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H Tachida

Publications and source records attributed to H Tachida.

At least 19 recordsLinked to original sources
PubMed1992

Persistence of repeated sequences that evolve by replication slippage.

The evolution of short repeated sequences by replication slippage under the assumption of selective neutrality is modeled using a linear birth and death process. The equilibrium distribution, the distribution of the life expectancy of a repeated sequence when the process starts from two repeats, the age distribution of repeats, the probability of obtaining two genes with i and j copies which diverged t generations ago and the conditional variance of copy number given the repeat number is more than one are computed. The distributions of life expectancy and age are shown to have long tails. Also the statistic which estimates the conditional variance is shown to have a large coefficient of variation. Using these theoretical results, we develop an approximate test of our model and analyze persistent repeated sequences found in the primate beta-globin gene region and Oenothera chloroplast DNA which are polymorphic within species. We found one sequence in Oenothera chloroplast DNA which does not fit to our neutral model.

Animals↗
PubMed1992

Variance component analysis of bristle characters in local populations of Drosophila melanogaster.

The genetic variabilities of sternopleural and abdominal bristle numbers existing in local natural populations were assessed. Using second chromosome lines of Drosophila melanogaster extracted from three natural populations in Japan (the Ishigakijima, Ogasawara and Aomori populations), experiments were conducted to estimate the components of genetic variances, additive and dominance variances. The following results were obtained: For both sternopleural and abdominal bristle numbers, the additive genetic variances (sigma 2A) were much larger than the dominance variances (sigma 2D) especially in the southern populations. For example, in the Ishigakijima population, for females sternopleural bristle numbers of the inversion-free chromosome group, the additive and dominance variances were estimated to be 1.255 +/- 0.2034 and 0.0552 +/- 0.0180, respectively. The magnitudes of the estimates of additive genetic variances were nearly equal from north to south. By comparing the additive genetic variances of the inversion-free chromosome group with those of the In(2L)t-carrying chromosome group, it was inferred that sufficient number of generations to achieve the equilibrium state has not passed since the introduction of a single or a small number of the In(2L)t-carrying chromosomes to the Ishigakijima population.

Animals↗
PubMed1991

Fixation probability in spatially changing environments.

The fixation probability of a mutant in a subdivided population with spatially varying environments is investigated using a finite island model. This probability is different from that in a panmictic population if selection is intermediate to strong and migration is weak. An approximation is used to compute the fixation probability when migration among subpopulations is very weak. By numerically solving the two-dimensional partial differential equation for the fixation probability in the two subpopulation case, the approximation was shown to give fairly accurate values. With this approximation, we show in the case of two subpopulations that the fixation probability in subdivided populations is greater than that in panmictic populations mostly. The increase is most pronounced when the mutant is selected for in one subpopulation and is selected against in the other subpopulation. Also it is shown that when there are two types of environments, further subdivision of subpopulations does not cause much change of the fixation probability in the no dominance case unless the product of the selection coefficient and the local population size is less than one. With dominance, the effect of subdivision becomes more complex.

Biological Evolution↗
PubMed1991

A study on a nearly neutral mutation model in finite populations.

As a nearly neutral mutation model, the house-of-cards model is studied in finite populations using computer simulations. The distribution of the mutant effect is assumed to be normal. The behavior is mainly determined by the product of the population size, N, and the standard deviation, sigma, of the distribution of the mutant effect. If 4N sigma is large compared to one, a few advantageous mutants are quickly fixed in early generations. Then most mutation becomes deleterious and very slow increase of the average selection coefficient follows. It takes very long for the population to reach the equilibrium state. Substitutions of alleles occur very infrequently in the later stage. If 4N sigma is the order of one or less, the behavior is qualitatively similar to that of the strict neutral case. Gradual increase of the average selection coefficient occurs and in generations of several times the inverse of the mutation rate the population almost reaches the equilibrium state. Both advantageous and neutral (including slightly deleterious) mutations are fixed. Except in the early stage, an increase of the standard deviation of the distribution of the mutant effect decreases the average heterozygosity. The substitution rate is reduced as 4N sigma is increased. Three tests of neutrality, one using the relationship between the average and the variance of heterozygosity, another using the relationship between the average heterozygosity and the average number of substitutions and Watterson's homozygosity test are applied to the consequences of the present model. It is found that deviation from the neutral expectation becomes apparent only when 4N sigma is more than two. Also a simple approximation for the model is developed which works well when the mutation rate is very small.

Computer Simulation↗
PubMed1990

A population genetic model of selection that maintains specific trinucleotides at a specific location.

