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Friday, June 23rd, 2017
Table of Contents

1 Introduction
5 PMID
 [F] Diseases Research  / PubMed Research Articles  /
Sex and genetic background influence Superoxide dismutase (cSOD) related phenotypic variation in Drosophila melanogaster.

PubMed

 

Resource

G3 (Bethesda, Md.) 2017 Jun 18; ()

Authors

Lessel CE1; Parkes TL2; Dickinson J3; Merritt TJS4;

Author Information
  • 1Laurentian University.
  • 2Nipissing University.
  • 3Laurentian University.
  • 4Laurentian University; tmerritt@laurentian.ca.

Abstract

Mutations often have drastically different effects in different genetic backgrounds; understanding a gene's biological function then requires an understanding of its interaction with genetic diversity. The antioxidant enzyme cytosolic superoxide dismutase, cSOD, catalyzes the dismutation of the superoxide radical, a molecule that can induce oxidative stress if its concentration exceeds cellular control. Accordingly, Drosophila melanogaster lacking functional cSOD exhibit a suite of phenotypes including decreased longevity, hypersensitivity to oxidative stress, impaired locomotion, and reduced NADP(H) enzyme activity in males. To date, cSOD-null phenotypes have primarily been characterized using males carrying one allele, cSod(n108)red, in a single genetic background. We used analysis of variance, and the effect size partial eta squared, to partition the amount of variation attributable to cSOD activity, sex, and genetic background across a series of life history, locomotor, and biochemical phenotypes associated with the cSOD-null condition. Overall, the results demonstrate that the cSOD-null syndrome is largely consistent across sex and genetic background, but also significantly influenced by both. The sex-specific effects are particularly striking and our results support the idea that phenotypes cannot be considered fully defined if they are examined in limited genetic contexts.

Copyright © 2017 Author et al.

PMID

28624774

Others

Publication Type: Journal Article


This article is licensed under the the National Library of Medicine License. It uses material from the PubMed National Library of Medicine Data.


Last Modified:   2016-03-27


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