The effect of population density on the elimination dynamics of a recessive lethal mutation l(2)M167 DTS from experimental populations of Drosophila melanogaster

2005 ◽  
Vol 41 (3) ◽  
pp. 249-255 ◽  
Author(s):  
A. M. Kulikov ◽  
F. Marec ◽  
V. G. Mitrofanov
Keyword(s):  
Drosophila Melanogaster ◽  
Population Density ◽  
Lethal Mutation ◽  
Recessive Lethal ◽  
Recessive Lethal Mutation ◽  
Experimental Populations

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 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.

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.

‘Immobile’ (im), a recessive lethal mutation of Xenopus laevis tadpoles

Development ◽  
1975 ◽  
Vol 34 (2) ◽  
pp. 435-449
Author(s):  
A. Droin ◽  
M. L. Beauchemin
Keyword(s):  
Xenopus Laevis ◽  
Lethal Mutation ◽  
Recessive Lethal ◽  
Recessive Lethal Mutation ◽  
Lower Jaw ◽  
Advanced Stages ◽  
Development Proceeds ◽  
Neurula Stage ◽  
Normal Controls ◽  
Muscular Tissues

‘Immobile’ (im) is a recessive lethal mutation discovered in the F3 of a Xenopus (Xenopus laevis laevis) originating from a mesodermal nucleus of a neurula transplanted into an enucleated egg. The im embryos do not contract after mechanical stimulation nor do they present any spontaneous contraction from the neurula stage onwards. Development proceeds normally during the first days after which deformation of the lower jaw and tail are observed. The im tadpoles die when normal controls are at the feeding stage. Nervous and muscular tissues are histologically normal in the mutant tadpoles; at advanced stages, however, an irregularity in the path of the myofibrils is observed which is especially conspicuous in the electron microscope. Cholinesterases and ATPase are present in the mutant muscles. Parabiosis and chimerae experiments have shown that parabionts and grafts behave according to their own genotype. Cultures of presumptive axial systems with or without ectoderm lead to the conclusion that, first of all, the abnormality is situated in the mesodermal cells and secondly that the first muscular contractions in normal Xenopus laevis are of myogenic origin. The banding pattern of the myofibrils is normal as was shown by obtaining contractions of glycerol extracted im myoblasts with ATP. It seems therefore that in this mutation, the abnormality is situated in the membranous system of the muscular cell, sarcoplasmic reticulum and/or tubular system as is probably the case in the mdg mutation of the mouse.

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