Reduction in Productivity and Recessive Lethal Mutation Following X-Irradiation CF Female Drosophila melanogaster

1952 ◽  
Vol 86 (831) ◽  
pp. 391-398 ◽  
Author(s):  
R. C. King
Keyword(s):  
Drosophila Melanogaster ◽  
Lethal Mutation ◽  
Recessive Lethal ◽  
Recessive Lethal Mutation ◽  
X Irradiation

scholarly journals THE INTERCELLULAR DISTRIBUTION OF MUTATIONS INDUCED IN OOCYTES OF DROSOPHILA MELANOGASTER BY CHEMICAL AND PHYSICAL MUTAGENS

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 151-160
Author(s):  
H Traut
Keyword(s):  
Drosophila Melanogaster ◽  
Mitomycin C ◽  
Mutation Frequency ◽  
Lethal Mutation ◽  
X Rays ◽  
Mutagenic Treatment ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
X Irradiation

ABSTRACT When females of Drosophila melanogaster are treated with chemical or physical mutagens, not only in one but also in both of the two homologous X chromosomes of a given oocyte, a recessive sex-linked lethal mutation may be induced. A method is described that discriminates between such "single" and "double mutations." A theory is developed to show how a comparison between the expected and the observed frequency of double mutations yields an indication of the intercellular distribution (random or nonrandom) of recessive lethal mutations induced by mutagenic agents in oocytes and, consequently, of the distribution (homogeneous or nonhomogeneous) of those agents.—Three agents were tested: FUdR (12.5, 50.0 and 81.0,μg/ml), mitomycin C (130.0 μg/ml) and X rays (2000 R, 150 kV). After FUdR feeding, no increase in the mutation frequency usually observed in D. melanogaster without mutagenic treatment was obtained (u=0.13%, namely three single mutations among 2332 chromosomes tested). After mitomycin C feeding, 104. single and three double mutations were obtained. All of the 50 mutations observed after X irradiation were single mutations. The results obtained in the mitomycin C and radiation experiments favor the assumption of a random intercellular distribution of recessive lethal mutations induced by these two agents in oocytes of D. melanogaster. Reasons are discussed why for other types of mutagenic agents nonrandom distributions may be observed with our technique.

scholarly journals HOMOEOSIS IN DROSOPHILA: A NEW ENHANCER OF POLYCOMB AND RELATED HOMOEOTIC MUTATIONS

Genetics ◽  
1983 ◽  
Vol 105 (2) ◽  
pp. 357-370
Author(s):  
Takashi Sato ◽  
Michael A Russell ◽  
R E Denell
Keyword(s):  
Drosophila Melanogaster ◽  
Gene Product ◽  
Point Mutations ◽  
Lethal Mutation ◽  
Chromosome 2 ◽  
Gene Complex ◽  
Recessive Lethal ◽  
Recessive Lethal Mutation ◽  
Sex Comb

ABSTRACT A new recessive lethal mutation in Drosophila melanogaster, Enhancer of Polycomb [E(Pc)], and chromosomal deficiencies lacking this locus act as dominant enhancers of the Polycomb mutant syndrome in adults. Thus, although E(Pc)/+ flies are phenotypically normal, this locus is haplo-abnormal with respect to its effect on the Polycomb phenotype. Recombinational and deficiency mapping localize the E(Pc) locus on chromosome 2 proximally and very closely linked (∼0.1 map unit) to the engrailed gene. E(Pc) enhances the expression of all Polycomb point mutations examined including that of a deficiency, indicating that this interaction does not depend on the presence of an altered Polycomb gene product. In several respects the mutations extra sex comb, lethal(4)29, and Polycomblike resemble those at the Polycomb locus. In the presence of E(Pc), recessive alleles of extra sex comb and lethal(4)29 are rendered slightly pseudodominant, and the homoeotic effects of Polycomblike heterozygotes are also enhanced. However, E(Pc) does not affect the expression of dominant mutations within the Bithorax gene complex (Cbx) or Antennapedia gene complex (AntpNs, Antp  73b, Antpscx, AntpEfW15, ScrMsc) which give homoeotic transformations resembling those of the Polycomb syndrome. Available evidence from the study of adult phenotypes suggests that mutations at E(Pc) do not result in homoeotic changes directly but instead modify the expression of a specific set of functionally related homoeotic variants.

