The lateral signal for LIN-12/Notch in C-elegans vulval development comprises redundant secreted and transmembrane DSL proteins
The lateral signal for LIN-12/Notch in C-elegans vulval development comprises redundant secreted and transmembrane DSL proteins
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DOI：
10.1016/s1534-5807(04)00021-8
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发表时间：
2004-02-01
影响因子：
11.8
通讯作者：
Greenwald, I
中科院分区：
文献类型：
--
作者：
Chen, N;Greenwald, I
外阴前体细胞（VPC）通过LET-23/EGF受体介导的诱导信号和LIN-12/Notch介导的侧向信号在空间上形成图案。横向信号已经逃避识别，所以横向信号被激活的机制还不清楚。在这里，我们计算确定了10个基因编码潜在的配体LIN-12，并表明，这些基因中的三个，apx-1，dsi-1，和滞后2，功能冗余的组件的横向信号。我们还表明，所有这三个基因的转录启动或上调VPC中的诱导信号，这表明直接转录控制的横向信号的诱导信号是这些细胞信号事件的协调机制的一部分。此外，我们表明，DSL-1，它缺乏一个预测的跨膜结构域，是一种天然分泌的配体，可以取代跨膜配体LAG-2在不同的功能测定。
The vulval precursor cells (VPCs) are spatially patterned by a LET-23/EGF receptor-mediated inductive signal and a LIN-12/Notch-mediated lateral signal. The lateral signal has eluded identification, so the mechanism by which lateral signaling is activated has not been known. Here, we computationally identify ten genes that encode potential ligands for LIN-12, and show that three of these genes, apx-1, dsi-1, and lag-2, are functionally redundant components of the lateral signal. We also show that transcription of all three genes is initiated or upregulated in VPCs in response to inductive signaling, suggesting that direct transcriptional control of the lateral signal by the inductive signal is part of the mechanism by which these cell signaling events are coordinated. In addition, we show that DSL-1, which lacks a predicted transmembrane domain, is a natural secreted ligand and can substitute for the transmembrane ligand LAG-2 in different functional assays.