scholarly journals Selection on heritable heterozygosity but no response to selection. Why?

2015 ◽  
Author(s):  
Tim Coulson ◽  
Sonya Clegg
Keyword(s):  
Allele Frequencies ◽  
Heterozygote Advantage ◽  
Response To Selection ◽  
Quantitative Genetic ◽  
In The Wild

The realisation that heterozygosity can be heritable has recently generated some elegant research. However, none of this work has discussed the fact that when heterozygote advantage occurs, heterozygosity can be heritable, yet allele frequencies remain at equilibrium and do not evolve with time. From a quantitative genetic perspective this means the character is heritable, is under selection, yet no response to selection is observed. We explain why this is the case, and discuss potential implications for the study of evolution in the wild.

scholarly journals Evolution of quantitative traits in the wild: mind the ecology

2010 ◽  
Vol 365 (1552) ◽  
pp. 2431-2438 ◽  
Author(s):  
Josephine M. Pemberton
Keyword(s):  
Quantitative Genetics ◽  
Quantitative Traits ◽  
Natural Populations ◽  
Response To Selection ◽  
Genetic Response ◽  
Quantitative Genetic ◽  
Animal Populations ◽  
In The Wild ◽  
Gradient Variation

Recent advances in the quantitative genetics of traits in wild animal populations have created new interest in whether natural selection, and genetic response to it, can be detected within long-term ecological studies. However, such studies have re-emphasized the fact that ecological heterogeneity can confound our ability to infer selection on genetic variation and detect a population's response to selection by conventional quantitative genetics approaches. Here, I highlight three manifestations of this issue: counter gradient variation, environmentally induced covariance between traits and the correlated effects of a fluctuating environment. These effects are symptomatic of the oversimplifications and strong assumptions of the breeder's equation when it is applied to natural populations. In addition, methods to assay genetic change in quantitative traits have overestimated the precision with which change can be measured. In the future, a more conservative approach to inferring quantitative genetic response to selection, or genomic approaches allowing the estimation of selection intensity and responses to selection at known quantitative trait loci, will provide a more precise view of evolution in ecological time.

scholarly journals Estimation of Cry3Bb1 resistance allele frequency in field populations of western corn rootworm using a genetic marker

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Alan Willse ◽  
Lex Flagel ◽  
Graham Head
Keyword(s):  
Allele Frequency ◽  
Western Corn Rootworm ◽  
Allele Frequencies ◽  
Chromosome 8 ◽  
Corn Belt ◽  
Corn Rootworm ◽  
Resistance Allele ◽  
Response To Selection ◽  
The Us ◽  
Causal Allele

Abstract Following the discovery of western corn rootworm (WCR; Diabrotica virgifera virgifera) populations resistant to the Bacillus thuringiensis (Bt) protein Cry3Bb1, resistance was genetically mapped to a single locus on WCR chromosome 8 and linked SNP markers were shown to correlate with the frequency of resistance among field-collected populations from the US Corn Belt. The purpose of this paper is to further investigate the relationship between one of these resistance-linked markers and the causal resistance locus. Using data from laboratory bioassays and field experiments, we show that one allele of the resistance-linked marker increased in frequency in response to selection, but was not perfectly linked to the causal resistance allele. By coupling the response to selection data with a genetic model of the linkage between the marker and the causal allele, we developed a model that allowed marker allele frequencies to be mapped to causal allele frequencies. We then used this model to estimate the resistance allele frequency distribution in the US Corn Belt based on collections from 40 populations. These estimates suggest that chromosome 8 Cry3Bb1 resistance allele frequency was generally low (<10%) for 65% of the landscape, though an estimated 13% of landscape has relatively high (>25%) resistance allele frequency.

scholarly journals ADAPTATION AT SPECIFIC LOCI. IV. DIFFERENTIAL MATING SUCCESS AMONG GLYCOLYTIC ALLOZYME GENOTYPES OF COLIAS BUTTERFLIES

