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Biomedical subjects

M Nei

Publications and source records attributed to M Nei.

At least 91 records · Page 5Linked to original sources
PubMed1975

Interlocus variation of genetic distance and the neutral mutation theory.

Theoretical distributions of genetic distance between reproductively isolated taxa are derived by means of computer simulation, taking into account mutation and random genetic drift. The distributions obtained are in good agreement with the observed distributions of interracial and interspecific genetic distances for enzymes loci in Drosophila. This indicates that the gene substitution at enzyme loci can be explained by the neutral mutation theory.

Animals↗
PubMed1974

Sampling variances of heterozygosity and genetic distance.

Mathematical formulae for the sampling variances of average heterozygosity and Nei's genetic distance are developed. These sampling variances are decomposed into their two components, i.e. the inter-locus and intra-locus variances. The relationship between the number of loci and the number of individuals per locus to be examined for estimating average heterozygosity and genetic distance is also discussed. The utility of the inter-locus variance of heterozygosity for studying the mechanism of maintenance of genetic variability in populations is indicated.

Alleles↗
PubMed1973

Analysis of gene diversity in subdivided populations.

A method is presented by which the gene diversity (heterozygosity) of a subdivided population can be analyzed into its components, i.e., the gene diversities within and between subpopulations. This method is applicable to any population without regard to the number of alleles per locus, the pattern of evolutionary forces such as mutation, selection, and migration, and the reproductive method of the organism used. Measures of the absolute and relative magnitudes of gene differentiation among subpopulations are also proposed.

Alleles↗
PubMed1973

Probability of fixation and mean fixation time of an overdominant mutation.

The probability of fixation of an overdominant mutation in a finite population depends on the equilibrium gene frequency in an infinite population (m) and the product (A) of population size and selection intensity. If m < 0.5 (disadvantageous overdominant genes), the probability is generally much lower than that of neutral genes; but if m is close to 0.5 and A is relatively small, it becomes higher. If m > 0.5 (advantageous overdominant genes), the probability is largely determined by the fitness of heterozygotes rather than that of mutant homozygotes. Thus, overdominance enhances the probability of fixation of advantageous mutations. The average number of generations until fixation of an overdominant mutation also depends on m and A. This average time is long when m is close to 0.5 but short when m is close to 0 or 1. This dependence on m and A is similar to that of Robertson's retardation factor.

Gene Frequency↗
PubMed1973

A case of high rate of spontaneous mutation affecting viability in Drosophila melanogaster.

A spontaneous lethal mutation rate approximately twenty to thirty times greater than normal has been discovered in second and third chromosomes derived from an irradiated isogenic line and paired with marked inversion chromosomes. Mutations resulting in reductions of viability of varying magnitude short of complete lethality apparently also occur at a very high rate in the third but not in the second chromosome. The pattern of accumulation of lethal mutations over several generations and viability frequency distributions within generations have been studied in a number of independent experiments. High mutation rate occurs in heterozygous isogenic-derived second and third chromosomes, either together or apart, irrespective of the genetic constitution of nonhomologous chromosomes. High mutation rates were not observed using the same methods with chromosomes of an inbred line from a different source. The possible mechanisms responsible for these results are discussed.

Animals↗
PubMed1973

Linkage disequilibrium in subdivided populations.

The linkage disequilibrium in a subdivided populaton is shown to be equal to the sum of the average linkage disequilibrium for all subpopulations and the covariance between gene frequencies of the loci concerned. Thus, in a subdivided population the linkage disequilibrium may not be 0 even if the linkage disequilibrium in each subpopulation is 0. If a population is divided into two subpopulations between which migration occurs, the asymptotic rate of approach to linkage equilibrium is equal to either r or 2(m(1) + m(2)) - (m(1) + m(2))(2), whichever is smaller, where r is the recombination value and m(1) and m(2) are the proportions of immigrants in subpopulations 1 and 2, respectively. Thus, if migration rate is high compared with recombination value, the change of linkage disequilibrium in subdivided populations is similar to that of a single random mating population. On the other hand, if migration rate is low, the approach to lnkage equilibrium may be retarded in subdivided populations. If isolated populations begin to exchange genes by migration, linkage disequilibrium may increase temporarily even for neutral loci. If overdominant selection operates and the equilibrium gene frequencies are different in the two subpopulations, a permanent linkage disequilibrium may be produced without epistasis in each subpopulation.

Blood Group Antigens↗
PubMed1972

Gene differences between Caucasian, Negro, and Japanese populations.

The numbers of gene (codon) differences per locus between two randomly chosen genomes within and between Caucasian, Negro, and Japanese populations have been estimated from gene frequency data for protein loci. The estimated number of gene differences between individuals from different populations is only slightly greater than the number between individuals from the same population.

Asian People↗