for aging and age-related diseases.