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Genetic and molecular analysis of repression in the P–M system of hybrid dysgenesis in Drosophila melanogaster

Published online by Cambridge University Press:  14 April 2009

Ellen M. Heath  and
Michael J. Simmons
Ellen M. Heath
Affiliation:
Department of Genetics and Cell Biology, University of Minnesota, St Paul, Minnesota 55108–1095, U.S.A.
Michael J. Simmons*
Affiliation:
Department of Genetics and Cell Biology, University of Minnesota, St Paul, Minnesota 55108–1095, U.S.A.
*
* Corresponding author.
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Twelve inbred lines derived from an M′ strain of Drosophila melanogaster were used to study the repression of P-element-mediated hybrid dysgenesis. Initial assessments indicated that the lines differed in the ability to repress gonadal dysgenesis, and that this ability was highly correlated with the ability to repress snw hypermutability. Later assessments indicated that most of the lines with low or intermediate repression potential evolved to a state of higher repression potential; however, Southern analyses failed to reveal significant changes in the array of genomic P elements that could account for this evolution. In addition, none of the lines possessed the incomplete P element known as KP, which has been proposed to explain repression in some D. melanogaster strains. One of the lines maintained intermediate repression potential throughout the period of study (52 generations), indicating that the intermediate condition was not intrinsically unstable. Genetic analyses demonstrated that in some of the lines, repression potential was influenced by factors that were inherited maternally through at least two generations; however, these factors were not as influential as those in a classic P cytotype strain. Additional tests with a dysgenesis-inducing X chromosome called T-5 indicated that repression itself was mediated by a combination of maternal effects and paternally inherited factors that were expressed after fertilization. These tests also suggested that in some circumstances, the P transposase, or its message, might be transmitted through the maternal cytoplasm.

Information

Type
Research Article
Information
Genetics Research , Volume 57 , Issue 3 , June 1991 , pp. 213 - 226
Copyright
Copyright © Cambridge University Press 1991

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