Hostname: page-component-586b7cd67f-t8hqh Total loading time: 0 Render date: 2024-11-26T22:21:39.521Z Has data issue: false hasContentIssue false
  • English
  • Français

The molecular basis of instability of the singedvery weak mutation in Drosophila melanogaster

Published online by Cambridge University Press:  14 April 2009

C. A. Ortori ,
D. Chambers  and
J. F. Y. Brookfield
C. A. Ortori
Affiliation:
Department of Genetics, University of Nottingham, Queens Medical Centre, Nottingham NG7 2UH, UK
D. Chambers
Affiliation:
Department of Genetics, University of Nottingham, Queens Medical Centre, Nottingham NG7 2UH, UK
J. F. Y. Brookfield*
Affiliation:
Department of Genetics, University of Nottingham, Queens Medical Centre, Nottingham NG7 2UH, UK
*
† Corresponding author.
Rights & Permissions [Opens in a new window]

Summary

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

The singedvery weak mutation was created by the sequential addition of two P transposable elements to the singed gene. The mutation can be somatically unstable through the action of a dominant maternal effect mutation on the second chromosome. It is also unstable in the germ line in these conditions. Sequencing of the region of the P insertions in the mutation reveals that the two inserted elements have single internal deletions, and the larger of the two is a copy of the KP element. The mutation will generate, at high frequencies, strongly singed and pseudo-wild type products by reversions occurred in the germline. These are the result of the precise excision of the smaller and the larger elements respectively. By PCR amplification of dissected thoraces we show that the somatic instability of the mutation, from a weak to a strong singed phenotype, is also caused by the excision of the smaller of the two elements.

Type
Research Article
Information
Genetics Research , Volume 63 , Issue 1 , February 1994 , pp. 19 - 26
Copyright
Copyright © Cambridge University Press 1994

