PubMed Health⌕ Search

Biomedical subjects

M N Nesbitt

Publications and source records attributed to M N Nesbitt.

At least 37 records · Page 2Linked to original sources

Susceptibility to urethan-induced pulmonary adenomas between A/J and C57BL/6J mice: use of AXB and BXA recombinant inbred lines indicating a three-locus genetic model.

For insight into the number of genes governing differential susceptibility such as in mice of the inbred strain A/J (A) highly susceptible to the induction of pulmonary adenomas by urethan in comparison to resistant strain C57BL/6J (B6) mice, tumor induction was studied in the AXB and BXA series of recombinant inbred (RI) strains derived respectively from A female X B6 male and B6 female X A male ancestral lines. Mice from 46 of these lines were given injections with 1 mg urethan/g (body wt), and the tumor number was assessed 4 months later. Lung tumor multiplicity for several RI lines was independently characterized in the Boulder, CO, and Montreal laboratories, and very similar numbers were obtained. Most lines had multiplicities intermediate to those of the progenitor strains, clearly indicating that more than a single gene accounted for the differences in lung tumor susceptibility between A and B6. The tumor incidence and multiplicity data fit very closely to what would be expected under a three-locus model, and we designated these genes "Pas" for pulmonary adenoma susceptibility. One locus called "Pas-1" had an effect on tumor multiplicity greater than that of the other loci.

Adenoma↗

Genetic control of macrophage activation for killing of extracellular targets.

Activated peritoneal macrophages from Corynebacterium parvum-treated mice of most inbred strains, including C57BL/6J (B), are cytotoxic to adherent 1023 sarcoma target cells as well as to larvae of Schistosoma mansoni. Macrophages from A/J (A) strain mice, on the other hand, are defective in this function. Segregation analysis of these two traits was compatible with the hypothesis that effective activation is, in each case, controlled by a single, dominant, autosomal gene. Typing of individual animals of the segregating backcross progeny and of AXB/BXA recombinant inbred strains for the expression of macrophage activation for tumoricidal and schistosomulicidal activity indicates that the genetic control of these two traits is closely linked or identical.

Animals↗

Regulation of resistance to leprosy by chromosome 1 locus in the mouse.

Mice of different inbred strains vary in their resistance to intravenous infection with Mycobacterium lepraemurium (MLM). The mean survival time of MLM-infected A/J and DBA/2 mice is significantly longer than that of similarly infected C57BL/6 and BALB/c mice. The typing of AXB/BXA recombinant inbred strains (A = A/J,B = C57BL/6) for the trait of relative resistance/susceptibility to MLM revealed a perfect match with the strain distribution pattern of resistance/susceptibility to Mycobacterium bovis (BCG), the trait which is controlled by the Bcg (Ity, Lsh) locus on chromosome 1. The control, by this gene, of response to MLM was further confirmed by the demonstration that BALB/c-Bcgr congenic mice, which carry the DBA/2-derived Bcgr (resistant) allele on chromosome 1, are significantly more resistant to MLM infection than their BALB/c (Bcgs, susceptible) counterparts.

Animals↗

Chromosomal mapping of murine c-fes and c-src genes.

The murine homologs of two viral oncogenes associated with tyrosine-specific kinase activity have been assigned to different loci in the mouse genome. The segregation of restriction site polymorphisms, as detected by probes that are specific for endogenous c-fes and c-src sequences, was followed in the DNA of recombinant inbred strains. The c-fes gene was mapped to the proximal portion of chromosome 7, very close to the Gpi-1 locus, whereas c-src was linked to the Psp locus on the distal half of chromosome 2.

Alleles↗

Chromosomal mapping of the mink cell focus-inducing and xenotropic env gene family in the mouse.

Chromosomal locations of members of the xenotropic-related env gene family in the mouse genome have been determined. Endonuclease restriction site polymorphisms detected by molecular hybridization were used to study the inheritance of mink cell-focus inducing and xenotropic env gene-related sequences in recombinant inbred strains of mice. Some of the endogenous env sequences appear to be closely linked to genes determining leukemia virus induction and to genes involved in the immune response, such as the heavy and light chains of the immunoglobulin molecules or allotypic determinants on B and T lymphocytes. The use of probes that detect restriction fragment length polymorphisms in a small family of dispersed sequences promises to yield a large number of markers that can be used together with recombinant inbred strains for efficient mapping of the mouse genome.

