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Biomedical subjects

M E Wallace

Publications and source records attributed to M E Wallace.

At least 37 records · Page 2Linked to original sources
PubMed1979

An inherited mild middle-aged adiposity in wild mice.

In a warfarin-resistant population of wild mice reared in the laboratory, a dominant gene for adiposity, Ad, was found to segregate. The onset of obesity is at 4--6 months, and adipose mice suffer from hyperinsulinaemia; the sexes differ in penetrance, males having greater penetrance then females. Linkage backcrosses show the gene to be situated on chromosome 7 with about 25% recombination with the closely linked warfarin-resistance genes War, and frizzy, fr. The finding of adipose in two other wild populations also carrying War is discussed as an ecological and physiological problem.

Animal Population Groups↗
PubMed1979

Analysis of genetic control of chylous ascites in ragged mice.

Chylous ascites is a disorder visible as a white fluid in the peritoneal cavity of suckling mice. It is due to inadequate lymphatic drainage from the small intestine. An initial genetic study showed it to be a pleiotropic effect of ragged, Ra. There were four main studies. These involved seven major mutants segregating with ragged. Four of the mutants had no effect on chylous ascites, but two mutants linked with ragged, and one unlinked, showed a complex situation involving enhancement, inhibition, epistacy and other interactions. The overall phenotypic effects which these mutants are known to have do not explain how they produce their interaction with ragged in terms of chylous ascites. The studies also indicate the existence of a single major modifier controlling penetrance and expression, and there is evidence for cumulatively acting minor modifiers. In neonates the male sex is more liable to chylous ascites, and in adults this condition affects fertility and fecundity.

Animals↗
PubMed1979

Studies in mice on the mutagenicity of two contraceptive drugs.

An experiment is described which tests for visible and invisible mutants in mice treated with four different doses each of the contraceptives Gynanovlar and Lyndiol. The results show that there is no reason to suppose that either substance has an appreciable mutagenic effect, expressed as an increase of antenatal and postnatal lethals or visibles. The substrain CBA/CagCam, used throughout, has an incidence of 0.27% of singly occurring abnormalities, mainly of the appendicular skeleton, which distinguishes it from the parent CBA strain and its axial variation described by Gruneberg (1963).

Abnormalities, Drug-Induced↗
PubMed1979

Crinkly-tail, a mild skeletal mutant in the mouse.

Crinkly-tail, cy, is a new recessive mutant with imperfect penetrance, in chromosome 4 of the mouse. The only abnormality is in the shape of the vertebrae for one, more rarely two, lengths of the region C9 to C14. This is expressed briefly in the 11-day-old embryo as a duplicated tail gut. None of the mechanisms operating in most of the 20 known tail mutants in the mouse operates in crinkly-tail. The defect is probably due to misallocation of the tissue derived from the primitive streak.

Animals↗
PubMed1978

Genetics of warfarin-resistance in house mice of three separate localities.

Mice from Loughborough and Nottingham were obtained in order to compare the inheritance of warfarin resistance in these populations with that established for a Cambridge population (Wallace & MacSwiney, 1976). Using the same breeding programme and warfarin testing technique, it is established that resistance in the new areas is, as in the Cambridge area, controlled by the major resistance gene, War, in chromosome 7, with penetrance affected by sex and modifiers. In addition, survival differences in males of different ages strongly suggests that War+ has less penetrance with age. Penetrance differences between the experiments establishes that wild populations differ in their modifier complex and that more than one modifier, probably several, exist. Questions are posed as to the adaptive significance of the phenomena, and the way in which they work, in the patchwork of warfarin baited and unbaited areas in this country.

Animals↗
PubMed1978

A new type of chondrodystrophic mutant in the mouse.

Stumpy is a new chondrodystrophic mutant in the mouse. The condition is inherited as a fully penetrant Mendelian recessive, and is not allelic with brachymorphic, achondroplasia, or stubby-three similar, previously described mutants. No chromosomal position has yet been assigned to the gene. Phenotypically, stumpy mice are chondrodystrophic dwarfs with all cartilage-formed bones in the skeleton affected. The condition differs from the usual chondrodystrophy described in mice in that proximal elements in the limbs are affected more than distal ones.

Achondroplasia↗
PubMed1976

Hydronephrosis in the mouse: the effects of the short-ear gene, sex and ureteral vascular system.

