Year: 1998
Type: preprint
Abstract: LIN-12/Notch proteins function as receptors for inter-cellular signals during development. Many aspects of LIN-12/Notch-mediated signaling have been elucidated through studies of cell–cell interactions that occur dur-ing Caenorhabditis elegans and Drosophila melanogas-ter development. The basic principles that operate in these lower organisms have also been shown to apply to vertebrates (for review, see Gridley 1997). Molecular fea-tures defined in lower organisms have also been shown to be conserved in vertebrates, including components of the signaling and signal transduction systems (for re-view, see Weinmaster 1997). The focus of this paper is on what has been learned about LIN-12/Notch signaling from invertebrates. First, a description of roles for LIN-12/Notch proteins in development is given, using differ-ent model cell fate decisions to illustrate various fea-tures. A discussion of the mechanism of LIN-12/Notch signal transduction follows, including new in vivo evi-dence that favors the direct participation of the intracel-lular domain of LIN-12/Notch proteins in regulating tar-get gene expression. Finally, other influences on LIN-12/ Notch activity are discussed, particularly protein turnover and protein processing. The LIN-12/Notch ‘‘pathway’’ Genetic studies have identified many conserved compo-nents that are important for LIN-12/Notch signaling. Table 1 summarizes the C. elegans and Drosophila genes involved in LIN-12/Notch signaling mentioned here, and their vertebrate counterparts. Of particular note is that transmembrane protein ligands of the conserved Delta/Serrate/LAG-2 (DSL) family activate LIN-12/ Notch signal transduction (for review, see Weinmaster 1997) and that many LIN-12/Notch outputs are medi-ated by a transcription factor named Suppressor of Hair-
Source: Genes & Development
Author: Iva Greenwald
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
Funder: Howard Hughes Medical Institute
OpenAlex ID: W7096867565