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内源性FGF驱动ERK依赖的细胞命运模式在2D人类胃体中

Kyoung Jo¹, Zong-Yuan Liu¹, Gauri Patel²

¹Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan.

bioRxiv : the preprint server for biology

|July 19, 2024

概括

纤维细胞生长因子 (FGF) 信号驱动人体胃口通过ERK激活在2D胃口. 通过FGFR1作用的FGF4和FGF17配体诱导原始的条状细胞,揭示了在人类早期发育中的新角色.

科学领域:

发育生物学是发展生物学.
干细胞生物学干细胞生物学
分子信号传递是分子信号传递.

背景情况:

纤维细胞生长因子 (FGF) 信号传递对于哺乳动物的胃流动至关重要,但其在人类发育中的确切作用尚不清楚.
了解FGF的功能需要人类早期发育的强大模型,例如2D胃类动物.

研究的目的:

为了研究FGF信号的功能,在人类胃流的2D胃类模型中进行信号传递.
阐明FGF依赖ERK激活的机制及其在原始链状 (PS) 细胞分化中的作用.

主要方法:

使用来自人类干细胞的二维胃.
使用成像分析了依赖FGF的ERK活动模式.
通过在位杂交和单细胞RNA测序 (scRNA-seq) 调查基因表达.
操纵FGF受体和连接体活动以评估功能影响.

主要成果:

鉴定了一种FGF依赖的ERK活动环,该环在PS样细胞出现之前出现.
证明了这种ERK活动对于PS类差异化至关重要.
表明FGF连接体FGF4和FGF17,通过基底局部化的FGFR1发出信号,诱导PS类细胞.
确认了人类和小鼠胃流动之间的FGF通路成分表达差异.

结论:

发现了FGF-依赖的ERK信号在使用2D胃体进行人体胃化中的新型作用.
建立了一种涉及FGF4/FGF17和FGFR1诱导PS样细胞的机制.
突出了哺乳动物胃流动期间FGF信号的特定物种差异.

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