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Notch signaling in the nervous system. Pieces still missing from the puzzle
Author(s) -
Baker Nicholas E.
Publication year - 2000
Publication title -
bioessays
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.175
H-Index - 184
eISSN - 1521-1878
pISSN - 0265-9247
DOI - 10.1002/(sici)1521-1878(200003)22:3<264::aid-bies8>3.0.co;2-m
Subject(s) - notch signaling pathway , notch proteins , hes3 signaling axis , biology , neurogenesis , signal transduction , lateral inhibition , neuroscience , cell fate determination , nervous system , microbiology and biotechnology , neural stem cell , neural cell , mechanism (biology) , cell , gene , genetics , stem cell , transcription factor , philosophy , epistemology
Notch has been known for many years as a receptor for inhibitory signals that shapes the pattern of the nervous system during its development. Genes in the Notch pathway function to prevent neural determination so that only a subset of the available ectodermal cells become neural precursors. The localization of Notch signaling is crucial for determining where neural precursor cells arise on a cell‐by‐cell basis. The unresolved problem is that studies of the expression of Notch protein and its ligands are inconsistent with the pattern of neurogenesis. During neural cell fate specification, distributions of Notch protein and of its ligand Delta appear uniform. Under the reigning paradigm, such widespread expression should lead to N signal transduction in all cells and thereby prevent any neural specification. Yet, contrary to this expectation, neural elements still form, in characteristic patterns, hence, Notch signal transduction must have been inactive in the precursor cells. The mechanism preventing Notch signaling in certain cells must be posttranslational but it has not yet been identified. This review will outline the experimental evidence supporting this view of Notch signaling, and briefly evaluate some of the possible mechanisms that have been suggested. BioEssays 22:264–273, 2000. © 2000 John Wiley & Sons, Inc.