Showing papers on "Mutation (genetic algorithm) published in 1977"
TL;DR: A more detailed analysis of oocyte-stage sensitivity to killing and mutation induction shows that there is no consistent correlation, either negative or positive, between the two, which indicates that the sensitivity to cell killing of the mouse immature oocytes may not be sufficient reason to prevent its use in predicting the mutational response of the human immature oocyte.
Abstract: Estimation of the genetic hazards of ionizing radiation in men is based largely on the frequency of transmitted specific-locus mutations induced in mouse spermatogonial stem cells at low radiation dose rates. The publication of new data on this subject has permitted a fresh review of all the information available. The data continue to show no discrepancy from the interpretation that, although mutation frequency decreases markedly as dose rate is decreased from 90 to 0.8 R/min (1 R = 2.6 x 10(-4) coulombs/kg) there seems to be no further change below 0.8 R/min over the range from that dose rate of 0.0007 R/min. Simple mathematical models are used to compute: (a) a maximum likelihood estimate of the induced mutation frequency at the low dose rates, and (b) a maximum likelihood estimate of the ratio of this to the mutation frequency at high dose rates in the range of 72 to 90 R/min. In the application of these results to the estimation of genetic hazards of radiation in man, the former value can be used to calculate a doubling dose--i.e, the dose of radiation that induces a mutation frequency equal to the spontaneous frequency. The doubling dose based on the low-dose-rate data compiled here is 110 R. The ratio of the mutation frequency at low dose rate to that at high dose rate is useful when it becomes necessary to extrapolate from experimental determinations, or from human data, at high dose rates to the expected risk at low dose rates. The ratio derived from the present analysis is 0.33.
251 citations
TL;DR: The present models show that with the additional features of mutation and selection, in a large population, the mating system has no influence on the amount of genetic variability maintained by additive genes.
Abstract: The traditional models of the effect of assortative mating and inbreeding on the genetic variance of polygenic characters (Fisher 1918; Wright 1921) presume that there is no natural selection or mutation. In a large population, the genetic variance determined by additive genes may then increase by up to a factor of two with local inbreeding, and even more with assortative mating. The classical models are still used to interpret data from natural populations. But contrary to their assumptions, most metrical characters in natural populations are usually thought to be under a type of selection which depletes polygenic variation. Mutation is then necessary to maintain genetic variation. The present models show that with the additional features of mutation and selection, in a large population, the mating system has no influence on the amount of genetic variability maintained by additive genes.
133 citations
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TL;DR: Observed differences in the slope m when different mutagens induce the same mutation in a given kind of cell imply that mutation and cellular inactivation do not arise from one type of DNA lesion only.
Abstract: Summary Many mutagens are known to induce a variety of different types of lesions in DNA. Cellular repair systems may eliminate some of these; some unrepaired lesions may lead to loss of reproductive capacity and others to viable mutations. Simple considerations of these three alternative fates of an exposed cell show that there should be a linear relation between the logarithm of the surviving fraction (log S/S0) and log(1 — M) where M is the mutant frequency. For low frequencies the relation assumes the simpler form M = —m log S/S0. The published literature on experimental mutagenesis in eukaryotes confirms these expectations. Observed differences in the slope m when different mutagens induce the same mutation in a given kind of cell (or a given mutagen induces the same mutation in different kinds of cell) imply that mutation and cellular inactivation do not arise from one type of DNA lesion only.
61 citations
TL;DR: The hexose monophosphate shunt is probably a minor pathway of NADPH formation in wild type E. coli and in mutants affected, directly or indirectly, in the NADPH-forming reactions glucose-6-phosphate dehydrogenase, isocitrate dehydration, malate dehydration, and energy-linked transhydrogenase.
60 citations
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55 citations
TL;DR: The result indicates that the electrochemical gradient, although necessary, is not sufficient to drive the active transport of amino acids and /3-methyl-n-thiogalactoside in the mutant, which could be ascribed to an inhibition of the energy-coupling process by glucose metabolites.
49 citations
31 Dec 1977
TL;DR: The implications of the results for the common alleles at protein loci in related Drosophila species and for the degeneration of unused characters in cave animals are discussed.
Abstract: Mathematical studies are conducted on three problems that arise in molecular population genetics. (1) The time required for a particular allele to become extinct in a population under the effects of mutation, selection, and random genetic drift is studied. In the absence of selection, the mean extinction time of an allele with an initial frequency close to 1 is of the order of the reciprocal of the mutation rate when 4 Nv N is the effective population size and v is the mutation rate per generation. Advantageous mutations reduce the extinction time considerably, whereas deleterious mutations increase it tremendously even if the effect on fitness is very slight. (2) Mathematical formulae are derived for the distribution and the moments of extinction time of a particular allele from one or both of two related populations or species under the assumption of no selection. When 4 Nv t th generation after their separation are studied. It is shown that if 4 Nv is small, the two species are expected to share a high proportion of common alleles even 4 N generations after separation. In addition to the above mathematical studies, the implications of our results for the common alleles at protein loci in related Drosophila species and for the degeneration of unused characters in cave animals are discussed.
