%0 Journal Article
%9 ACL : Articles dans des revues avec comité de lecture répertoriées par l'AERES
%A De Meeûs, Thierry
%T Revisiting F-IS, F-ST, Wahlund effects, and Null alleles
%D 2018
%L fdi:010073032
%G ENG
%J Journal of Heredity
%@ 0022-1503
%K differentiation ; F-statistics ; genetic identities ; inbreeding
%M ISI:000432311600010
%N 4
%P 446-456
%R 10.1093/jhered/esx106
%U https://www.documentation.ird.fr/hor/fdi:010073032
%> https://www.documentation.ird.fr/intranet/publi/2018/06/010073032.pdf
%V 109
%W Horizon (IRD)
%X Null alleles and Wahlund effects are well known causes of heterozygote deficits in empirical population genetics studies as compared to Hardy-Weinberg genotypic expectations. Some authors have theoretically studied the relationship of Wright's F-IS computed from subsamples displaying a Wahlund effect and F-ST before the Wahlund effect, as can occasionally be obtained from populations of long-lived organisms. In the 2 subsample case, a positive relationship between these 2 parameters across loci would represent a signature of Wahlund effects. Nevertheless, for most organisms, getting 2 independent subsamples of the same cohort and population, one with a Wahlund effect and the other without, is almost never achieved and most of the time, empirical population geneticists only collect a single sample, with or without a Wahlund effect, or with or without null alleles. Another issue is that null allele increase F-IS and F-ST altogether and thus may also create such correlation. In this article, I show that, for organisms collected in a single sample, which corresponds to the most common situation, Wahlund effects and null alleles affect the values of both F-Is and F-ST though in the opposite direction. I also show that Wahlund effect produces no or weak positive correlation between the 2 F-statisties, while null alleles generate a strong positive correlation between them. Variation of these F-statistics is small and even minimized for F-ST under Wahlund effects as compared to null alleles. I finally propose a determination key to interpret data with heterozygote deficits.
%$ 020