Quantitative genetics studies how genetic and environmental variation contribute to continuously varying traits.
The difference between the mean phenotype of selected parents and the biological population mean under a specified selection scheme. It differs from the partial regression coefficients in a multivariate selection gradient.
A one-trait short-term response model , where is the inherited change in mean, the phenotypic selection differential and narrow-sense heritability. It assumes an appropriate additive inheritance model and does not turn environmental phenotype change into inherited response.
A mixed model using pedigree or genomic relationships to estimate genetic contributions to phenotypic variation. A donor identity effect alone is not proof of an indirect genetic effect.
A breeding design in which offspring share a sire but have different dams. Relatedness patterns help distinguish inherited covariance from shared full-family environment.
An influence of the mother on offspring phenotype beyond simply transmitting offspring alleles. It can include genetic and non-genetic components.
An effect of an individual's own genotype on its phenotype, defined relative to the model and its other genetic and environmental contributions.
An effect of one individual's genotype on another individual's phenotype, mediated through the environment or social interaction. Maternal effects are genetic only insofar as maternal genetic variation contributes to them.
A genomic region statistically associated with variation in a quantitative trait. A mapped interval can contain multiple causal variants or genes.
The genetic variants, their effects, interactions and arrangement that contribute to a specified phenotype in a stated biological population and environment.
The relationship between environment and the phenotype expressed by a specified genotype. In the illustrative form , describes baseline expression and describes responsiveness to cue .
A relation between an individual’s behaviour and social conditions. Baseline differences and differences in responsiveness are separate components.
A phenotypic trait influenced by variation at multiple genetic loci. Absence of a single shared large-effect region does not exclude repeated evolution through many small inherited effects.
Dependence of a difference between genotypes on the environment. Crossing reaction norms provides a clear example: one genotype can outperform another in one environment but reverse rank elsewhere.
Mapping inherited differences in a quantitative phenotypic trait to genomic intervals through segregation and genetic recombination. A detected interval need not contain only one causal gene or genetic variant.
pleiotropy in which a change has benefits and costs in different traits, environments, sexes or life stages. Whether an allele spreads depends on its net contribution to genotype fitness, rather than the sign of any one effect.
Shared variation in inherited contributions to different phenotypic traits. It can arise from pleiotropy or associations between separate causal genetic loci; measuring it does not distinguish these mechanisms by itself.
The component of variation in a specified trait attributable to differences among genotypes in the stated environment and biological population. Additive genetic variance is distinguished from contributions due to dominance and epistasis.
The covariance matrix of additive inherited contributions to a collection of phenotypic traits. Its diagonal entries are additive genetic variances; off-diagonal entries describe additive genetic covariance. It summarizes available local directions of response but can change as allele frequencies and associations change.
The local response approximation , where is the additive genetic covariance matrix and is a phenotypic selection gradient. Correlated inheritance can facilitate one direction of response and inhibit another.[ref]
A vector describing direct selection on measured phenotypic traits, conditional on the other measured traits. In a local deterministic fitness model it can be written ; biological population regression estimates require their own sampling and fitness assumptions. This differs in context from a rare-mutant invasion selection gradient.
A proposed decrease in the rate of adaptation when mutations affect more independently selected dimensions. In Fisher's geometric model, a large random step can improve one component while damaging others. The prediction depends on the scaling of mutational effects and need not follow from a simple count of organismal traits.
An effect of one gene or genetic variant on multiple distinguishable phenotypic traits. It can constrain evolution when effects oppose simultaneous improvement, or facilitate coordinated improvement when their directions align with natural selection. Distinguish a single causal change from several linked changes.
A genetic risk score combines allele counts from several genetic variants, usually using specified weights. In Mendelian randomization it can act as a combined instrumental variable for an exposure; interpretation still requires instrument relevance, instrumental-variable independence, and the exclusion restriction.
Heritability is the fraction of phenotypic variance in a specified biological population and environment attributed to genetic variation. It is a biological population parameter, not the genetic fraction of one individual's trait.
If observed variation is true-score variation plus independent measurement error , and genetic variance is part of , then . Writing measurement reliability as gives the displayed identity. Removing independent error can raise the heritability estimate without changing the genetic contribution to the true score. The result requires this measurement model; it does not identify measurement reliability by dividing arbitrary estimates from different longitudinal models.
The ratio of additive genetic variance to total phenotypic variance in a specified biological population and environment. It is not the fraction of one individual attributable to genes.
A twin study compares trait resemblance between twins with different degrees of genetic relatedness to separate genetic and environmental variance components.
The assumption that environmental similarity relevant to the measured outcome does not systematically account for the additional resemblance of monozygotic compared with dizygotic twins in the genetic model. It does not require identical treatment of all twins in every respect.
Monozygotic twins develop from one zygote and are modeled as sharing essentially all additive genetic variation.
Dizygotic twins develop from two zygotes and, absent assortative mating and other complications, share one half of additive genetic variation on average.
The ACE model decomposes trait variation into additive genetic effects , common environmental effects , and unique environmental effects .
Falconer's formula estimates narrow-sense heritability from monozygotic and dizygotic twin correlations:It relies on equal relevant environments and a dizygotic additive-genetic correlation of one half.
Assortative mating is nonrandom mating in which partners are more or less similar than random pairs for a trait or correlated characteristic. Positive assortment can increase genetic similarity among siblings.
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Quantitative genetics is a branch of genetics that deals with the inheritance of traits that are determined by multiple genes (polygenic traits) rather than a single gene. This field focuses on understanding how genetic and environmental factors contribute to the variation in traits within a population. Key aspects of quantitative genetics include: 1. **Traits**: Quantitative traits are typically measurable and can include characteristics such as height, weight, yield in crops, or susceptibility to diseases.