Population genetics

Population genetics is the study of genetic variation in populations. Basic concepts of population genetics allow us to understand how and why the prevalence of various genetic diseases differs among populations. 

An essential step in understanding genetic variation is to measure it in populations. This is done by estimating genotype and gene frequencies. 

The genotype frequency is then obtained by dividing the count for each genotype by the total number of individuals. Thus, the firequency of genotype 1-1 is 49/100 = 0.49, and the fi-equen-cies of genotypes 1-2 and 2-2 are 0.42 and 0.09, respectively. 

The gene frequency measures the proportion of chromosomes that contain a specific allele. To continue the RFLP example given above, we wish to estimate the frequencies of alleles 1 and 2 in our population. Each individual with the 1-1 genotype has two copies of allele 1, and each heterozygote (1-2 genotype) has one copy of allele 1. Because each diploid somatic ceU contains 

Genotype frequencies measure the proportion of each genotype in a population. Gene frequencies measure the proportion of chromosomes that contain a specific allele (gene). 

Population genetics describes interactions among alleles. The system (in the simplest case it is a one gene locus) is composed of alleles The 

The reconciliation of the Darwinian theory of natural selection and of Mendelian population genetics has been based on this model (Fisher, 1930 Wright, 1931). 

According to Fisher s theorem, the mean fitness w increases steadily along the trajectory of (7.18). Technically it means that w is Lyapunov function. 

Kimura (1958) stated that the trajectories of (7.8) point in the direction of maximal increase of w. Technically it would mean that (7.18) is a gradient system. However, the system is not a gradient system, at least not in the traditional sense. Maximal increase implies that the direction of the trajectories is orthogonal to the contour lines of w, and this is not the case in general. The spirit of Kimura s maximum principle have been saved by a redefinition of orthogonality by Shahshahani (1979) who introduced a new Riemannian metric at every point of the state-space. 

It can be shown more generally (Sigmund, 1984) that a difierential equation 

As explained in Chapter 1, the toxicity of natural xenobiotics has exerted a selection pressure upon living organisms since very early in evolutionary history. There is abundant evidence of compounds produced by plants and animals that are toxic to species other than their own and which are nsed as chemical warfare agents (Chapter 1). Also, as we have seen, wild animals can develop resistance mechanisms to the toxic componnds prodnced by plants. In Anstralia, for example, some marsupials have developed resistance to natnrally occnrring toxins produced by the plants upon which they feed (see Chapter 1, Section 1.2.2). 

It is only very recently that organic componnds synthesized by humans have begun to exert a selection pressure upon natural populations, with the consequent emergence of resistant strains. Pesticides are a prime example and will be the principal subject of the present section. It should be mentioned, however, that other types of biocides (e.g., antibiotics and disinfectants) can produce a similar response in microbial populations that are exposed to them. 

Organic Pollutants An Ecotoxicological Perspective, Second Edition 

The development of resistant strains of pest species of insects has been intensively studied for sound economic reasons, and there are many good examples. For further information, see Brown (1971), Georghiou and Saito (1983), McCaffery (1998), and Oppenoorth and Welling (1976). Some examples of mechanisms of insect resistance are given in Table 4.3. 

Resistance mechanisms associated with changes in toxicokinetics are predominately cases of enhanced metabolic detoxication. With readily biodegradable insecticides such as pyrethroids and carbamates, enhanced detoxication by P450-based monooxygenase is a common resistance mechanism (see Table 4.3). 

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C. Winstanley and J. A. W. Morgan, The bacterial flagellin gene as a biomarker for detection, population genetics and epidemiological analysis. Microhiolof y 143 . 3071 (1997). 

Bursill CA, Channon KM, Greaves DR. The role of chemokines in atherosclerosis recent evidence from experimental models and population genetics. Curr Opin Lipidol 2004 15(2) 145-149. 

Hoss, M. (2000), Ancient DNA Neanderthal population genetics, Nature 404,453-454. 

Leaves, N. I. Sisson, P. R. Freeman, R. Jordens, J. Z. Pyrolysis mass spectrometry in epidemiological and population genetic studies of Haemophilus influenzae. J. Med. Microbiol. 1997, 46, 204-207. 

Provine, W. B. (1971), The Origins of Theoretical Population Genetics, University of Chicago Press,... 

The accurate analysis of genetic variation in nematodes has major implications for parasite identification and for investigating population genetic structures (Lejambre, 1993 Grant, 1994). Conventional DNA methods have been valuable and their application has provided a wealth of molecular data (reviewed by McManus and Bowles, 1996), but little attention has been paid to their capacity to resolve sequence variation (reviewed by Gasser, 1997). For instance, PCR-RFLP analysis using (multiple) restriction endonucleases is useful, but sequence variation may go undetected as... 

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