Periodic appearances of specific trinucleotides along the DNA sequence have been reported in the chicken core DNA, and the phenomenon has been suggested to be related to the supercoiling of DNA around nucleosomes. A population genetic model is constructed in which selection is operating to maintain specific trinucleotides at a specific location on the DNA sequence. Assuming low mutation rates, equilibrium probabilities of the appearances of respective trinucleotides were computed. Vague patterns appeared if the product of the effective size and the selection coefficient was 0.1-2.0. The genetic load and substitution rates in the equilibrium state were also computed. When the model was applied to the chicken DNA data, the product of the effective size and the selection coefficient was estimated to be 0.1-0.2. With this intensity of selection, the substitution rate was hardly different from that in the case without selection. However, the genetic load became fairly large. Considering the large number of times that DNA coils about nucleosomes, the number of trinucleotide sites must be very large, and thus the total load might be too large. Epistasis among these sites to reduce the total load is suggested to exist if selection is responsible for this periodic pattern observed in the chicken core DNA.

Alleles↗
PubMed1990

Theoretical study of near neutrality. I. Heterozygosity and rate of mutant substitution.

In order to clarify the nature of "near neutrality" in molecular evolution and polymorphism, extensive simulation studies were performed. Selection coefficients of new mutations are assumed to be small so that both random genetic drift and selection contribute to determining the behavior of mutants. The model also incorporates normally distributed spatial fluctuation of selection coefficients. If the system starts from "average neutrality," it will move to a better adapted state, and most new mutations will become "slightly deleterious." Monte Carlo simulations have indicated that such adaptation is attained, but that the rate of such "progress" is very low for weak selection. In general, the larger the population size, the more effective the selection becomes. Also, as selection becomes weaker, the behavior of the mutants approaches that of completely neutral genes. Thus, the weaker the selection, the smaller is the effect of population size on mutant dynamics. Increase of heterozygosity with population size is very pronounced for subdivided populations. The significance of these results is discussed in relation to various observed facts on molecular evolution and polymorphism, such as generation-time dependency and overdispersion of the molecular clock, or contrasting patterns of DNA and protein polymorphism among some closely related species.

Biological Evolution↗
PubMed1990

Increased variation in ADH enzyme activity in Drosophila mutation-accumulation experiment is not due to transposable elements at the Adh structural gene.

We present here a molecular analysis of the region surrounding the structural gene encoding alcohol dehydrogenase (Adh) in 47 lines of Drosophila melanogaster that have each accumulated mutations for 300 generations. While these lines show a significant increase in variation of alcohol dehydrogenase enzyme activity compared to control lines, we found no restriction map variation in a 13-kb region including the complete Adh structural gene and roughly 5 kb of both 5' and 3' sequences. Thus, the rapid accumulation of ADH activity variation after 28,200 allele generations does not appear to have been due to the mobilization of transposable elements into or out of the Adh structural gene region.

Alcohol Dehydrogenase↗
PubMed1989

Effects of identity disequilibrium and linkage on quantitative variation in finite populations.

Identity disequilibrium, ID, is the difference between joint identity by descent and the product of the separate probabilities of identity by descent for two loci. The effects of ID on the additive by additive (a*a) epistatic variance and joint dominance component between populations and in the additive, dominance and a*a variance within populations, including the effects on covariances of relatives within populations, were studied for finite monoecious populations. The effects are formulated in terms of three additive partitions, eta b, eta a and eta d, of the total ID, each of which increases from zero to a maximum at some generation dependent upon linkage and population size and decreases thereafter. eta d is about four times the magnitude of the other two but none is of any consequence except for tight linkage and very small populations. For single-generation bottleneck populations only eta d is not zero. With random mating of expanded populations eta b remains constant and eta a and eta d go to zero at a rate dependent upon linkage, very fast with free recombination. The contributions of joint dominance to the genetic components of variance within and between populations are entirely a function of the eta's while those of a*a variance to the components are functions mainly of the coancestry coefficient and only modified by the eta's. The contributions of both to the covariances of half-sibs, full-sibs and parent-offspring follow the pattern expected from their contributions to the genetic components of variance within populations except for minor terms which most likely are of little importance.

Chromosome Mapping↗
PubMed1989

Restriction map and alpha-amylase activity variation among Drosophila mutation accumulation lines.

