Journal ArticleDOI
Notch Signaling: Cell Fate Control and Signal Integration in Development
TLDR
Notch signaling defines an evolutionarily ancient cell interaction mechanism, which plays a fundamental role in metazoan development, providing a general developmental tool to influence organ formation and morphogenesis.Abstract:
Notch signaling defines an evolutionarily ancient cell interaction mechanism, which plays a fundamental role in metazoan development. Signals exchanged between neighboring cells through the Notch receptor can amplify and consolidate molecular differences, which eventually dictate cell fates. Thus, Notch signals control how cells respond to intrinsic or extrinsic developmental cues that are necessary to unfold specific developmental programs. Notch activity affects the implementation of differentiation, proliferation, and apoptotic programs, providing a general developmental tool to influence organ formation and morphogenesis.read more
Citations
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Notch inhibition of RAS signaling through MAP kinase phosphatase LIP-1 during C. elegans vulval development.
TL;DR: During Caenorhabditis elegans vulval development, a signal from the anchor cell stimulates the RTK/RAS/MAPK signaling pathway in the closest vulval precursor cell P6.p, where LIP-1 inactivates the MAP kinase to inhibit primary fate specification and links the two signaling pathways to generate a pattern.
Journal ArticleDOI
Glial cell fate specification modulated by the bHLH gene Hes5 in mouse retina
Masato Hojo,Toshiyuki Ohtsuka,Nobuo Hashimoto,Gerald Gradwohl,Francois Guillemot,Ryoichiro Kageyama +5 more
TL;DR: It is found that, in mouse retina, the bHLH gene Hes5 was specifically expressed by differentiating Müller glial cells and that misexpression of Hes5 with recombinant retrovirus significantly increased the population ofglial cells at the expense of neurons.
Journal ArticleDOI
Notch Activation Results in Phenotypic and Functional Changes Consistent With Endothelial-to-Mesenchymal Transformation
Michela Noseda,Graeme W. McLean,Kyle Niessen,Linda Chang,Ingrid L. Pollet,Rachel Montpetit,Réza Shahidi,Katerina Dorovini-Zis,Linheng Li,Benjamin Beckstead,Ralph E. Durand,Pamela A. Hoodless,Aly Karsan +12 more
TL;DR: This is the first evidence that Jagged1-Notch interactions induce endothelial-to-mesenchymal transformation, and the findings suggest that Notch signaling may be required for proper endocardial cushion differentiation and/or vascular smooth muscle cell development.
Journal ArticleDOI
Genetic control of Drosophila nerve cord development
James B. Skeath,Stefan Thor +1 more
TL;DR: The Drosophila ventral nerve cord has been a central model system for studying the molecular genetic mechanisms that control CNS development, and studies show that the generation of neural diversity is a multistep process initiated by the patterning and segmentation of the neuroectoderm.
Journal ArticleDOI
SKIP, a CBF1-associated protein, interacts with the ankyrin repeat domain of NotchIC To facilitate NotchIC function.
Sifang Zhou,Masahiro Fujimuro,James J. Hsieh,Lin Chen,Alison Miyamoto,Gerry Weinmaster,S. Diane Hayward +6 more
TL;DR: The results suggest a model in which NotchIC activates responsive promoters by competing with the SMRT-corepressor complex for contacts on both CBF1 and SKIP.
References
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Journal ArticleDOI
Notch3 mutations in CADASIL, a hereditary adult-onset condition causing stroke and dementia
Anne Joutel,Christophe Corpechot,Anne Ducros,Katayoun Vahedi,Hugues Chabriat,Philippe Mouton,Sonia Alamowitch,Valérie Domenga,Michaelle Cécillion,Emmanuelle Maréchal,Jacqueline Maciazek,Céline Vayssière,Corinne Cruaud,E. A. Cabanis,Marie Madeleine Ruchoux,Jean Weissenbach,Jean Francois Bach,Marie-Germaine Bousser,Elisabeth Tournier-Lasserve +18 more
TL;DR: The characterization of the human Notch3 gene, which was previously mapped to the CADASIL critical region, is reported, indicating that Notch 3 could be the defective protein in CADASil patients.
Journal ArticleDOI
Notch-1 signalling requires ligand-induced proteolytic release of intracellular domain.
TL;DR: It is shown that signalling by a constitutively active membrane-bound Notch-1 protein requires the proteolytic release of the Notch intracellular domain (NICD), which interacts preferentially with CSL.
Journal ArticleDOI
Signalling downstream of activated mammalian Notch.
Sophie Jarriault,Christel Brou,Frédérique Logeat,Eric H. Schroeter,Raphael Kopan,Alain Israël +5 more
TL;DR: It is shown that activated forms of mNotch associate with the human analogue of Su(H), KBF2/RBP-JK and act as transcriptional activators through theKBF2-binding sites of the HES-1 promoter and block MyoD-induced myogenesis5-7.
Journal Article
Notch signaling : Signal transduction
TL;DR: The Notch/Lin-12/Glp-1 receptor family mediates the specification of numerous cell fates during development in Drosophila and Caenorhabditis elegans and putative components of the signaling cascade are identified, including a conserved family of extracellular ligands and two cellular factors that may associate with the Notch Intracellular domain.
Journal ArticleDOI
Alagille syndrome is caused by mutations in human Jagged1, which encodes a ligand for Notch1
Linheng Li,Ian D. Krantz,Yu Deng,Yu Deng,Anna Genin,Amy B. Banta,Colin Collins,Ming Qi,Barbara J. Trask,Wen Lin Kuo,Joanne Cochran,Teresa Costa,Mary Ella M Pierpont,Elizabeth B. Rand,David A. Piccoli,Leroy Hood,Nancy B. Spinner +16 more
TL;DR: Four distinct coding mutations in JAG1 are demonstrated, providing evidence that it is the causal gene for Alagille syndrome, and supporting the hypothesis that haploinsufficiency for this gene is one of the mechanisms causing the Alagile syndrome phenotype.