Animals↗

Isoenzyme pattern of HPRT in murine erythrocytes: control by an autosomal locus.

A locus on chromosome 7 controls the electrophoretic mobility of hypoxanthine phosphoribosyltransferase (HPRT) isoenzymes in mouse erythrocytes, but not in several other tissues. This locus is designated Hma (HPRT mobility alteration) and maps very close to the Hbb locus. The A/J, AKR/J, AU/SsJ, BALB/cJ, CBA/J, C3H/HeJ, DBA/2J, LP/J, RF/J, SEA/Gn, ST/BJ, and 129/J strains and our population of Swiss albino mice have the Hmaa allele. Hmaa is dominant to Hmab, which is found in the C57BL/6J, C57BL/KsJ, C58/J, LT/Sv, MA/MyJ, SJL/J, and SWR/J strains. Both alleles are found in feral Mus musculus. In our conditions, homozygotes for Hmab have two major bands of HPRT activity after electrophoresis of extracts of erythrocytes and of other tissues. Heterozygotes and Hmaa homozygotes have three bands in erythrocyte extracts but two band in other tissues.

Alleles↗

Behavior in chimeric mice combining differently behaving strains.

A/J and C57BL/6J mice behave differently in tests for alcohol preference, open-field activity, defecation in the open field, cricket attacking, and rope climbing. Chimeric mice, i.e., mice containing both A/J cells and C57BL/6J cells, were constructed and tested for these behaviors. Patterns of behavior among A/J in equilibrium with C57BL/6J chimeras are such as to suggest that none of these behavior differences is controlled by a single cell or clone and that the same cell population that gives rise to the strain difference in alcohol preference also gives rise to the differences in open-field activity and defecation, while separate cell populations control cricket killing and rope climbing.

Alcohol Drinking↗

Colinearity in the mouse genome: a study of chromosome 2.

The cytologic positions (determined by G-banding) of the breakpoints on mouse chromosome 2 of a series of ten reciprocal translocations were compared with their most probable genetic positions on the linkage map, as determined by studies on recombination with known chromosome 2 (= linkage group V) markers. The most probable proximaldistal orders of the genetic and cytologic breakpoints were found to be the same; i.e., the two sets of breakpoints were colinear. However, there was no close correspondence between these two measures of the distance apart of adjacent breakpoints, since some translocation breaks which were well separated in G-band positions seemed close together in terms of the linkage map, and vice versa. This helps to confirm LYON'S conclusion that in certain mouse chromosomes, including No. 2, the distribution of chiasmata is nonrandom.

Animals↗

Chromosome banding patterns in preimplantation mouse embryos.

The chromosomes of first cleavage mouse embryos show the same banding patterns after quinacrine mustard staining as do chromosomes of differentiated mouse cells. Whatever feature of chromosome structure the banding pattern reveals thus appears not to be altered during development and differentiation.

Animals↗

Cytological identification of the chromosomes involved in Searle's translocation and the location of the centromere in the X chromosome of the mouse.

The autosome in Searle's X-autosome translocation has been shown to be chromosome 16. The breakpoint in chromosome 16 is slightly proximal to the middle and in the X is slightly distal to the middle.-Available evidence indicates that either Linkage Group XV or Linkage Group XIX is carried on chromosome 16.-The centromere of the X chromosome is at the spf end of the linkage group.

Animals↗

Genetic control of thymus size in inbred mice.

Differences exist among inbred mouse strains in the size of the thymus relative to overall body size. These differences are controlled by several genes acting in different phases of thymus development. After 50 days of age, there is an approximately 2-fold difference in thymus size between C57BL/6J and AKR/J, and other strains (A/J, DBA/2J, BALB/cJ, CBA/J, C3H/HeJ, 129/J, C57BL/ 10J , MA/ MyJ ). The C57BL/6J and AKR/J mice have the larger thymus, and this characteristic is dominant in F1 animals derived from C57BL/6J and A/J strains. Studies on recombinant inbred strains derived from C57BL/6J and DBA/2J ( BXD strains), and C57BL/6J and A/J ( AXB and BXA strains) indicate that this difference is controlled by alleles at one locus, which we have designated Tsz -1 (thymus size 1). In the immediate postnatal period (0-23 days), while the relative size of the thymus is increasing, the thymus size of C57BL/6J mice is large relative to that of A/J mice, but the A/J character is dominant during this period, and this difference appears to be controlled by two genes.

Age Factors↗