The specific activities of alpha-amylase were measured for two sets of mutation accumulation lines, each set having originated from a different lethal-carrying second chromosome and SM1(Cy) chromosome and having been maintained by a balanced lethal system for about 300 generations. Significant variation was found to have accumulated among lines of both sets. Because of dysgenic crosses in the early generations of mutation accumulation, insertions or deletions of transposable elements in the Amy gene region were suspected of being the cause of this variation. In order to test this possibility, the structural changes in the 14 kb region of these chromosomes that includes the structural genes for alpha-amylase were investigated by restriction map analysis. We found that most part of the activity variation is due to replacements of a chromosomal region of SM1(Cy), including the structural genes for alpha-amylase, by the corresponding regions of the lethal chromosomes. One line also contained an insertion in this region but this line has an intermediate activity value. Thus, insertions of transposable elements into the Amy gene region were not found to be responsible for the new variation observed in alpha-amylase activity. If we remove those lines with structural changes from the analysis, the genetic variance of alpha-amylase specific activity among lines becomes non-significant in both sets of chromosomes.

Animals↗
PubMed1989

A building block model for quantitative genetics.

We introduce a quantitative genetic model for multiple alleles which permits the parameterization of the degree, D, of dominance of favorable or unfavorable alleles. We assume gene effects to be random from some distribution and independent of the D's. We then fit the usual least-squares population genetic model of additive and dominance effects in an infinite equilibrium population to determine the five genetic components--additive variance sigma 2 a, dominance variance sigma 2 d, variance of homozygous dominance effects d2, covariance of additive and homozygous dominance effects d1, and the square of the inbreeding depression h--required to treat finite populations and large populations that have been through a bottleneck or in which there is inbreeding. The effects of dominance can be summarized as functions of the average, D, and the variance, sigma 2 D. An important distinction arises between symmetrical and nonsymmetrical distributions of gene effects. With symmetrical distributions d1 = -d2/2 which is always negative, and the contribution of dominance to sigma 2 a is equal to d2/2. With nonsymmetrical distributions there is an additional contribution H to sigma 2 a and -H/2 to d1, the sign of H being determined by D and the skew of the distribution. Some numerical evaluations are presented for the normal and exponential distributions of gene effects, illustrating the effects of the number of alleles and of the variation in allelic frequencies. Random additive by additive (a*a) epistatic effects contribute to sigma 2 a and to the a*a variance, sigma 2/aa, the relative contributions depending on the number of alleles and the variation in allelic frequencies.(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗
PubMed1989

Effects of mutation on selection limits in finite populations with multiple alleles.

The ultimate response to directional selection (i.e., the selection limit) under recurrent mutation is analyzed by a diffusion approximation for a population in which there are k possible alleles at a locus. The limit mainly depends on two scaled parameters S (= 4Ns sigma a) and theta (= 4Nu) and k, the number of alleles, where N is the effective population size, u is the mutation rate, s is the selection coefficient, and sigma 2a is the variance of allelic effects. When the selection pressure is weak (S less than or equal to 0.5), the limit is given approximately by 2S sigma a[1 - (1 + c2)/k]/(theta + 1) for additive effects of alleles, where c is the coefficient of variation of the mutation rates among alleles. For strong selection, other approximations are devised to analyze the limit in different parameter regions. The effect of mutation on selection limits largely relies on the potential of mutation to introduce new and better alleles into the population. This effect is, however, bounded under the present model. Unequal mutation rates among alleles tend to reduce the selection limit, and can have a substantial effect only for small numbers of alleles and weak selection. The selection limit decreases as the mutation rate increases.

Alleles↗
PubMed1988

Permanency of response to selection for quantitative characters in finite populations.

To study the permanency of response to selection for a quantitative character in finite populations and the nature of the genetic effects that contribute to this response, we have used the covariance between ancestors and descendents within populations. Effects and variances are defined for an initial equilibrium random mating monoecious population that gives rise to replicate finite populations. After a prescribed history of restricted population size, the replicate populations are expanded, and the covariance between ancestors and descendents is quantified in terms of descent measures and genetic components in the initial population as a means of determining the additive variance within populations. Several dominance components including joint dominance effects of loci contribute to the additive variance, some of which can be negative. There is always a positive contribution of additive by additive variance to the additive variance within populations, which can be large. With the new definitions of components of genetic variance within populations, selection response is formulated in the same manner as for the initial random mating population, but the components have been modified considerably by the restricted population size.

Biological Evolution↗
PubMed1987

Quantitative genetic variation in an ecological setting.