TL;DR: Within each group there was a negative relationship obtained between growth rate and longevity, and peak body weight was positively correlated with longevity for all mouse groups.
Abstract: Body weights were obtained monthly for mutant groups with the C57BL/6J genetic background which differ in body weight ( bg , cJ, A y ,
TL;DR: Exonuclease activity other than RNase II (EC 3.4.1.23) was detected and purified from Escherichia coli, using HlrRNA, T4 phage-specific mRNA, and poly(U) as substrates, and seems to be forms of a single new enzyme.
TL;DR: The nematode Caenorhabditis elegans may, according to some workers, become the Escherichia coli or at least the bacteriophage T4 of the animal world.
Abstract: At a recent conference (1) in Woods Hole, Massachusetts, investigators (2) met to discuss the nematode Caenorhabditis elegans. This free-living worm may, according to some workers, become the Escherichia coli or at least the bacteriophage T4 of the animal world. Small (about I mm in length) and semitransparent, C. elegans provides for research the advantages of a short life cycle (3 days) and a simple anatomy-it contains about 810 nongonadal nuclei. It is both easy to cultivate, on E. coli as a food source, and convenient for genetic analysis. Its genes are carried on five autosomes and a sex chromosome (X), and it has a genome size about 20 times that of E. coli. It generally reproduces as
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TL;DR: Fibroblasts from three chronically affected, beta-galactosidase deficient adults were shown to synthesize nearly normal quantities of immunologically reactive catalytically deficient beta-GalactOSidase, indicating that they are CRM + structural mutants.
Abstract: Fibroblasts from three chronically affected, beta-galactosidase deficient adults were shown to synthesize nearly normal quantities of immunologically reactive catalytically deficient beta-galactosidase, indicating that they are CRM + structural mutants.
TL;DR: Hydrazine was found to be mutagenic for yeast at exposures ranging over nearly three orders of magnitude and results suggest that, in this eukaryote, HZ-induced lesions lead to mutation by causing base mispairing at DNA replication rather than by means of an error-prone repair mechanism.
Abstract: Hydrazine was found to be mutagenic for yeast ( Saccharomyces cerevisiae ) at exposures (concentration × time) ranging over nearly three orders of magnitude. Little or no forward mutation from CAN1 to can1 was detectable upon immediate plating following treatment in neutral buffer suspension. Post-treatment cell division in yeast extract peptone dextrose complex growth medium was required for expression of induced mutation to canavanine resistance. Frequencies of induced mutation rose to levels approximately 10-fold higher than spontaneous levels for exposures between 0.1 and 12.0 min mol/l. Survival remained at 100%. For exposures greater than 80 min mol/l viability and mutation frequency began to decrease sharply. By contrast, single treatments of ethyl methanesulfonate, methyl methanesulfonate, N -methyl- N ′-nitro- N -nitro-soguanidine, nitrous acid, hydroxylamine, and ultraviolet light were able to increase mutation frequency with this system upon immediate assay. Further growth-dependent increases in mutation frequency were not observed with HA and UV. Expression of HZ-induced mutation was detectable after treated cells had undergone less than one population doubling in YEPD. Such mutation expression could be blocked by the inhibitors cycloheximide and hydroxyurea, which block protein synthesis and DNA synthesis respectively. Results were similar to those obtained previously with Haemophilus influenzae and similarly suggest that, in this eukaryote, HZ-induced lesions lead to mutation by causing base mispairing at DNA replication rather than by means of an error-prone repair mechanism.
TL;DR: A spontaneous mutation conferring white plasmodial color on the Myxomycete Physarum polycephalum has been analysed in this article, and the mutant whi-1 allele is recessive to whi+ in both heterokaryotic and heterozygous PLAsmodia.
Abstract: A spontaneous mutation conferring white plasmodial colour on the Myxomycete Physarum polycephalum has been analysed. The mutant whi-1 allele is recessive to whi+ in both heterokaryotic and heterozygous plasmodia. The whi locus is unlinked to mt, npfA, fusA and leu.
TL;DR: In this article, the authors show that with stochastic migration, whether of fixed or variable numbers of individuals, a positive term Δm is added to the variance, and that the equilibrium value of the between-population variability is increased compared to the corresponding value for deterministic migration by a factor of approximately (1 − m)−2 for small m.
