Showing papers on "Mutation (genetic algorithm) published in 1984"

Ecological determinants of genetic structure in plant populations

Abstract: Plant populations are not randomly arranged assemblages of genotypes but are structured in space and time (2, 29, 49, 58, 84, 112). This structure may be manifested among geographically distinct populations, within a local group of plants, or even in the progeny of individuals. Genetic structure results from the joint action of mutation, migration, selection, and drift, which in tum must operate within the historical and biological context of each plant species. Ecological factors affecting reproduction and dispersal are likely to be particularly important in determining genetic structure (2, 31, 58). Reproduction is the process that translates the current genotypic array into that of subsequent generations, while the dispersal of pollen and seeds determines the postreproductive pattems of gene dispersion within and among populations. Although the concept of genetic structure has been used in various ways (58, 130, 154), we limit our definition to the nonrandom distribution of alleles or genotypes in space or time and disregard genome organization and meiotic processes that can also affect allele and genotype frequencies. Because of the limited mobility of plants, their genetic structure implies spatial structure, or the actual physical distribution of individuals. While spatial pattems often have genetic implications, nonrandom genetic pattems can exist without a nonrandom distribution of individuals. Conversely, a population may have a nonrandom spatial distribution without any accompanying genetic structure. Spatial and genetic patterns are often assumed to result from environmental heterogeneity and differential selection pressures (22, 53, 131, 132). Selection is a ubiquitous feature of natural populations; it alters gene and

Nonrandomness of point mutation as reflected in nucleotide substitutions in pseudogenes and its evolutionary implications

Abstract: We have obtained a revised estimate of the pattern of point mutation by considering more pseudogene sequences. Compared with our previous estimate, it agrees better with expectations based on the double-strand structure of DNA. The revised pattern, like the previous one, indicates that mutation occurs nonrandomly among the four nucleotides. In particular, the proportion of transitional mutations (59%) is almost twice as high as the value (33%) expected under random mutation. The same high proportion of transitions is observed in synonymous substitutions in genes. The proportion of transitional changes observed among electrophoretic variants of human hemoglobin is about the same as that predicted by the revised pattern of mutation. We also show that nonrandom mutation increases, by about 15%, the proportion of synonymous mutations due to single-nucleotide changes in the codon table, and increases, from 10% to 50%, the rate of synonymous mutation in the seven genes studied. However, nonrandom mutation reduces (by about 10%) the proportion of polar changes among nonsynonymous mutations in a gene. As far as single-nucleotide changes (in the codon table) are concerned, nonrandom mutation only slightly favors relatively conservative amino acid interchanges, and has virtually no effect on the proportions of radical changes and nonsense mutations.

Origin of the beta S-globin gene in blacks: the contribution of recurrent mutation or gene conversion or both.

Abstract: In order to investigate the origin(s) of the mutation(s) leading to the beta S-globin gene in North American populations of African ancestry, we analyzed DNA polymorphisms in the beta-globin gene cluster in a large number of both beta A- and beta S-globin gene-bearing chromosomes in U.S. and Jamaican Blacks. We found 16 different haplotypes of polymorphic sites associated with 170 beta S-globin gene-bearing chromosomes. The three most common beta S haplotypes, which account for 151/170 of the beta S-globin gene-bearing chromosomes, are only rarely seen in the chromosomes bearing the beta A-globin gene in these populations (6/47). Two observations suggest multiple origins or interallelic gene conversion, or both, of the beta S mutation. First, the mutation is present in all three beta-globin gene frameworks. Second, the beta S haplotypes can be divided into four groups, each of which cannot be derived from any other by less than two crossing-over events. In summary, our observation of the beta S mutation on 16 different haplotypes in African populations can be best explained by (i) a number of simple recombination events 5' to the beta-globin gene and (ii) up to four independent mutations and/or interallelic gene conversions.

The genetic correlation between characters maintained by selection, linkage and inbreeding.