scholarly journals GENETIC EFFECTS OF ACUTE SPERMATOGONIAL X-IRRADIATION OF THE LABORATORY RAT

Genetics ◽  
1977 ◽  
Vol 85 (2) ◽  
pp. 309-317
Author(s):  
J R Chambers ◽  
A B Chapman
Keyword(s):  
Genetic Effects ◽  
Lethal Mutation ◽  
Mutation Rates ◽  
Recessive Mutation ◽  
Significant Other ◽  
Recessive Lethal ◽  
Recessive Lethal Mutation ◽  
Dominant Lethal Mutation ◽  
X Irradiation ◽  
Rats And Mice

ABSTRACT The genetic effects of one generation of spermatogonial X-irradiation in rats, by a single dose of 600r in one experiment and by a fractionated dose of 450r in another, were measured in three generations of their descendants. Estimates of dominant lethal mutation rates—(2 to 3) × 10 -4/gamete/r—from litter size differences between irradiated and nonirradiated stock were consistent with previous estimates from rats and mice. Similar consistency was found for estimates of sex-linked recessive mutation rates—(1 to 2) × 10-4 chromosome/r—from male proportions within strains; however, when measured in crossbreds the proportion of males was higher in the irradiated than in the nonirradiated lines. This inconsistency in results is in keeping with the contradictory results reported for recessive sex-linked lethal mutation rates in mice. The effects used to estimate recessive lethal mutation rates which were unusually high—(2 to 14) × 10-4/gamete/r—were not significant. Other factors that could have contributed to the observed effects are postulated.

Normale Entwicklung der Fliege Drosophila in Niederfrequenten Magnetfeldern / Normal Development of the Fruitfly Drosophila in VLF Magnetic Fields

1977 ◽  
Vol 32 (1-2) ◽  
pp. 125-132 ◽  
Author(s):  
Karl Georg Götz ◽  
Simon Götz
Keyword(s):  
Drosophila Melanogaster ◽  
Magnetic Fields ◽  
Normal Development ◽  
Control Group ◽  
Wild Type ◽  
Recessive Lethal ◽  
Recessive Lethal Mutation ◽  
Observed Damage ◽  
Mutagenic Effects ◽  
Pulsed Fields

Abstract Attempts to substantiate irreversible actions of a variety of magnetic fields on the fruitfly, Drosophila melanogaster, have been successful and unsuccessful in about equal numbers. The most conspicuous mutagenic effects apparently induced by pulsed H F-fields failed to appear under continuous electromagnetic irradiation. This seems to correlate the observed damage with the VLF-components of the pulsed fields. The present investigation is motivated by the occurrence of these components both in the atmosphere and in the vicinity of electrical appliances. A strain of normally viable wild type males and subnormally viable Attached-X γ ω females was used in which the yield, and the sex ratio, of the progeny indicate, respectively, the extent of developmental damage and of sex-linked recessive lethal mutation induced by the exposure to detrimental conditions. Evaluation of 73,800 flies from subsequent generations of a control group and two test groups raised in steady, or rotating, homogeneous 9.6 kHz magnetic fields of about 2.5 G did not reveal any development of hereditare load in the test groups.

scholarly journals The histology and self-differentiating capacity of the abnormal cartilage in a new lethal mutation in the rat ( Rattus norvegicus )

1939 ◽  
Vol 127 (847) ◽  
pp. 257-277 ◽  
Keyword(s):  
Rattus Norvegicus ◽  
Physiological Condition ◽  
The Body ◽  
Lethal Mutation ◽  
The Other ◽  
Recessive Lethal ◽  
Recessive Lethal Mutation ◽  
Previous Communication

In a previous communication (Grüneberg 1938), a new recessive lethal mutation has been described in the rat which produces a variety of ano­malies in various parts of the body. It was shown that all these deviations from the normal, including those disturbances which lead to the death of the lethals, are ultimately caused by an anomaly of the cartilage. All the other manifestations of the gene are therefore of a secondary nature. The histology of the abnormal cartilage will be described in the first part of this paper. For the anomaly of the cartilage, no obvious cause could be discovered by morphological means. It was pointed out, however, that this does not necessarily mean that the gene acts primarily on the cartilage. There remained the possibility that the cartilage itself was only secondarily affected by some general physiological condition of the body which pro­duced no other visible changes.

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