AFF-1, a FOS-1-regulated fusogen, mediates fusion of the anchor cell in C-elegans
AFF-1, a FOS-1-regulated fusogen, mediates fusion of the anchor cell in C-elegans
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DOI：
10.1016/j.devcel.2007.03.003
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发表时间：
2007-05-01
影响因子：
11.8
通讯作者：
Podbilewicz, Benjamin
中科院分区：
文献类型：
--
作者：
Sapir, Amir;Choi, Jaebok;Podbilewicz, Benjamin
细胞融合是生殖和器官形成的基础。大多数C。EFF-1融合子介导的EFF-1在Elegans上皮细胞中的表达。然而，锚细胞和utse合胞体之间的融合建立了一个连续的子宫-外阴管在eff-1突变体中正常进行。通过分离锚细胞不能融合的突变体，我们鉴定了aff-1。AFF-1异位表达结果。注入在C中通常不融合的细胞。优雅AFF-1融合异源细胞的能力进一步证实了其融合活性。AFF-1和EFF-1的融合活性和表达模式不同，但在其胞外域共有8个保守的预测二硫键，包括一个推定的TGF-β-I型受体结构域。我们发现，FOS-1，Fos转录因子直系同源物，控制锚细胞入侵线虫发展过程中，是一个特定的激活因子aff-l介导的锚细胞融合。因此，FOS-1在发育级联中连接细胞侵袭和融合。
Cell fusion is fundamental for reproduction and organ formation. Fusion between most C. elegans epithelial cells is mediated by the EFF-1 fusogen. However, fusion between the anchor cell and the utse syncytium that establishes a continuous uterine-vulval tube proceeds normally in eff-1 mutants. By isolating mutants where the anchor-cell fails to fuse, we identified aff-1. AFF-1 ectopic expression results. infusion of cells that normally do not fuse in C. elegans. The fusogen activity of AFF-1 was further confirmed by its ability to fuse heterologous cells. AFF-1 and EFF-1 differ in their fusogenic activity and expression patterns but share eight conserved predicted disulfide bonds in their ectodomains, including a putative TGF-beta-type-I-Receptor domain. We found that FOS-1, the Fos transcription factor ortholog that controls anchor-cell invasion during nematode development, is a specific activator of aff-l-mediated anchor-cell fusion. Thus, FOS-1 links cell invasion and fusion in a developmental cascade.