Abstract: Mutation is modelled in two quantitative characters under separate genetic control in a large population. A bivariate pattern of selection acts to correlate the characters and, without pleiotropy, their genetic correlation is due entirely to linkage disequilibrium. Data on spontaneous mutation, the effective number of genes, and the intensity of natural selection on quantitative characters are used to evaluate the models. It is concluded that, even when selection favors a high correlation between the characters, with random mating and no linkage between loci influencing different traits the genetic correlation between characters is likely to be small in magnitude. A genetic correlation of large magnitude can be maintained only if the loci influencing different characters are tightly linked, or there is a high level of inbreeding in the population created by frequent mating between closely related individuals.

Human-murine hybridoma fusion partner

Abstract: By careful screening and mutation, a human-murine hybridoma suitable as a fusion partner for immortalizing an antibody-secreting B cell has been generated. The trioma fusion products of this immortalizing partner are stable producers of human monoclonal antibodies. A trioma which produces monoclonal human anti-varicella zoster is disclosed.

Pleiotropic overdominance and the maintenance of genetic variation in polygenic characters.

Abstract: A model of selection is described in which optimizing phenotypic selection is combined with pleiotropic overdominance. Thus, the role that mutation commonly plays in models of phenotypic evolution is replaced by balancing selection. Expressions are provided for the equilibrium genetic variance in phenotype and for the heterozygosity. An approximate analysis of the transient properties of the model shows that, in certain circumstances, the behavior is quite similar to that of models based on the interaction of mutation and selection.

Cultural and biological evolutionary processes: gene-culture disequilibrium.

Abstract: The dynamics of the interaction between genetic and cultural transmission are studied by using a simple two-phenotype diallelic haploid genetic system. The value of an individual's phenotype is determined by cultural transmission from its parent or by a randomly chosen member of the parental population. In the absence of phenotypic selection, polymorphic equilibria of the gene and trait frequencies are obtained. The correlation between genotype and phenotype within or between populations depends on a quantity formally similar to linkage disequilibrium and is determined by a relationship among transmission coefficients analogous to a coefficient of epistasis. With natural selection on the phenotype and no mutation, only degenerate transmission rules allow polymorphic equilibria to be attained, and, in general, the genotype allowing the strongest transmission of the favored phenotype is successful.

Retention of cryptic genes in microbial populations.

Abstract: Cryptic genes are silenced genes that can still be reactivated by mutation. Since they can make no positive contribution to the fitness of their carriers, it is not clear why many cryptic genes in microbial populations have not degenerated into useless DNA sequences. Hall et al. (1983) have suggested that cryptic genes have persisted because of occasional strong environmental selection for reactivated genes. The present mathematical study supports their suggestion. It shows that a cryptic gene can be retained without having any selective advantage over a useless DNA sequence, if selection for the reactivated gene occasionally occurs for a substantially long time.

Evolutionary constraints and the neutral theory.

Abstract: The neutral theory of molecular evolution postulates that nucleotide substitutions inherently take place in DNA as a result of point mutations followed by random genetic drift. In the absence of selective constraints, the substitution rate reaches the maximum value set by the mutation rate. The rate in globin pseudogenes is about 5 X 10(-9) substitutions per site per year in mammals. Rates slower than this indicate the presence of constraints imposed by negative (natural) selection, which rejects and discards deleterious mutations.

Hemoglobin E in Europeans: further evidence for multiple origins of the beta E-globin gene.

Abstract: We have determined haplotypes for the known restriction site polymorphisms in the beta-globin gene cluster in two families of European ancestry containing individuals who are heterozygous for hemoglobin E. In both families, the beta E mutation is associated with a haplotype not previously found among the haplotypes of beta E chromosomes in Southeast Asia. Moreover, in one family, the mutation is present in a beta-gene framework not found in beta E chromosomes of Southeast Asia. These data provide further evidence of multiple independent origins of the beta E mutation in human populations.

Mutation tests in Neurospora crassa. A report of the U.S. Environmental Protection Agency Gene-Tox Program.

