In other words, there are other components of phenotypic variance, such as environmental variance, which may not be heritable from parent to offspring, and so there is a regression toward the population mean. This is all good & well, just like using the ideal gas law, pV = nRT, is often very useful.
But, we can obtain the breeder’s equation, and ergo quantitative genetical processes, from population genetic theory. Nature is one. First, let’s use a simple “counting” example.
The mean value for the distribution of phenotypic values obtained from the genotypes in the case of dominance is 1.5. You can confirm this numerically, or simply derive it from the expression 2p (1 + q), where q = 1 – p, and in this case q = p (both being 0.5).
The breeder’s equation comes out of applied quantitative genetics, so in a sense it is “gene blind,” it simply describes and projects evolutionary processes without any exploration of a deeper framework. But, we can obtain the breeder’s equation, and ergo quantitative genetical processes, from population genetic theory.
The majority of populations have a certain degree of variation in their genetic pools.
Natural selection can induce microevolution, in other words, a change in allele frequencies over a given time or generations, as fitness-increasing alleles are more common in the population over generations. Microevolution is a change in the frequency of gene variants, alleles in a population, typically occurring over a relatively short period.
Phenotype frequency is the number of individuals in a population having a specific observable trait or phenotype. Briefly, it is a ratio depicting the number of times a specific phenotype occurs in a population at a given period in a single generation
Allele frequency is determined as the ratio of the frequency of appearance of an allele in a population to the total number of copies of the alleles present at a specific genetic locus. Allele frequencies can be represented as a decimal, a percentage, or a fraction.
When alleles from more than one locus (position on chromosome) are considered, it results in gamete frequency. Every new gamete being considered contains an allele from each locus.
Similarly, the characterization of single nucleotide polymorphisms (SNPs) has gained considerable interest in the discovery as it facilitates the analysis of the potential interaction between human genotype and phenotype.
1. Trying to find p First- One common mistake students commonly make calculating p by observing the population and calculating the square root later. This strategy does not work in typical recessive/dominant allele relationships, as the dominant allele can hide a recessive allele.
The breeder’s equation is proximately useful, but to explore its boundaries and limitations we need to comprehend how it relates to Mendelian genetics.
There is only one way you can obtain a genotype of all “upper case” or “lower case” alleles, so you just multiply the expectations across each slot, 1/24, and you get 1/16. In contrast, there are multiple ways that you can obtain an AaBb genotype.
By basic algebra that means that the narrow sense heritability is 1.0. The way I framed the genetic architecture as additive and independent means that all the variation is due to additive genetic variance, so we should expect that the heritability in the narrow sense should account for the full phenotype range.
In other words, there are other components of phenotypic variance, such as environmental variance, which may not be heritable from parent to offspring, and so there is a regression toward the population mean. This is all good & well, just like using the ideal gas law, pV = nRT, is often very useful.