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.

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 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.

Embryological study of a T/t locus mutation (t w73) affecting trophectoderm development

Development ◽  
1976 ◽  
Vol 36 (2) ◽  
pp. 373-381
Author(s):  
Martha Spiegelman ◽  
Karen Artzt ◽  
Dorothea Bennett
Keyword(s):  
Close Association ◽  
Mouse Embryos ◽  
Embryological Study ◽  
Lethal Mutation ◽  
Recessive Lethal ◽  
Recessive Lethal Mutation ◽  
Ectoplacental Cone ◽  
T Locus

Mouse embryos homozygous for the recessive lethal mutation tw73 show specific defects in trophectoderm shortly after implantation. The trophectoderm and ectoplacental cone fail to form the usual close association with the uterine decidua, and proliferation is markedly reduced. The embryo proper ceases to develop beyond the two-layered stage and degenerates and dies within 5 days of implantation.

Cartilage matrix deficiency (cmd): a new autosomal recessive lethal mutation in the mouse

Development ◽  
1978 ◽  
Vol 43 (1) ◽  
pp. 71-84
Author(s):  
E. Rittenhouse ◽  
L. C. Dunn ◽  
J. Cookingham ◽  
C. Calo ◽  
M. Spiegelman ◽  
...  
Keyword(s):  
Autosomal Recessive ◽  
Spinal Column ◽  
Recessive Gene ◽  
Cartilage Matrix ◽  
Lethal Mutation ◽  
Electron Microscopic ◽  
Human Infants ◽  
Recessive Lethal ◽  
Recessive Lethal Mutation ◽  
Trunk Limbs

A new autosomal recessive lethal mutation in the mouse designated cartilage matrix deficiency (cmd) is described. Homozygotes are dwarfed, and have abnormally short trunk, limbs, tail and snout, as well as a protruding tongue and cleft palate. The abdomen is distended because the foreshortened rib cage and spinal column forces the liver ventrad from its normal location. Histological and electron microscopic study reveals a deficiency of cartilage matrix in tracheal cartilage and in all cartilagenous bones examined. The syndrome closely resembles the rare lethal condition achondrogenesis, found in human infants, which is also believed to be due to an autosomal recessive gene.

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