What refers to the total number of genes of every individual in a population?

For more information about genes:

MedlinePlus Genetics provides consumer-friendly gene summaries that include an explanation of each gene's normal function and how variants in the gene cause particular genetic conditions.

More information about how genetic conditions and genes are named is also available from MedlinePlus Genetics.

The Centre for Genetics Education offers a fact sheet that introduces genes and chromosomes.

The Tech Museum of Innovation at Stanford University describes genes and how they were discovered.

The Virtual Genetics Education Centre, created by the University of Leicester, offers additional information on DNA, genes, and chromosomes.

Topics in the Cells and DNA chapter

• What is a cell?
• What is DNA?
• What is a gene?
• What is a chromosome?
• How many chromosomes do people have?
• What is noncoding DNA?

Other chapters in Help Me Understand Genetics

The information on this site should not be used as a substitute for professional medical care or advice. Contact a health care provider if you have questions about your health.

Here, we will limit ourselves to the theoretical framework of population genetics under the Mendelian approach and, unless otherwise stated explicitly, to the diploid model of sexual reproduction.

Scope of Population Genetics

Population genetics seeks to understand how and why the frequencies of alleles and genotypes change over time within and between populations. It is the branch of biology that provides the deepest and clearest understanding of how evolutionary change occurs. Population genetics is particularly relevant today in the expanding quest to understand the basis for genetic variation in susceptibility to complex diseases. Many of the factors that affect allelic frequency and associations among alleles of linked genes have been first characterized in Drosophila and other model organisms, but the same principles apply to virtually all organisms.

Shortly after the rediscovery of Mendel's laws in 1900, a raging controversy developed over the relevance of the kind of variation and transmission that Mendel characterized to the smooth, continuous variation that biologists had noted and measured in virtually all organisms. Could the continuous variation in stature, for example, be explained by underlying genes of the sort Mendel described? One of the arguments against Mendel's genes was that recessive alleles would soon be lost from a population by virtue of its recessiveness. Godfrey Hardy and Wilhelm Weinberg independently demonstrated the folly of this argument, and showed instead that randomly mating populations would be expected to retain the allelic variation by simple Mendelian principles unless some other force acted on the variation. But this did not fully resolve the question of why parents and offspring have correlated phenotypes for continuously varying traits.

It was the theoretical population geneticist Ronald Fisher who developed the mathematics to show exactly how many genes acting together could produce the precise quantitative degrees of familial resemblance that are observed. This was one of many instances in the history of population genetics in which a formal mathematical model of the problem paved the way to understanding what empirical data needed to be gathered to test the new conceptualization. Fisher went on to develop, along with Sewall Wright and J. B. S. Haldane, much of the theory for allelic frequency change under simple models of natural selection. Wright and Fisher developed the theoretical machinery needed to understand the complex process of recurrent sampling that we now call random genetic drift. By 1940 much of the theory for the ‘modern synthesis’ of Darwinian evolution and Mendelian transmission genetics had been developed.

Before considering the development of the empirical aspects of population genetics, the basic mechanisms that underlie the modern synthesis are briefly reviewed below.

Abstract

Population genetics is the study of genetic variation within and among populations and the evolutionary factors that explain this variation. Its foundation is the Hardy - Weinberg law, which is maintained as long as population size is large, mating is at random, and mutation, selection and migration are negligible. If not, allele frequencies and genotype frequencies may change from one generation to the next. Ethnic variation in allele frequencies is found throughout the genome, and by examining this genetic diversity, evolutionary patterns can be inferred, and variants contributing to the cause of common diseases can be identified. As a result of major international initiatives, extensive databases containing millions of genetic variants are available. Together with automated technology for genotyping, sequencing and bioinformatic analysis, these datasets provide the population geneticist with a huge set of densely mapped polymorphisms for reconciling genome variation with population histories of bottlenecks, admixture, and migration, for revealing evidence of natural selection, and for advancing understanding of many diseases.

IV.A.3. The Island Model

Although the previously mentioned measures of population differentiation are useful as descriptive tools, they can also be used to estimate the evolutionary parameters that determine the extent of population differentiation. This requires the development of models of the joint effects of genetic drift, mutation, and migration, one of the most complex problems in theoretical population genetics. The simplest and most widely used model is the island model, which assumes that the species is divided into n distinct subpopulations or demes, which each behave according to the Wright–Fisher model with population size N. After reproduction has occured within each deme, a fraction mof each deme's genes are replaced with genes drawn randomly from the other n− 1 demes. Coalescent theory can be used to determine the mean coalescence times of pairs of alleles sampled from the same population (t0) or from different populations (t1); t0= 2Nand t1=2Nn(l+[n−1]/[4Nnm]). In the infinite sites model, the mean fraction of nucleotides that differ between a pair of alleles is equal to the product of the mutation rate per site and twice their coalescence time (see Section III,D) so that the expected nucleotide site differences between alleles can be derived directly from the corresponding coalescence times.

An important and somewhat counterintuitive conclusion is that the within-population nucleotide site diversity, πS, is equal to 4Ndu, that is, it depends on the total number of individuals in the set of populations in the same way as the diversity in a panmictic population under the infinite sites model, and it is independent of the migration rate (with the proviso that m>0). As expected, the other diversity measures depend inversely on Nm, with large between-population divergence being possible only when Nm<1; for large d, KST is approximately equal to 1/(1+4Nm). Values of these statistics that are close to zero are generally taken to indicate relatively little population differentiation, whereas values close to one imply considerable differences among local populations relative to the within-population variability.

Is the sum total of all the genes in a population?

What is the total number of genes and their different alleles in a population called?

What is genotype population?

Is the total collection of genes in a population at any one time?