The Effects of Larval Crowding and Body Size on the Longevity of Adult Drosophila Melanogaster

Ecology ◽  
1958 ◽  
Vol 39 (1) ◽  
pp. 118 ◽  
Author(s):  
Richard S. Miller ◽  
J. L. Thomas
Keyword(s):  
Drosophila Melanogaster ◽  
Body Size ◽  
Larval Crowding ◽  
Adult Drosophila

Testing for Asymmetrical Gene Flow in aDrosophila melanogasterBody-Size Cline

Genetics ◽  
2003 ◽  
Vol 165 (2) ◽  
pp. 667-673 ◽  
Author(s):  
W Jason Kennington ◽  
Julia Gockel ◽  
Linda Partridge
Keyword(s):  
Drosophila Melanogaster ◽  
Gene Flow ◽  
Body Size ◽  
Genetic Parameter ◽  
Good Evidence ◽  
Microsatellite Data ◽  
Eastern Australia ◽  
The Difference ◽  
Two Populations ◽  
Private Alleles

AbstractAsymmetrical gene flow is an important, but rarely examined genetic parameter. Here, we develop a new method for detecting departures from symmetrical migration between two populations using microsatellite data that are based on the difference in the proportion of private alleles. Application of this approach to data collected from wild-caught Drosophila melanogaster along a latitudinal body-size cline in eastern Australia revealed that asymmetrical gene flow could be detected, but was uncommon, nonlocalized, and occurred in both directions. We also show that, in contrast to the findings of a previous study, there is good evidence to suggest that the cline experiences significant levels of gene flow between populations.

scholarly journals Effect of a Dipeptide-Enriched Diet in an Adult Drosophila melanogaster Laboratory Strain

2013 ◽  
Vol 77 (4) ◽  
pp. 836-838 ◽  
Author(s):  
Shigenobu SHIOTANI ◽  
Nobuya YANAI ◽  
Takanori SUZUKI ◽  
Shiho TUJIOKA ◽  
Yurie SAKANO ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Laboratory Strain ◽  
Adult Drosophila

Towards a Drosophila model of Hutchinson–Gilford progeria syndrome

2008 ◽  
Vol 36 (6) ◽  
pp. 1389-1392 ◽  
Author(s):  
Gemma S. Beard ◽  
Joanna M. Bridger ◽  
Ian R. Kill ◽  
David R.P. Tree
Keyword(s):  
Drosophila Melanogaster ◽  
Premature Aging ◽  
Lamin A ◽  
Wild Type ◽  
Drosophila Model ◽  
Numerous Cell ◽  
Cellular Abnormalities ◽  
Progeria Syndrome ◽  
Hutchinson Gilford Progeria Syndrome ◽  
Adult Drosophila

The laminopathy Hutchinson–Gilford progeria syndrome (HGPS) is caused by the mutant lamin A protein progerin and leads to premature aging of affected children. Despite numerous cell biological and biochemical insights into the basis for the cellular abnormalities seen in HGPS, the mechanism linking progerin to the organismal phenotype is not fully understood. To begin to address the mechanism behind HGPS using Drosophila melanogaster, we have ectopically expressed progerin and lamin A. We found that ectopic progerin and lamin A phenocopy several effects of laminopathies in developing and adult Drosophila, but that progerin causes a stronger phenotype than wild-type lamin A.

The Transplantation of Ovaries between Genetically Sterile and Wild Type Drosophila melanogaste

1965 ◽  
Vol 20 (4) ◽  
pp. 292-297 ◽  
Author(s):  
Robert C. King ◽  
Dietrich Bodenstein
Keyword(s):  
Drosophila Melanogaster ◽  
Body Cavity ◽  
Ovarian Tumors ◽  
Wild Type ◽  
Adult Females ◽  
Recessive Genes ◽  
Initiating Factors ◽  
Adult Drosophila ◽  
Do So ◽  
Drosophila Melanogaste

Ovarian tumors are characteristically found in adult Drosophila melanogaster females homozygous for certain recessive genes (fes, nw and fu). Ovaries genetically destined to become tumorous do so even when they are transplanted to a normal abdomen. Normal ovaries transplanted to the abdomen of females homozygous for such tumor genes do not become tumorous. Therefore there is no evidence for diffusible tumorigenic agents as initiating factors in the development of the ovarian tumors characteristic of females homozygous for fes, nw or fu. Vitellogenesis is retarded in adult females homozygous for certain recessive genes (fs 2.1, ty and ap4). Transplantation of ovaries from homozygous females to the abdominal body cavity of females carrying the + alleles of the gene in question fails to cure the implant in the case of fs 2.1 and ty. Ovaries of ap4/ap4 genotype produce abundant yolk when implanted into wild type abdomens. Thus it is the abdominal environment of ap4 which is at fault, rather than a malfunctioning of the ovary.

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