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Biomedical subjects

M E Wallace

Publications and source records attributed to M E Wallace.

53 records · Page 3Linked to original sources
PubMedDate not supplied

Variant of type B blood in an El Salvador family. Expression of a variant B gene enhanced by the presence of an A2 gene.

A variant of type B blood was found in three members of a family from El Salvador. In two members, both genotype BO, the blood and saliva had the characteristics of the phenotype Be1 . In the third member, genotype A2B, the red cell B antigen was stronger than in his BO genotype relatives. Thus, in this family, the presence of the A2 gene appeared to enhance the expression of the B gene.

ABO Blood-Group System↗
PubMedDate not supplied

Continued high incidence of mutants in a Peruvian population of mice.

A second trapping of wild mice from two sites in a Peruvian river valley confirms the unprecedented high mutant incidence established by a previous trapping. It also shows that the population may be localized. The new mutants are different from those found in the first trapping, and thus indicate a continued source of mutagenic activity either external or within the gene pool of the population. A third study is underway.

Animals↗
PubMedDate not supplied

A tiger mouse and relatives. Variants caused by an activated transposable element?

In a laboratory-bred population of wild Peruvian house mice, one male had an excessive rate of non-pairing of the X and Y chromosomes. After crossing him with laboratory stock mice, a mouse of very unusual phenotype appeared from a yellow (AyA) mother. He was yellow with black dorsal stripes; hence Tiger. He was mated to many females, and inbred F2 and F3 generations were raised. There were no more tiger phenotypes, but his F1 contained an excess of black-and-tans over yellows, showing him to be a gonosomic mosaic Ayat/atat; the homozygous cell line probably arose from the heterozygous one. The mitotic karyotype was normal. Some of Tiger's mates were of known allozyme types and their progeny were scored. The allozyme segregations were normal, except at the Es-3 locus (esterase-3), for which Tiger was typed as homozygous. Several unusual events among Tiger's close relatives included a mutation to an unstable pattern mutant, three probable translocations, and several cases of somatic defect. All unusual mice derived from Tiger's yellow mother, whose genome was one-quarter Peruvian. Yellow is associated with an ecotropic murine leukemia virus. The Peru genome is characterized by a high occurrence of mutation and aberrant karyotypes. It is suggested that something from the Peru genome in Tiger's mother caused instability of the DNA sequence associated with yellow, with related disturbance at different locations thereafter. The nature of this instability, and of the Peru genome, is discussed.

Animals↗
PubMedDate not supplied

An inherited agent of mutation with chromosome damage in wild mice.

A population of wild mice in Peru was sampled three times over a period of 20 years. Inbreeding from each sample has shown the population to carry an unusually high frequency of visible mutants and nestling lethals. Preliminary evidence of chromosomal damage suggests an inherited tendency to some form of genetic instability.

Alleles↗
PubMedDate not supplied

Chubby: a new autosomal recessive skeletal mutation producing dwarfism in the mouse.

The chubby (cby) mutant is a previously undescribed skeletal mutation in the mouse. Breeding experiments showed that cby is a recessive mutant with complete viability, full penetrance and fertility in both sexes. Tests for allelism showed that the cby mutant is genetically unlike the somewhat similar mutants, stumpy (stm), pituitary dwarf (dw), spondylometaphyseal chondrodysplasia (smc), brachymorphic (bm), and achondroplasia (cn). The defects seem to occur mainly in growth cartilage. Microradiography revealed increased height of the epiphyseal growth plate and irregular bone trabeculae in the metaphysis. Light microscopy showed disturbed columnar organization of proliferative chondrocytes and pronounced signs of cellular disintegration. The hypertrophic zone, however, contained normally shaped chondrocytes arranged in regular columns. In spite of the normal cellular hypertrophy the pattern of cartilage mineralization was disturbed. The electron microscopy studies revealed very high amounts of matrix vesicles and numerous larger membrane coated structures in the extracellular matrix. Biochemical analysis of the affected growth cartilage revealed a slightly modified pattern of proteoglycan subpopulations and considerably longer chondroitin sulfate chains when compared with controls. From the present study it can be concluded that the cby mutant is a genetically and morphologically distinct condition with characteristic, somewhat rickets-like stigmata. The pathogenetic mechanism underlying the condition remains to be clarified.

Animals↗