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通过代谢重编程,Irg1l调节神经质的大小,以促进支持细胞增殖

Xin Wang¹, Ruijun Shi¹, Yuqing Xiang²

¹Institute of Special Environmental Medicine, Affiliated Hospital 2, Nantong University , Nantong, China.

The Journal of cell biology

|October 28, 2025

概括

伊塔科纳酸是一种内源代谢物,通过影响支持细胞增殖来调节斑马鱼神经的大小. 这一发现揭示了代谢物和器官发育之间的新联系.

科学领域:

发展生物学发展生物学
代谢学代谢学代谢学
遗传学遗传学是一个

背景情况:

器官尺寸调节对于胚胎发育和器官功能至关重要.
控制器官大小的内源代谢物以前没有被确定.
在哺乳动物中已知itaconate通路,但其在器官生成中的作用尚不清楚.

研究的目的:

研究内源代谢物在胚胎发育过程中调节器官大小中的作用.
为了确定特定的代谢物和途径,涉及斑马鱼神经的发展.
阐明代谢物影响器官大小的机制.

主要方法:

斑马鱼神经质的单细胞转录组测序.
基因淘汰和irg1l (Irg1同类) 的过度表达.
用4-octyl itaconate (4-OI) 进行治疗,它是一种 itaconate衍生物.
对支持细胞增殖和Yap通路激活的分析.

主要成果:

编码产生伊塔康酸盐的酶的irg1l基因在斑马鱼神经支细胞中高度表达.
缺少irg1l会导致神经母细胞变小和听力功能障碍.
过度表达irg1l或治疗4-OI通过促进支持细胞增殖,增加神经巨的大小.
该Irg1l/itaconate通路重编程新陈代谢,激活Yap,并驱动细胞增殖.

结论:

伊塔科纳酸是第一个确定能调节器官大小的内源代谢物.
1l/伊塔康酸轴是斑马鱼神经尺寸的关键调节器.
这一途径涉及代谢重编程,雅普激活和支持细胞增殖,为器官发育提供了新的见解.

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