University of Illinois Urbana-Champaign

Somatic Effects of P Element Activity in Drosophila melanogaster: Pupal Lethality

Engels, William R.; Benz, Wendy K.; Preston, Christine R.; Graham, Patricia L.; Phillis, Randall W.; Robertson, Hugh M.

Content Files
Robertson_Genetics_1987.pdf

Permalink

https://hdl.handle.net/2142/217

Description

Title
Somatic Effects of P Element Activity in Drosophila melanogaster: Pupal Lethality
Author(s)
  • Engels, William R.
  • Benz, Wendy K.
  • Preston, Christine R.
  • Graham, Patricia L.
  • Phillis, Randall W.
  • Robertson, Hugh M.
Issue Date
1987-12
Keyword(s)
  • Drosophila melanogaster
  • Genetics
Date of Ingest
2007-02-13T20:09:44Z
Abstract
Nonautonomous P elements normally excise and transpose only when a source of transposase is supplied, and only in the germline. The germline specificity depends on one of the introns of the transposase gene which is not spliced in somatic cells. To study the effects of somatic P activity, a modified P element (A2-3) lacking this intron was used as a source of transposase. Nonautonomous P elements from a strain called Birmingham, when mobilized in somatic cells by A2-3, were found to cause lethality, although neither component was lethal by itself. The three major Birmingham chromosomes acted approximately independently in producing the lethal effect. This lethality showed a strong dependence on temperature. Although temperature sensitivity was limited to larval stages, the actual deaths occurred at the pupal stage. Survivors, which could be recovered by decreasing the temperature or by reducing the proportion of the Birmingham genome present, often showed multiple developmental anomalies and reduced longevity reminiscent of the effects of cell death from radiation damage. Although the genetic damage occurred in dividing imaginal disc cells, the phenotypic manifestations-death and abnormalities-are not observed until later. The survivors also showed gonadal dysgenic (GD) sterility, a well-known characteristic of P-M hybrid dysgenesis. To explain these findings, we suggest that pupal lethality and GD sterility are both caused by massive chromosome breakage in larval cells, resulting from excision and transposition of genomic P elements acting as substrate for the transposase.
Publisher
Genetics Society of America
Type of Resource
text
Genre of Resource
Article
Language
en
Permalink
http://hdl.handle.net/2142/217
Copyright and License Information
Copyright owned by Genetics Society of America

Owning Collections

Illinois Research and Scholarship (Open Collection) PRIMARY
This is the default collection for all research and scholarship developed by faculty, staff, or students at the University of Illinois at Urbana-Champaign