title: Essential role for Notch signaling in restricting developmental plasticity.
abstract: 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.
authors.affiliation: Department of Molecular, Cellular, and Developmental Biology, Neuroscience Research Institute, University of California at Santa Barbara, Santa Barbara, CA 93106, USA.
authors.forename: Nareg J-V
authors.initials: NJ
authors.lastname: Djabrayan
authors.forename: Nathaniel R
authors.initials: NR
authors.lastname: Dudley
authors.forename: Erica M
authors.initials: EM
authors.lastname: Sommermann
authors.forename: Joel H
authors.initials: JH
authors.lastname: Rothman
mesh_terms: D000818:Animals; D017173:Caenorhabditis elegans / Q000166:cytology / Q000196:embryology* / Q000235:genetics; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism*; D002454:Cell Differentiation; D065150:Cellular Reprogramming; D047108:Embryonic Development; D018507:Gene Expression Regulation, Developmental; D051880:Receptors, Notch / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D029742:Caenorhabditis elegans Proteins; D051880:Receptors, Notch