Abstract: Migration has in the past been introduced deterministically into stochastic gene frequency models. Migration at rate m then reduces the between-population variability by a factor of (1 − m)2 each generation. We show that with stochastic migration, whether of fixed or variable numbers of individuals, a positive term Δm is added to the variance. As a result of the Δ
m
term, the equilibrium value of the between-population variability is increased compared to the corresponding value for deterministic migration by a factor of approximately (1 − m)−2 for small m. An equivalent result is derived for mutation, using the infinite allele model for a single population. We show in addition that these results may be derived much more simply by use of identity-by-descent probability methods, but only if a modified definition of the probability of identity-by-descent is used, involving the sampling with instead of without replacement of pairs of genes from the population.
TL;DR: It is suggested that the creation of individual and family histories, using large scale automatic record linkage and existing files of vital and ill-health records, may be a useful approach to these kinds of problems.
Abstract: In order to adequately assess the genetic risks to man of an altered mutation rate, it is necessary to know the naturally occurring frequency of mutation-maintained genetic ill-health and the burde...
TL;DR: It is colclude that most HLA variants arise by mutation and the mutation rate for HLA-B27 loss is 8 x 10(-7) per cell per generation.
Abstract: Variants of a diploid lymphoid cell line that show a loss of HLA-B27 antigen occur randomly in time and independently of exposure to the alloantiserum used for their isolation. From these and previous findings of variant stability, inducibility by mutagens, and the absence of linked variation, we colclude that most HLA variants arise by mutation. The mutation rate for HLA-B27 loss is 8 x 10(-7) per cell per generation.
TL;DR: The effect of different mutagens on brewing yeast is described together with the results of selection for strains possessing improved commercial properties.
Abstract: The effect of different mutagens on brewing yeast is described together with the results of selection for strains possessing improved commercial properties. The mutagens n-methyl-n-nitroso nitrogua...
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TL;DR: Compared with chromosome anomalies, congenital abnormalities, and inborn errors of metabolism, the schizophrenic and manic depressive psychoses present greater problems both as regards the sense in which they may be considered to be genetic diseases and as regards their incidence in the population.
Abstract: Compared with chromosome anomalies, congenital abnormalities, and inborn errors of metabolism, the schizophrenic and manic depressive psychoses present greater problems both as regards the sense in which they may be considered to be genetic diseases and as regards their incidence in the population. They do not usually become manifest until adult life and are very variable in age at onset, symptomatology, and course. They are sensitive to variation in the postnatal environment. Compared with peptic ulcer, diabetes, and Parkinson's disease, with which there are parallels, the psychoses present much greater problems of diagnosis. Inheritance is certainly complex. Simple Mendelian ratios are not found. At present it is not known whether schizophrenia and manic depression are essentially monogenic, genetically heterogeneous (like deafness and blindness), or polygenic disorders. Despite these uncertainties, there can be little doubt that genetic factors make an important difference to the risk an individual runs of developing a psychosis and, if so, to its probable type. The evidence comes from the rates of similar psychoses in first degree relatives of cases, in second-degree relatives, and in members of the general population; further, from the psychosis rates in monozygotic compared with dizygotic twins of psychotic probands; and lastly, in the case of schizophrenia, from a few pairs of monozygotic twins reared apart, and interesting recent studies using adoptions (Gottesman and Shields, 1972). In the case of the depressive psychoses there is some evidence of at least partially different genetic factors in bipolar manic depressive psychosis and unipolar endogenous depression without mania (Angst and Perris, 1972). However, the dictum that one gene can have many effects and that a syndrome can be caused by different genes is particularly true for psychiatry. In patients with schizophrenia the risk that their sibs and their children will be similarly affected is about 10%. It thus lies in between that in high risk genetic disease (usually 25 to 50%) and low risk genetic disease (where it is usually not more than about 5 %). In manic depressive psychosis the morbid risk is usually higher than in schizophrenia, rising to about 20% for affective disorder in the first degree relatives of bipolar cases. Despite the higher morbid risk for relatives and the increased suicide risk for patients, the affective psychoses are best regarded as being less detrimental than schizophrenia. Schizophrenia generally has an earlier onset and, despite advances in treatment, is still liable to run a chronic course; and there is a greater reduction in fertility. But the illnesses in both groups can vary widely in severity.
TL;DR: The rates of mutation in germ cells are the principal determinant of the incidence of genetically predisposed individuals, whereas the rate in somatic cells is the principaleterminant in those not sopredisposed.
Abstract: The risk of cancer can be increased by both genetic predisposition and environmental exposure. A common mechanism, mutation, may be involved in both. The rate of mutation in germ cells is the principal determinant of the incidence of genetically predisposed individuals, whereas the rate in somatic cells is the principal determinant in those not so predisposed. Many environmental carcinogens produce their effects via increased somatic mutation rates. The individuals of a population may be classified according to the operation of genetic predisposition, exposure to environmental carcinogens (mutagens), both, or neither. This last group reflects "background" somatic mutation rates.