The short-ear gene in the mouse, se, affects a number of soft tissues; skeletal effects result in reduced body cavities. A high incidence of hydronephrosis in short-ear genotypes has been ascribed to pressure on the lower ureter resulting from crowding of organs in the body cavity. This study concerns the ureteral vascular system as observed in 861 autopsies of mice of varying age, of the three short-ear genotypes, drawn from ten stocks. Incidence and expression of hydronephrosis is greater in short-ear males than in females, and the ratio between the two varies from one stock to another. This study seeks an explanation. Short-ear genotypes have an abnormally high incidence of unusual ureteral veins, hydronephrosis being strongly associated with the more posterior ones. Ureteraonadal and iliac veins. The spermatic vein's more posterior position, compared with the ovarian, is strongly correlated with the sex difference in posterior ureteral venation and thus with the sex difference in incidence of hydronephrosis. Stocks are compared according to the amount of selection for fitness of short-ear genotypes; there is a reduced incidence of hydronephrosis with selection, accompanied by fewer posterior ureteral veins. Age also affects hydronephrosis; its expression increases slightly with age, and the male sese progeny of young mothers appear to be particularly prone to hydronephrosis. Three skeletal mutants segregate; of these fidget, fi, causes a type of hydronephrosis differing somewhat from that caused by se.

Age Factors↗
PubMed1976

A major gene controlling warfarin-resistance in the house mouse.

The spread of a "cream" mutant in a wild population of house mice is reported. The hypothesis that the gene responsible for the colour, extreme chinchilla, ce, has spread because of linkage with a major gene for warfarin-resistance, is tested by a linkage backcross. The results prove that a major gene does exist, that it is very closely linked with frizzy, fr, in chromosome 7, which in turn is linked with ce, that it is fully dominant in females at 4 months of age, and that its partial dominance in males is under the control of modifiers. The symbol War is proposed for the gene. Its position in chromosome 7 is analagous with the position of the resistant gene, Rw2, in the rat in the analagous chromosome. The adaptive significance of the finding is discussed, as also are reports of certain other mutants in wild populations of mice.

Animals↗
PubMed1976

Inherited resistance to Corynebacterium kutscheri in mice.

An analysis of the factors responsible for inherited resistance to Corynebacterium kutscheri was undertaken. Various inbred mouse strains were examined; these included the Swiss Lynch and C57Bl/l mice, their F1 and F2 progeny, and the progeny of the F1 backcrossed to each parent strain. Two modes of inherited resistance are described. An examination suggested that resistance as measured by the mean lethal dose of C. kutscheri was under polygenic control and was inherited continuously. However, the efficiency with which C. kutscheri was eliminated by the mononuclear phagocyte cells of the liver over 3 days differed markedly among strains. A genetic analysis of this mononuclear phagocyte microbicidal efficiency (MPME) in Swiss Lynch and C57Bl/6 mice was undertaken. The trait, MPME, was present, but did not segregate, in the F1 progeny or in the progeny of the backcross to the resistant C57Bl/6 parent; this was clear evidence of dominance. Moreover, MPME segregated in a ratio of 1:1 in the progeny of the backcross to the sensitive Swiss Lynch parent and in a ratio of 3:1 in the F2 progeny. It was concluded that MPME was inherited discontinuously and was controlled by a single dominant autosomal gene (or closely linked group); the recessive allele was assigned the gene symbol ack. Linkage experiments showed there to be no association between the ack locus and any of the immune-response genes.

Animals↗
PubMed1976

Effects of stress due to deprivation and transport in different genotypes of house mouse.

The importance of various stress factors involved in boxing and transit of wild and laboratory mice on a 28 hour journey was studied. Transference from laboratory cage to transit box alone caused weight loss; under the best conditions the laboratory mice lost 5% of their initial weight and wild ones 8%. Deprivation of food resulted in absolute loss of weight; from this death ensued when 20% of initial weight was lost: the smaller wild mice died sooner than the larger laboratory ones. Water deprivation resulted in retarding recovery of weight lost; wild mice took longer to recover than laboratory ones. It also caused weight loss and, in conjunction with deprivation of food, poor condition and death. Transit itself affected percentage weight loss and wheat consumption; wild mice were affected differently from laboratory mice in both respects. Genotype is seen to be important not only in controlling initial weight and activity level, but also--and independently of weight--the total food requirement. In the light of these findings current literature giving guidance on shipment of small mammals is shown to be inadequate, and certain recommendations are given.

Animals↗