The Abruptex Mutations of Notch Disrupt the Establishment of Proneural Clusters in Drosophila

The receptor encoded by the Notch gene plays a central role in preventing cells from making decisions about their fates until appropriate signals are present. This function of Notch requires the product of the Suppressor of Hairless gene. Loss of either Notch or Suppressor of Hairless function resul...

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Bibliographic Details
Published in:Developmental biology 1999-12, Vol.216 (1), p.230-242
Main Authors: Brennan, Keith, Tateson, Richard, Lieber, Toby, Couso, Juan Pablo, Zecchini, Vincent, Arias, Alfonso Martinez
Format: Article
Language:English
Subjects:
animal breeding
animal genetics
animal physiology
Animals
arthropods
Basic Helix-Loop-Helix Transcription Factors
Cell Differentiation
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Drosophila - embryology
Drosophila - genetics
Drosophila Proteins
entomology
Epidermal Growth Factor - genetics
Gene Expression Regulation, Developmental
Membrane Proteins - genetics
Mutation
Phenotype
Receptors, Notch
Repressor Proteins - metabolism
Signal Transduction
signalling
Transcription Factors - genetics
Transcription Factors - metabolism
Wings, Animal - embryology
Wings, Animal - growth & development
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Summary:The receptor encoded by the Notch gene plays a central role in preventing cells from making decisions about their fates until appropriate signals are present. This function of Notch requires the product of the Suppressor of Hairless gene. Loss of either Notch or Suppressor of Hairless function results in cells making premature and incorrect cell fate decisions, whilst increases in Notch signalling prevent cells from making these decisions. Here we find that the proneural clusters are not established correctly in certain Abruptex mutations of Notch and this failure to establish proneural clusters correctly is not due to increased Notch signalling during lateral inhibition. In addition we show that the overexpression of certain dominant negative Notch molecules can disrupt the initiation of proneural cluster development in a manner similar to the Abruptex mutants.
ISSN:0012-1606
1095-564X
DOI:10.1006/dbio.1999.9501