References

Black, D. M., Jackson, M. S., Kidwell, M. G. & Dover, G. A. (1987). KP-elements repress P-induced dysgenesis in Drosophila melanogaster. EMBO Journal 6, 4125–4135.CrossRefGoogle ScholarPubMed
Boussey, I. A., Healy, M. J., Oakeshott, J. G. & Kidwell, M. G. (1988). Molecular analysis of the P-M gonadal dysgenesis cline in Eastern Australian Drosophila melanogaster. Genetics 119, 889–902.CrossRefGoogle Scholar
Brookfield, J. F. Y. (1991). Models of repression of transposition in P-M hybrid dysgenesis by P cytotype and by zygotically encoded repressor proteins. Genetics 128, 471–486.CrossRefGoogle Scholar
Brookfield, J. F. Y. & Lewis, A. P. (1989). Somatic reversion of P transposable element insertion mutations at the singed locus of Drosophila melanogaster requiring specific P insertions and a trans-acting factor. Genetical Research 54, 101–112.CrossRefGoogle Scholar
Brookfield, J. F. Y. & Mitchell, S. F. (1985). P-M hybrid dysgenesis using geographically separate P strains of Drosophila melanogaster. Heredity 55, 163–165.CrossRefGoogle Scholar
Engels, W. R. (1989). P elements in Drosophila melanogaster. In Mobile DNA (ed. Berg, D. E. and Howe, M. M.), pp. 437–484. Washington D.C.: American Society for Microbiology.Google Scholar
Engels, W. R., Johnson-Schlitz, D. M., Eggleston, W. B. & Sved, J. (1990). High-frequency P element loss in Drosophila is homolog dependent. Cell 62, 515–525.CrossRefGoogle ScholarPubMed
Gloor, G. B., Nassif, N. A., Johnson-Schlitz, D. M., Preston, C. R. & Engels, W. R. (1991). Targeted gene replacement in Drosophila via P-element-induced gap repair. Science 253, 1110–1117.CrossRefGoogle ScholarPubMed
Heath, E. M. & Simmons, M.J. (1991). Genetic and molecular analysis of repression in the P-M system of hybrid dysgenesis in Drosophila melanogaster. Genetical Research 57, 213–226.CrossRefGoogle Scholar
Higuet, D., Anxolabéhère, D. & Nouaud, D. (1992). A particular P-element insertion is correlated to the P-induced hybrid dysgenesis repression in Drosophila melanogaster. Genetical Research 60, 15–24.CrossRefGoogle Scholar
Jackson, M. S., Black, D. M. & Dover, G. A. (1988). Amplification of P elements associated with the repression of hybrid dysgenesis in Drosophila melanogaster. Genetics 120, 1003–1013.CrossRefGoogle ScholarPubMed
Jowett, T. (1986). Preparation of nucleic acids. In Drosophila: a practical approach (ed. Roberts, D. B.), pp. 275–286. Oxford: IRL Press.Google Scholar
Kitamura, T., Kobayashi, S. & Okada, M. (1993). Developmentally-regulated splicing of the third intron of the P element in somatic tissues of Drosophila embryos. Development, Growth and Differentiation 35, 67–73.CrossRefGoogle Scholar
Kobayashi, S., Kitamura, T., Sasaki, H. & Okada, M. (1993). Two types of pole cells are present in the Drosophila embryo, one with and one without splicing activity for the third P element intron. Development 117, 885–893.CrossRefGoogle ScholarPubMed
Lewis, A. P. (1987). Ph.D. thesis, University of Leicester.Google Scholar
Misra, S. & Rio, D. C. (1990). Cytotype control of Drosophila P element transposition: the 66 kD protein is a repressor of transposase activity. Cell 62, 269–284.CrossRefGoogle ScholarPubMed
Monastiroti, M., Hatzopoulos, P., Stamatis, N., Yanno-poulos, G. & Louis, C. (1988). Cohabitation of KP and full-length P elements in the genome of MR strains inducing P-M-like hybrid dysgenesis in Drosophila melanogaster. Molecular and General Genetics 215, 94–99.CrossRefGoogle Scholar
Nitasaka, E., Mukai, T. & Yamazaki, T. (1987). Repressor of P elements in Drosophila melanogaster: cytotype determination by a defective P element with only open reading frames 0 through 2. Proceedings of the National Academy of Science U.S.A. 84, 7605–7608.CrossRefGoogle Scholar
O'Hare, K. & Rubin, G. M. (1983). Structures of P transposable elements and their sites of insertion and excision in the Drosophila melanogaster genome. Cell 34, 25–35.CrossRefGoogle ScholarPubMed
O'Hare, K., Driver, A., McGrath, S. & Johnson-Schlitz, D. M. (1992). Distribution and structure of cloned P elements from the Drosophila melanogaster P strain Π2. Genetical Research 60, 33–41.CrossRefGoogle Scholar
Paterson, J. & O'Hare, K. (1991). Structure and transcription of the singed locus of Drosophila melanogaster. Genetics 129, 1073–1084.CrossRefGoogle ScholarPubMed
Raymond, J. D., Ojala, T. A., White, J. & Simmons, M. J. (1991). Inheritance of P-element regulation in Drosophila melanogaster. Genetical Research 57, 227–234.CrossRefGoogle ScholarPubMed
Rio, D. C. (1990). Molecular mechanisms regulating Drosophila P element transposition. Annual Review of Genetics 24, 543–578.CrossRefGoogle ScholarPubMed
Roiha, H., Rubin, G. M. & O'Hare, K. (1987). P-element insertions and rearrangements at the singed locus of Drosophila melanogaster. Genetics 119, 75–83.CrossRefGoogle Scholar
Ronsseray, S., Lehmann, M. & Anxolabéhère, D. (1991). The maternally inherited regulation of P elements in Drosophila melanogaster can be elicited by two P copies at cytological site 1A on the X chromosome. Genetics 129, 501–512.CrossRefGoogle ScholarPubMed
Sambrook, J., Fritsch, E. F. & Maniatis, T. (1989). Molecular cloning: a laboratory manual. Cold Spring Harbor Press. Cold Spring Harbor, New York.Google Scholar
Simmons, M. J. & Buchholz, L. M. (1985). Transposase titration in Drosophila melanogaster: a model of cytotype in the P-M system of hybrid dysgenesis. Proceedings of the National Academy of Sciences USA 82, 8119–8123.CrossRefGoogle Scholar
Simmons, M. J., Raymond, J. D., Boedigheimer, M. J. & Zunt, J. R. (1987). The influence of nonautonomous P elements on hybrid dysgenesis in Drosophila melanogaster. Genetics 117, 671–685.CrossRefGoogle ScholarPubMed
Simmons, M. J., Raymond, J. D., Rasmusson, K. E., Miller, L. M., McLarnon, C. F. & Zunt, J. R. (1990). Repression of P element-mediated hybrid dysgenesis in Drosophila melanogaster. Genetics 124, 663–676.CrossRefGoogle ScholarPubMed
Winship, P. R. (1989). An improved method for directly sequencing PCR-amplified material using DMSO. Nucleic Acids Research 17, 1266.CrossRefGoogle Scholar