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Studies on the sterility induced by the male recombination factor 31.1 MRF in Drosophila melanogaster

Published online by Cambridge University Press:  14 April 2009

George Yannopoulos
George Yannopoulos
Affiliation:
Department of Genetics, University of Patras, Greece
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The sterility which is associated with male recombination induced by 31.1 MRF was studied genetically and cytologically. In all crosses it was found that female sterility mainly involves failure of the heterozygous females to lay eggs because their ovaries are atrophic. Under the optical microscope, the atrophic ovaries were seen to contain only germaria in their ovarioles. It was also found that in some cases 31.1 MRF affects only one of the two ovaries of the same female. This observation suggests that defective development of atrophic ovaries is not due to influences from the rest of the body but should be attributed to the inability of the germ cells to differentiate. Moreover, various stocks as well as homologous chromosomes were found to react differently to 31.1 MRF with respect to female sterility. In their effect on male sterility it was observed that some strains behave as neutral and others as reactive when mated with 31.1/Cy L4 males.

Type
Research Article
Information
Genetics Research , Volume 32 , Issue 3 , November 1978 , pp. 239 - 247
Copyright
Copyright © Cambridge University Press 1978

References

REFERENCES

Brink, B. A. (1973). Paramutation. Annual Review of Genetics 7, 129–152.CrossRefGoogle ScholarPubMed
Kidwell, M. G. & Kidwell, J. F. (1975). Cytoplasmic–chromosome interactions in Drosophila melanogasier. Nature 253, 755–756.CrossRefGoogle Scholar
King, R. C. (1970). Ovarian Development in Drosophila melanogaster. New York: Academic Press.Google Scholar
Lindsley, D. L. & Grell, E. H. (1968). Genetic variation of Drosophila melanogaster. Carnegie Institute of Washington publication, p. 627.Google Scholar
McClintock, B. (1965). The control of gene action in maize. Brookhaven Symposia in Biology 18, 162–184.Google Scholar
Picard, G. (1976). Non-Mendelian female sterility in Drosophila melanogaster: hereditary transmission of I factor. Genetics 83, 107–123.CrossRefGoogle ScholarPubMed
Sved, J. A. (1976). Hybrid dysgenesis in Drosophila melanogaster: a possible explanation in terms of spatial organization of chromosomes. Australian Journal of Biological Science 29, 375–386.CrossRefGoogle ScholarPubMed
Woodruff, R. C. & Thompson, J. N. Jr (1977). An analysis of spontaneous recombination in Drosophila melanogaster males. Isolation and characterization of male recombination lines. Heredity 38 (3), 291–307.CrossRefGoogle Scholar
Yannopoulos, G. (1978 a). Studies on male recombination in a Southern Greek Drosophila melanogaster population, (c) Chromosomal abnormalities at male meiosis. (d) Cytoplasmic factor responsible for the reciprocal cross effect. Genetical Research 31, 187–196.CrossRefGoogle Scholar
Yannopoulos, G. (1978 b). Progressive resistance against the male recombination factor 31.1 MRF acquired by Drosophila melanogaster. Experientia 34, 8, 1000–1002.CrossRefGoogle ScholarPubMed
Yannopoulos, G. & Pelecanos, M. (1977). Studies on male recombination in a Southern Greek Drosophila melanogaster population, (a) Effect of temperature. (b) Suppression of male recombination in reciprocal crosses. Genetical Research 29, 231–238.CrossRefGoogle Scholar