Establishment of ventral cell fates in the Drosophila embryonic ectoderm requires DER, the EGF receptor homolog.
Open accessAbstract
The embryonic ectoderm in Drosophila displays a highly organized arrangement of specific structures along the dorsal-ventral axis. To establish this characteristic design, cells must receive instructive cues regarding their position. We present evidence that during stages 8-9 of embryonic development, the Drosophila EGF receptor homolog (DER) is essential for determining the identity of cells within the ventral ectoderm. In the absence of DER activity at this phase, alterations in cell fate are observed: Ventral cells acquire more dorsal fates, as visualized by the expression profile of specific markers. The ventralizing effect of DER appears to function later than that of the dorsalizing dpp pathway, and the spatial overlap between them is minimal. A model for the determination of cell fates along the dorsal-ventral axis involving the two pathways is presented. Some aspects of the mutant ectodermal and CNS phenotypes of the DER locus (faint little ball, flb) resemble the phenotype of mutations from the spitz group. Synergistic interactions between flb and spitz or Star mutations suggest that these genes participate in a common signaling pathway.
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Research works printed but not linked: 3
- Ashbumer, M. 1989. Drosophila: A laboratory manual. Cold Spring Harbor Laboratory Press, Cold Spring Harbor, New York.
- Campos-Ortega, J.A. and V. Hartenstein. 1985. The embryonic development of Drosophila melanogaster. Springer-Verlag, Berlin/Heidelberg, Germany.
- Wieschaus, E. and C. Nfisslein-Volhard. 1986. Looking at em- bryos. In Drosophila, a practical approach (ed. D.B. Roberts), pp. 199-227, IRL press, Oxford, England.
Cited by
Sorted by citations
Schweitzer, R., Shaharabany, M., Seger, R., & Shilo, B. Z. (1995) · Genes & Development · doi:10.1101/gad.9.12.1518 · Cited by 317 · see citing works
Self-citationWeiss, J. B., Von Ohlen, T., Mellerick, D. M., Dressler, G., Doe, C. Q., & Scott, M. P. (1998) · Genes & Development · doi:10.1101/gad.12.22.3591 · Cited by 250 · see citing works
“Signaling via the EGF receptor is required to establish ventral and/or intermediate column fates in the neuroectoderm (Rutledge et al. 1992; Raz and Shilo 1993; Schweitzer et al. 1995).”
BackgroundIsshiki, T., Takeichi, M., & Nose, A. (1997) · Development · doi:10.1242/dev.124.16.3099 · Cited by 148 · see citing works
msh may play a conserved role in dorsoventral patterning of the neuroectoderm and mesoderm
D'Alessio, M., & Frasch, M. (1996) · Mechanisms of Development · doi:10.1016/s0925-4773(96)00583-7 · Cited by 126 · see citing works
- Authors
- Raz, E., & Shilo, B. Z.
- Affiliations
- Weizmann Institute of Science (IL)
- ORCID
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1993-10
- Volume
- 7
- Issue
- 10
- Pages
- 1937-1948
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2102722477
- Cited by
- 113
- References
- 0
- Citations by year
- 2023: 3 · 2021: 1 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 2 · 2013: 1 · 2012: 1
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- Minerva Foundation
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurobiology and Insect Physiology Research
- Keywords
- cell fate determination, dorsal-ventral axis, ventralization, Dpp signaling, embryonic development
- MeSH terms
- Animals, Cell Communication, Drosophila, Ectoderm, Models, Biological, Morphogenesis, Protein Kinases, Time Factors, Genes, Insect, Genes, Reporter, Receptors, Invertebrate Peptide, Drosophila Proteins, ErbB Receptors
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