Department of Molecular, Cellular, and Developmental Biology, Neuroscience Research Institute, University of California at Santa Barbara, Santa Barbara, CA 93106, USA.
Genes Dev. 2012 Nov 1;26(21):2386-91. doi: 10.1101/gad.199588.112.
We report that Notch signaling is essential for the switch from developmental plasticity to commitment during Caenorhabditis elegans embryogenesis. The GLP-1 and LIN-12 Notch receptors act to set a memory state that affects commitment of cells arising from the major ectodermal progenitor (AB blastomere) several cell divisions later, thereby preventing their forced reprogramming by an endoderm-determining transcription factor. In contrast to Notch-dependent cell fate induction, this activity is autonomous to the AB lineage, is independent of the known cell fate-inducing Notch ligands, and requires a putative secreted Notch ligand, Delta Serrate Lag-3 (DSL-3). Thus, Notch signaling promotes developmental commitment by a mechanism that is distinct from that involved in specifying cell fates.
我们报告称，Notch 信号通路对于秀丽隐杆线虫胚胎发生过程中从发育可塑性到定型的转变是必需的。GLP-1 和 LIN-12 Notch 受体作用于建立一个记忆状态，该状态会影响几个细胞分裂后来自主要外胚层祖细胞（AB 卵裂球）的细胞的定型，从而防止它们被内胚层决定转录因子强行重编程。与 Notch 依赖性细胞命运诱导相反，这种活性是 AB 谱系自主的，不依赖于已知的细胞命运诱导 Notch 配体，并且需要假定的分泌 Notch 配体 Delta Serrate Lag-3（DSL-3）。因此，Notch 信号通路通过一种与指定细胞命运不同的机制促进发育定型。