The machinery was developed to investigate the behavior of quantitative genetic variation in an ecological model of a finite number of islands of finite size, with migration rate m and extinction rate e, for a quantitative genetic model general for numbers of alleles and loci and additive, dominance, and additive by additive epistatic effects. It was necessary to reckon with seven quadratic genetic components, whose coefficients in the genotypic variance components within demes, sigma Gw2, between demes within populations, sigma s2, and between replicate populations, sigma r2, are given by descent measures. The descent measures at any time are calculated with the use of transition equations which are determined by the parameters of the ecological model. Numerical results were obtained for the coefficients of the quadratic genetic components in each of the three genotypic variance components in the early phase of differentiation. The general effect of extinction is to speed up the time course leading to fixation, to increase sigma r2, and to decrease sigma s2 (with a few exceptions) in comparison with no extinction. The general effect of migration is to slow down the time course leading to fixation, to increase sigma Gw2, at least in the later generations, and to decrease sigma s2 (with a few exceptions) in comparison with no migration. Except for these, the effects of migration and extinction on the variance components are complex, depending on the genetic model, and sometimes involve interaction of migration and extinction. Sufficient details are given for an investigator to evaluate numerically the results for variations in the quantitative genetic and ecological models.

Alleles↗
PubMed1987

Evolution and maintenance of quantitative genetic variation by mutations.

The genotypic variance within, sigma 2w, and between, sigma 2b, random mating populations and rates and times for convergence to equilibrium values from different founder populations are formulated for an additive genetic model with an arbitrary number of alleles k, number of loci m, population size N, and mutation rate u, with unequal mutation rates for alleles. As a base of reference, the additive variance sigma 2a in an infinite equilibrium population is used. sigma 2a increases as k increases and decreases with variation in the mutation rates. Both transitional and equilibrium values of the variance within populations could be expressed as sigma 2w = (1 - theta)sigma 2a, where theta is the coancestry with mutations of individuals within populations. Thus, rates of convergence and evolutionary times are a function of those for theta, which involves both N and u. When the founder population is fixed, very long times are required to obtain a perceptible increase in sigma 2w and equilibrium values of sigma 2w are very small when 4Nu less than or equal to 10(-1). The variance between populations can be expressed as sigma 2b = 2 theta sigma 2a when the founder population is an infinite equilibrium population, and as sigma 2b = 2(theta - alpha)sigma 2a when the founder population is fixed, where alpha is a function only of u. In this latter case, rates of divergence, while affected by both N and u, are dominated by u and asymptotically a function of u only. With u = 10(-5), very long times (10(3) generations) are required for any perceptible divergence, even for N = 1-10. At equilibrium, most of the variance is between small populations and within very large populations. Migration increases the variance within populations and decreases the variance between populations.

Alleles↗
PubMed1986

Analysis of linkage disequilibrium in an island model.

Linkage disequilibria for two loci in a finite island model were parameterized. The total linkage disequilibrium was decomposed into three components, gametic, demic, and population, for which corresponding unbiased estimators were established. Other statistics encountered provided measures of differentiation corresponding to the hierarchical structure of the ecological model. Under the assumption of linkage equilibrium, the variances and covariances of these estimators and statistics were formulated in terms of descent measures, functions of gene frequencies, and the numbers of individuals, demes, and populations sampled. The functions of gene frequencies fall into two classes, one representing the differentiation of genes at each locus, and the other representing the association of genes between the loci. For a neutral model with extinction, migration, and linkage, transition equations were derived for the descent measures which also take into account deme size and numbers of dems within the population. With the addition of unequal mutation rates for a finite number of alleles at each locus, the transition equations were solved for the descent measures in the equilibrium state. This permitted the exact numerical evaluation of the effects of the sampling and ecological dimensions and of extinction, migration, and mutation rates in any parameter range. Some numerical results were presented for the effects of linkage, extinction, migration, and sampling on the variances of various measures of linkage disequilibrium and genetic differentiation. Also, some results were compared with the approximate numerical results of Ohta which agreed fairly well in the parameter ranges she considered, but not so well in other ranges.

Analysis of Variance↗
PubMed1986

Linkage disequilibria in finite populations.

Four-locus recombination frequencies are summarized into two-locus pair frequencies and three-locus frequencies, and further, into two-locus frequencies such that higher-order frequencies are linear functions of lower-order frequencies. Frequencies of gene combinations are defined according to their position on the same or distinct gametes, and linear functions of these provide the measures of linkage disequilibria. These concepts are utilized to derive the transitional behavior of the gene combinations frequencies and the linkage disequilibria in a finite monoecious population with random union of gametes for up to four loci. The transitions of lower-order disequilibria in a higher-order (more loci) setting involve the higher-order disequilibria which must be taken into account in arriving at the final (fixation) frequencies. The methods allow different initial conditions. Since corresponding data functions of the gene combination frequencies provide unbiased estimates of the parameters, estimators follow naturally.

Gene Frequency↗