Scholarlink

<p>Cuproptosis denotes cell death triggered by copper accumulation. However, its role in natural environmental responses remains unclear. Here, we demonstrate that cuproptosis contributes to cold-induced lethality in <i>C. elegans</i>. A mutant for the lysosomal copper transporter gene <i>slcr-46.1</i> exhibited defective cold tolerance due to copper accumulation in the pharyngeal muscle upon cold&#xa0;exposure. The abnormal cold tolerance of the <i>slcr-46.1</i> mutant was suppressed by interference with copper homeostasis and cuproptosis-signaling genes. Chelating copper ions in the&#xa0;<i>slcr-46.1</i> mutant rescued the abnormal cold tolerance, while inhibiting cuproptosis signaling in wild-type worms inhibited cold-induced lethality. In addition, the cold lethality in the <i>slcr-46.1</i> mutant was not caused by activation of the oxidative stress pathway observed in ferroptosis (iron-dependent&#xa0;cell death). Here, we show evidence that cuproptosis plays a critical role in cold-induced lethality in an animal.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Cuproptosis inducers mediate cold lethality via SLCR-46.1 in C. elegans

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月27日

查看全文
  • Serina Yamashiro,
  • Satomi Mizuno,
  • Haruka Motomura,
  • Aidan T. Pezacki,
  • Yukina Mori,
  • Christopher J. Chang,
  • Akane Ohta,
  • Atsushi Kuhara

摘要

Cuproptosis denotes cell death triggered by copper accumulation. However, its role in natural environmental responses remains unclear. Here, we demonstrate that cuproptosis contributes to cold-induced lethality in C. elegans. A mutant for the lysosomal copper transporter gene slcr-46.1 exhibited defective cold tolerance due to copper accumulation in the pharyngeal muscle upon cold exposure. The abnormal cold tolerance of the slcr-46.1 mutant was suppressed by interference with copper homeostasis and cuproptosis-signaling genes. Chelating copper ions in the slcr-46.1 mutant rescued the abnormal cold tolerance, while inhibiting cuproptosis signaling in wild-type worms inhibited cold-induced lethality. In addition, the cold lethality in the slcr-46.1 mutant was not caused by activation of the oxidative stress pathway observed in ferroptosis (iron-dependent cell death). Here, we show evidence that cuproptosis plays a critical role in cold-induced lethality in an animal.