Ras1-Mediated Modulation of Drosophila Homeotic Function in Cell and Segment Identity
Abstract
Mutations of the Drosophila homeotic proboscipedia gene (pb; the Hox-A2/B2 homologue) provoke dose-sensitive defects. These were used to search for dose-sensitive dominant modifiers of pb function. Two identified interacting genes were the proto-oncogene Ras1 and its functional antagonist Gap1, prominent intermediaries in known signal transduction pathways. Ras1+ is a positive modifier of pb activity both in normal and ectopic cell contexts, while the Ras1-antagonist Gap1 has an opposite effect. A general role for Ras1 in homeotic function is likely, since Ras1+ activity also modulates functions of the homeotic loci Sex combs reduced and Ultrabithorax. Our data suggest that the modulation occurs by a mechanism independent of transcriptional control of the homeotic loci themselves, or of the Ras1/Gap1 genes. Taken together our data support a role for Ras1-mediated cell signaling in the homeotic control of segmental differentiation.
Additional Information
© 1997 by the Genetics Society of America. Manuscript received June 17, 1996; Accepted for publication March 12, 1997. We thank K. MATTHEWS, S. ECK, D. SNEDEGAR, T. and T. KAUFMAN of the Indiana University Drosophila Stock Center for providing the stocks, including the autosomal Deficiency Kits, that permitted this study. We also thank G. RUBIN, E. HAFEN, R. ROGGE, U. BANERJEE, J. SCHNORR, C. BERG, N. PERRIMON and J. KENNISON for providing stocks; D. BROWER and J. LOPEZ for antisera; and J. BISHOP and U. GAUL for probes used for in situ hybridizations. The critical reading of the manuscript by our colleagues STEPHANE NOSELLI, BRUNO GLISE, ALAIN VINCENT and JULIAN SMITH was greatly appreciated. M.B., C.B. and L.S. were supported by graduate fellowships from the Ministere de l'Enseignement Superieur et de la Recherche (MESR); M.B. and L.S. also benefited from graduate training fellowships from the Association pour la Recherche contre le Cancer (ARC). This work was made possible by ongoing institutional funding from the Centre National de la Recherche Scientifique (CNRS), and grants from the Association pour la Recherche Contre le Cancer and the MESR.Attached Files
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Additional details
- PMCID
- PMC1208002
- Eprint ID
- 108341
- Resolver ID
- CaltechAUTHORS:20210308-104755322
- Ministere de l'Enseignement Superieur et de la Recherche
- Association pour la Recherche contre le Cancer
- Centre National de la Recherche Scientifique (CNRS)
- Created
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2021-03-08Created from EPrint's datestamp field
- Updated
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2021-03-10Created from EPrint's last_modified field