Abstract: Many mutation tests have been developed in Neurospora crassa during the almost 40 years of its use in mutation research These tests detect two major classes of mutation: gene mutation and meiotic nondisjunction Within the first class, forward- and reverse-mutation tests have been used The forward-mutation tests include those that detect mutations at many loci and at specific loci Both kinds of forward-mutation tests have been done in homokaryons ( n ) and heterokaryons ( n + n ′) From the publications that were not rejected by our pre-established criteria, data were extracted for 166 chemicals that had been tested for mutagenicity Only 6 of the 166 chemicals have been tested in one or more gene mutation test and the meiotic nondisjunction test; these 6 chemicals were positive in the first and negative in the second Of the 102 chemicals tested in one or more gene mutation tests, 94 were positive and 8 were negative Of the 70 chemicals tested in the meiotic nondisjunction test, 7 were positive and 63 were negative Two tests, the ad-3 ) forward-mutation test and the meiotic nondisjunction test, have been used most frequently These two tests are especially important for hazard evaluation, because each detects a class of mutations that is likely to be deleterious or lethal in the F 1 - disomics by the meiotic nondisjunction test and multilocus deletions by the ad-3 forward-mutation test in heterokaryons Generally, direct-acting chemicals are mutagenic in the gene mutation tests, but few chemicals that required metabolic activation have been tested Only 31 of the 166 chemicals tested in N crassa have been tested for carcinogenicity Among these chemicals, there is a good association between mutagenicity in gene mutation tests and carcinogenicity but a poorer association between meiotic nondisjunction and carcinogenicity; however, only a small number of chemicals has been tested in the meiotic nondisjunction test Further use and development of certain mutation tests in N crassa are desirable

Mutation and selection in the marker (X) syndrome A hypothesis

Abstract: Summary Sherman et at. (1984) concluded from a cytogenetic and genetic analysis of families with the marker (X) syndrome that the rate of the mutation leading to this syndrome is extraordinarily high (7×2 times 10–4 in male germ cells), and that these mutations occur exclusively in male germ cells. It is shown by some model calculations that the empirical evidence can be reconciled with more conventional assumptions on the mutation rate if a moderately increased fertility of clinically unaffected female and possibly male carriers in the past is assumed. Indirect evidence for such an increased fertility can be derived from old reports on higher reproduction of slightly subnormal individuals. On the other hand, complete compensation of gene loss in affected individuals by higher fertility of unaffected carriers appears to be rather unlikely. At present, a moderately high mutation rate – as found, for example, in Duchenne muscular dystrophy or haemophilia A – in combination with a moderately increased fertility of clinically unaffected carriers is the most likely alternative.

UV-mutagenesis at a cloned target sequence: converted suppressor mutation is insensitive to mutation frequency decline regardless of the gene orientation.

Abstract: Premutational lesions produced by ultraviolet radiation in the Gln2 tRNA genes of E. coli B/r show differing sensitivities to a mutation avoidance phenomenon known as mutation frequency decline (MFD). A mutation event that changes the wild-type gene to an amber (UAG) suppressor is normally sensitive to MFD. Mutation of this amber suppressor to an ochre (UAA) suppressor is not sensitive to MFD. These two mutation events occur in the same anticodon region of the DNA. The dissimilarity of MFD sensitivity between these two mutations may result because of the respective premutational photoproducts for the two are located in opposite strands of duplex DNA. To examine the effect of strand position of the premutational lesions of MFD, recombinant lambda phage were constructed that contained the amber suppressor as a mutation target in the two possible orientations. Comparison of MFD in bacterial lysogens containing either of the two types of recombinant prophage indicated that reversing the orientation of the target sequence relative to adjacent bacterial DNA had no effect on MFD. Since rotational inversion of the target sequence did not alter the sensitivity to MFD of mutation occurring at the cloned target gene, the antimutation process inherent to FMD can not be attributed to an asymmetrical interaction between the template strands and the DNA-replication complex.