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Publication : Deficiency of serum IgG1 subclass.

First Author  Ito M Year  1989
Journal  Mouse News Lett Volume  84
Pages  95 Mgi Jnum  J:14258
Mgi Id  MGI:62430 Citation  Ito M, et al. (1989) Deficiency of serum IgG1 subclass. Mouse News Lett 84:95
abstractText  Full text of MNL contribution: Research News: c. Deficiency of Serum IgGl subclass. We found mutant mice lacking the serum IgGl subclass in the research stock of the MRL/MPJ-lpr strain (abbreviated MRL/lpr in this report). Serum IgGl subclass levels in 8 month-old MRL/lpr were 0.42-2.5mg/ml, but that of the mutants was undetectable (lower than 0.2ug/ml). In order to demonstrate inheritance of the IgGl deficiency, mating experiments were done using MRL/lpr as a parent strain. The F1 mice showed normal values of serum IgGl subclass described above Three-fourths of the F2 generation mice showed normal levels of IgGl, but a quarter low levels (3.8-11.7ug/ml), although they were not deficient (unexplained at present). These data revealed that the mutant gene is an autosomal recessive gene. The gene related to deficiency of the serum IgGl subclass was tentatively named ggld (gamma globulin 1 deficiency). Linkage analyses were performed using BALB/cA (lpr+ : gg1d+ : Igh-Ca) as partner strain. The Fl was backcrossed with MRL/lpr (lpr : ggld : Igh-Cj), and the backcross progeny (N=107) were typed for IgGl levels (N=107), lymphoproliferation (N=107) and immunoglobulin allotypes (N=63). First, the relation between lpr and ggld was analysed using 107 backcross progeny. The segregating ratio of ggld/ggld-lpr/lpr : ggld/ggld-lpr/+ : ggld/+-lpr/lpr : ggld/+-lpr/+ was 29 : 24 : 25 : 29. These data showed that there was no linkage between the ggld and lpr genes. Next, linkage between ggld and immunoglobulin allotype (Igh-C) was studied. Sixty three BC progeny were segregated into ggld/ggld-a/j : ggld/ggld-j/j : ggld/+-a/j : ggld/+-j/j = 11 : 18 : 15 : 19. These data showed that there was no linkage between the ggld and Igh-C genes, and strongly suggested that the deficiency of serum IgGl is caused by a regulatory phenomenon in the process of IgGl expression, and not by a structural gene. At present, we are breeding three kinds of ggld congenic strains: MRL/n-ggld, BALB/cA-ggld and C57BL/6N-ggld. (M. Ito, K. Hioki and H. Katoh)
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