Cell-autonomous role of Notch, an epidermal growth factor homologue, in sensory organ differentiation in Drosophila.

The gene Notch (N) codes for a transmembrane protein with an extracellular domain that has homologies to epidermal growth factors and an intracellular domain that could be involved in signal transduction. N null alleles cause the transformation of most epidermal cells into neuroblasts in central and...

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Detalles Bibliográficos
Autores: Celis, José F. de, Marí-Beffa, Manuel, García-Bellido, Antonio
Tipo de recurso: artículo
Fecha de publicación:1990
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/47833
Acceso en línea:http://hdl.handle.net/10261/47833
Access Level:acceso embargado
Palabra clave:Drosophila
Melanogaster
Notch
Transmembrane
Cells
Growth
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network_acronym_str ES
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repository_id_str
spelling Cell-autonomous role of Notch, an epidermal growth factor homologue, in sensory organ differentiation in Drosophila.Celis, José F. deMarí-Beffa, ManuelGarcía-Bellido, AntonioDrosophilaMelanogasterNotchTransmembraneCellsGrowthThe gene Notch (N) codes for a transmembrane protein with an extracellular domain that has homologies to epidermal growth factors and an intracellular domain that could be involved in signal transduction. N null alleles cause the transformation of most epidermal cells into neuroblasts in central and peripheral nervous systems. Alleles of the same gene, called Abruptex (Ax), that map to the extracellular domain of N protein cause the absence of adult sensory organs. Both types of alleles show cell autonomy in mosaic analysis carried out in the last stages of the formation of adult sensory organs. The phenotypes are different: cells lacking N gene products differentiate as sensory organ mother cells early and as its neural sublineage later, whereas in the homozygous Ax condition epidermal cells do not enter the sensory organ mother cell pathway. The results indicate that N gene products act internally in the cell, probably as receptors of intercellular signals both in sensory organ mother cell singularization and in fate specification of its daughter cells. Ax mutations behave as an excess of N+ function in this signal transduction process. N proteins modified by these mutations act as constitutively activated.Peer reviewedNational Academy of Sciences (U.S.)Consejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]201220121990info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_6501http://hdl.handle.net/10261/47833reponame:DIGITAL.CSIC. Repositorio Institucional del CSICinstname:Consejo Superior de Investigaciones Científicas (CSIC)Ingléshttp://dx.doi.org/10.1073/pnas.88.2.632Síinfo:eu-repo/semantics/embargoedAccessoai:digital.csic.es:10261/478332026-05-22T06:33:51Z
dc.title.none.fl_str_mv Cell-autonomous role of Notch, an epidermal growth factor homologue, in sensory organ differentiation in Drosophila.
title Cell-autonomous role of Notch, an epidermal growth factor homologue, in sensory organ differentiation in Drosophila.
spellingShingle Cell-autonomous role of Notch, an epidermal growth factor homologue, in sensory organ differentiation in Drosophila.
Celis, José F. de
Drosophila
Melanogaster
Notch
Transmembrane
Cells
Growth
title_short Cell-autonomous role of Notch, an epidermal growth factor homologue, in sensory organ differentiation in Drosophila.
title_full Cell-autonomous role of Notch, an epidermal growth factor homologue, in sensory organ differentiation in Drosophila.
title_fullStr Cell-autonomous role of Notch, an epidermal growth factor homologue, in sensory organ differentiation in Drosophila.
title_full_unstemmed Cell-autonomous role of Notch, an epidermal growth factor homologue, in sensory organ differentiation in Drosophila.
title_sort Cell-autonomous role of Notch, an epidermal growth factor homologue, in sensory organ differentiation in Drosophila.
dc.creator.none.fl_str_mv Celis, José F. de
Marí-Beffa, Manuel
García-Bellido, Antonio
author Celis, José F. de
author_facet Celis, José F. de
Marí-Beffa, Manuel
García-Bellido, Antonio
author_role author
author2 Marí-Beffa, Manuel
García-Bellido, Antonio
author2_role author
author
dc.contributor.none.fl_str_mv Consejo Superior de Investigaciones Científicas [https://ror.org/02gfc7t72]
dc.subject.none.fl_str_mv Drosophila
Melanogaster
Notch
Transmembrane
Cells
Growth
topic Drosophila
Melanogaster
Notch
Transmembrane
Cells
Growth
description The gene Notch (N) codes for a transmembrane protein with an extracellular domain that has homologies to epidermal growth factors and an intracellular domain that could be involved in signal transduction. N null alleles cause the transformation of most epidermal cells into neuroblasts in central and peripheral nervous systems. Alleles of the same gene, called Abruptex (Ax), that map to the extracellular domain of N protein cause the absence of adult sensory organs. Both types of alleles show cell autonomy in mosaic analysis carried out in the last stages of the formation of adult sensory organs. The phenotypes are different: cells lacking N gene products differentiate as sensory organ mother cells early and as its neural sublineage later, whereas in the homozygous Ax condition epidermal cells do not enter the sensory organ mother cell pathway. The results indicate that N gene products act internally in the cell, probably as receptors of intercellular signals both in sensory organ mother cell singularization and in fate specification of its daughter cells. Ax mutations behave as an excess of N+ function in this signal transduction process. N proteins modified by these mutations act as constitutively activated.
publishDate 1990
dc.date.none.fl_str_mv 1990
2012
2012
dc.type.none.fl_str_mv info:eu-repo/semantics/article
http://purl.org/coar/resource_type/c_6501
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/10261/47833
url http://hdl.handle.net/10261/47833
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv http://dx.doi.org/10.1073/pnas.88.2.632
Sí
dc.rights.none.fl_str_mv info:eu-repo/semantics/embargoedAccess
eu_rights_str_mv embargoedAccess
dc.publisher.none.fl_str_mv National Academy of Sciences (U.S.)
publisher.none.fl_str_mv National Academy of Sciences (U.S.)
dc.source.none.fl_str_mv reponame:DIGITAL.CSIC. Repositorio Institucional del CSIC
instname:Consejo Superior de Investigaciones Científicas (CSIC)
instname_str Consejo Superior de Investigaciones Científicas (CSIC)
reponame_str DIGITAL.CSIC. Repositorio Institucional del CSIC
collection DIGITAL.CSIC. Repositorio Institucional del CSIC
repository.name.fl_str_mv
repository.mail.fl_str_mv
_version_ 1869414085601263616
score 15.812429

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