Epistasis as a Source of Increased Additive Genetic Variance at Population Bottlenecks

Evolution ◽  
1996 ◽  
Vol 50 (3) ◽  
pp. 1042 ◽  
Author(s):  
James M. Cheverud ◽  
Eric J. Routman
Genetics ◽  
1999 ◽  
Vol 152 (1) ◽  
pp. 345-353 ◽  
Author(s):  
Michael C Whitlock ◽  
Kevin Fowler

Abstract We performed a large-scale experiment on the effects of inbreeding and population bottlenecks on the additive genetic and environmental variance for morphological traits in Drosophila melanogaster. Fifty-two inbred lines were created from the progeny of single pairs, and 90 parent-offspring families on average were measured in each of these lines for six wing size and shape traits, as well as 1945 families from the outbred population from which the lines were derived. The amount of additive genetic variance has been observed to increase after such population bottlenecks in other studies; in contrast here the mean change in additive genetic variance was in very good agreement with classical additive theory, decreasing proportionally to the inbreeding coefficient of the lines. The residual, probably environmental, variance increased on average after inbreeding. Both components of variance were highly variable among inbred lines, with increases and decreases recorded for both. The variance among lines in the residual variance provides some evidence for a genetic basis of developmental stability. Changes in the phenotypic variance of these traits are largely due to changes in the genetic variance.


Genetics ◽  
2008 ◽  
Vol 179 (4) ◽  
pp. 2135-2146 ◽  
Author(s):  
Belinda van Heerwaarden ◽  
Yvonne Willi ◽  
Torsten N. Kristensen ◽  
Ary A. Hoffmann

Genetics ◽  
1974 ◽  
Vol 76 (3) ◽  
pp. 537-549
Author(s):  
Gunther Schlager

ABSTRACT Response to two-way selection for systolic blood pressure was immediate and continuous for about eight generations. In the twelfth generation, the High males differed from the Low males by 38 mmHG; the females differed by 39 mmHg. There was little overlap between the two lines and they were statistically significant from each other and from the Random control line. There appeared to be no more additive genetic variance in the eleventh and twelfth generations. Causes for the cessation of response are explored. This is probably due to a combination of natural selection acting to reduce litter sizes in the Low line, a higher incidence of sudden deaths in the High line, and loss of favorable alleles as both selection lines went through a population bottleneck in the ninth generation.—In the eleventh generation, the selected lines were used to produce F1, F2, and backcross generations. A genetic analysis yielded significant additive and dominance components in the inheritance of systolic blood pressure.


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