First Author | Kojima A | Year | 1988 |
Journal | Mouse News Lett | Volume | 80 |
Pages | 147 | Mgi Jnum | J:25317 |
Mgi Id | MGI:73049 | Citation | Kojima A (1988) New mutant: Sublingual gland differentiation arrest in the NFS/N subline. Mouse News Lett 80:147 |
abstractText | Full text of MNL contribution: New Mutant: Sublingual gland differentiation arrest in the NFS/M subline. In the course of studies on the single dosage effects of the nude gene (Kojima et al., Expl. Cell Biol. 52:107, 1984), we incidentally found that our NFS/N strain mice have the abnormal phenotype in the sublingual glands. The genetic basis for this abnormality (autosomal recessive) was determined by crossing these NFS/N mice to the BALB/c strain mice of normal phenotype. The normal mouse sublingual glands are predominantly mucous-secreting and composed of acini containing tall pyramidal cells with basally located nuclei and pale to blue-staining cytoplasm with hematoxylin and eosin. They stain intensely with periodic-acid-Schiff(PAS), Alcian blue or mucicarmine stains. In contrast, the mutant phenotype was characterized by the failure of the acinal cells to differentiate to the mucous-rich cells. Most endopieces consist of acini of Alcian blue-negative cuboidal cells. Normally-staining mucous cells, however, exist singly or in groups in a small number of acini from an early age, and their number apparently increases with age so as to occupy over half of the total acini. The expression of normal phenotype in the mutant mice appears to be a random event occurring at the cellular level. We obtained the NFS/N strain mice, together with a congenic line carrying the nude(nu) gene, in 1981 from the Central Institute for Experimental Animals, Kawasaki (Dr. T. Nomura). This NFS/N and congenic NFS/N-nu strains were originally derived from NIH, U.S.A. (Dr. C. Hansen) at F27 in 1977. The mutant phenotype appears to be fixed in the NFS/NJic subline, maintained in SPF in the Central Institute for Experimental Animals, and was so far confined to it and its congenic nude line among a number of inbred strains of mice, rats and other rodents examined. Interestingly, the other NFS/N I subline available in Japan, derived from NIH in 1977 and maintained in Kyoto Univ., Inst. for Virus Res. (Dr. A. Ishimoto), had the normal sublingual glands. Furthermore, more than ten colonies of wild mice (Prof. K. Moriwaki, National Institute of Genetics, Mishima) had also the wild type sublingual glands. At present, no information is at hand about where the mutation occurred. Since there is no report in mice concerning the mutant phenotype involving the sublingual gland, we provisionally propose sublingual gland differentiation arrest (sld) for this mutation. Based on these findings, we have developed a congenic normal strain to sld by introducing the normal wild gene Ò+Ó derived from a BALB/c mouse into the NFS/NJic strain. This congenic line and other NFS/N lines of normal phenotype (e.g. the Ishimoto's line) will serve controls. |