Genetics ◽  
1985 ◽  
Vol 109 (1) ◽  
pp. 157-175
Author(s):  
Ward B Watt ◽  
Patrick A Carter ◽  
Sally M Blower
Keyword(s):  
Mating Success ◽  
Initial Study ◽  
Heterozygote Advantage ◽  
Male Mating ◽  
Genotype Distribution ◽  
Male Mating Success ◽  
Evolutionary Forces ◽  
Fitness Index ◽  
In The Wild ◽  
Specific Variation

ABSTRACT Male mating success as a function of genotype is an important fitness component. It can be studied in wild populations, in species for which a given group of progeny has exactly one father, by determining genotypes of wild-caught mothers and of sufficient numbers of their progeny. Here, we study male mating success as a function of allozyme genotype at two glycolytic loci in Colias butterflies, in which sperm precedence is complete, so that the most recent male to mate fathers all of a female's subsequent progeny.—For the phosphoglucose isomerase, PGI, polymorphism, we predict mating advantage and disadvantage of male genotypes based on evaluation of their biochemical functional differences in the context of thermal-physiological-ecological constraints on the insects' flight activity. As predicted, we find major, significant advantage in mating success for kinetically favored genotypes, compared to the genotype distribution of males active with the sampled females in the wild. These effects are repeatable among samples and on different semispecies' genetic backgrounds.—Initial study of the phosphoglucomutase, PGM, polymorphism in the same samples reveals heterozygote advantage in male-mating success, compared to males active with the females sampled. This contrasts with a lack of correspondence between PGI and PGM genotypes in other fitness index or component differences.—Epistatic interactions in mating success between the two loci are absent.—There is no evidence for segregation distortion associated with the alleles of either primary locus studied, nor is there significant assortative mating.—These results extend our understanding of the specific variation studied and suggest that even loci closely related in function may have distinctive experience of evolutionary forces. Implications of the specificity of the effects seen are briefly discussed.

scholarly journals Phenotypic plasticity of labile traits in the wild

2013 ◽  
Vol 59 (4) ◽  
pp. 485-505 ◽  
Author(s):  
Jon E. Brommer
Keyword(s):  
Life History ◽  
Phenotypic Plasticity ◽  
Statistical Approach ◽  
Scale Up ◽  
Population Level ◽  
Wild Populations ◽  
Quantitative Genetic ◽  
In The Wild ◽  
The Individual ◽  
Quantitative Genetic Parameters

Abstract Individual-based studies allow quantification of phenotypic plasticity in behavioural, life-history and other labile traits. The study of phenotypic plasticity in the wild can shed new light on the ultimate objectives (1) whether plasticity itself can evolve or is constrained by its genetic architecture, and (2) whether plasticity is associated to other traits, including fitness (selection). I describe the main statistical approach for how repeated records of individuals and a description of the environment (E) allow quantification of variation in plasticity across individuals (IxE) and genotypes (GxE) in wild populations. Based on a literature review of life-history and behavioural studies on plasticity in the wild, I discuss the present state of the two objectives listed above. Few studies have quantified GxE of labile traits in wild populations, and it is likely that power to detect statistically significant GxE is lacking. Apart from the issue of whether it is heritable, plasticity tends to correlate with average trait expression (not fully supported by the few genetic estimates available) and may thus be evolutionary constrained in this way. Individual-specific estimates of plasticity tend to be related to other traits of the individual (including fitness), but these analyses may be anti-conservative because they predominantly concern stats-on-stats. Despite the increased interest in plasticity in wild populations, the putative lack of power to detect GxE in such populations hinders achieving general insights. I discuss possible steps to invigorate the field by moving away from simply testing for presence of GxE to analyses that ‘scale up’ to population level processes and by the development of new behavioural theory to identify quantitative genetic parameters which can be estimated.

scholarly journals Inheritance of Scottish-type resistance to warfarin in the Norway rat

1976 ◽  
Vol 28 (3) ◽  
pp. 231-239 ◽  
Author(s):  
J. H. Greaves ◽  
P. B. Ayres
Keyword(s):  
Resistance Gene ◽  
Rattus Norvegicus ◽  
Major Gene ◽  
Inheritance Of Resistance ◽  
Response To Selection ◽  
Norway Rat ◽  
Group I ◽  
Wild Rat ◽  
In The Wild ◽  
Warfarin Resistance

SUMMARYThe inheritance of resistance to the rodenticide, warfarin, in the Norway rat, Rattus norvegicus, derived from a wild rat population in Scotland was studied in the backcross, intercross and testcross. The resistance was found to be due to a major gene with about the same map position in Linkage Group I as the warfarin-resistance gene, Rw2, which occurs in the wild rat population in Wales. In heterozygotes, the Scottish resistance gene, unlike the Welsh gene, is incompletely penetrant in expression, though the penetrance was found to increase markedly in response to selection. Differences between the Scottish and Welsh types of resistance suggest that the two resistance genes are allelic.

scholarly journals Heritability, selection, and the response to selection in the presence of phenotypic measurement error: effects, cures, and the role of repeated measurements

2018 ◽  
Author(s):  
Erica Ponzi ◽  
Lukas F. Keller ◽  
Timothée Bonnet ◽  
Stefanie Muff
Keyword(s):  
Measurement Error ◽  
Repeated Measurements ◽  
Phenotypic Traits ◽  
Response To Selection ◽  
Transient Effects ◽  
Genetic Analyses ◽  
Selection Gradients ◽  
Quantitative Genetic ◽  
Selection Processes ◽  
Unbiased Estimates

Quantitative genetic analyses require extensive measurements of phenotypic traits, a task that is often not trivial, especially in wild populations. On top of instrumental measurement error, some traits may undergo transient (i.e. non-persistent) fluctuations that are biologically irrelevant for selection processes. These two sources of variability, which we denote here as measurement error in a broad sense, are possible causes for bias in the estimation of quantitative genetic parameters. We illustrate how in a continuous trait transient effects with a classical measurement error structure may bias estimates of heritability, selection gradients, and the predicted response to selection. We propose strategies to obtain unbiased estimates with the help of repeated measurements taken at an appropriate temporal scale. However, the fact that in quantitative genetic analyses repeated measurements are also used to isolate permanent environmental instead of transient effects, requires a re-assessment of the information content of repeated measurements. To do so, we propose to distinguish “short-term” from “long-term” repeats, where the former capture transient variability and the latter the permanent effects. We show how the inclusion of the corresponding variance components in quantitative genetic models yields unbiased estimates of all quantities of interest, and we illustrate the application of the method to data from a Swiss snow vole population.

Estimating Quantitative Genetic Parameters Using Sibships Reconstructed From Marker Data

Genetics ◽  
2000 ◽  
Vol 155 (4) ◽  
pp. 1961-1972 ◽  
Author(s):  
Stuart C Thomas ◽  
William G Hill
Keyword(s):  
Prior Knowledge ◽  
Genetic Parameters ◽  
Allele Frequencies ◽  
Parameter Estimates ◽  
Monte Carlo Techniques ◽  
Quantitative Genetic ◽  
Downward Bias ◽  
Mean Square Errors ◽  
Sibship Reconstruction ◽  
Quantitative Genetic Parameters

Abstract Previous techniques for estimating quantitative genetic parameters, such as heritability in populations where exact relationships are unknown but are instead inferred from marker genotypes, have used data from individuals on a pairwise level only. At this level, families are weighted according to the number of pairs within which each family appears, hence by size rather than information content, and information from multiple relationships is lost. Estimates of parameters are therefore not the most efficient achievable. Here, Markov chain Monte Carlo techniques have been used to partition the population into complete sibships, including, if known, prior knowledge of the distribution of family sizes. These pedigrees have then been used with restricted maximum likelihood under an animal model to estimate quantitative genetic parameters. Simulations to compare the properties of parameter estimates with those of existing techniques indicate that the use of sibship reconstruction is superior to earlier methods, having lower mean square errors and showing nonsignificant downward bias. In addition, sibship reconstruction allows the estimation of population allele frequencies that account for the relationships within the sample, so prior knowledge of allele frequencies need not be assumed. Extensions to these techniques allow reconstruction of half sibships when some or all of the maternal genotypes are known.

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