scholarly journals Paternal inheritance of egg traits in mice: a case of genomic imprinting

1989 ◽  
Vol 54 (3) ◽  
pp. 213-219 ◽  
Author(s):  
S. A. A. Bander ◽  
S. C. Watson ◽  
J. G. M. Shire

SummaryEggs from reciprocal hybrids between the C57BL/6By and BALB/cBy strains were tested for their susceptibility to attack by hyaluronidase and pronase. There were significant reciprocal differences between the F1 females in the responses of their unfertilized eggs to both enzymes. The F1 hybrids from BALB mothers showed the increased susceptibility characteristic of C57BL whilst the F1 hybrids with C57BL mothers were more resistant to both enzymes, like BALB mice. Eggs from the four kinds of reciprocal F2 hybrid females also showed patroclinous patterns of susceptibility. A patroclinous difference was found between reciprocal crosses of the CXBD and CXBE recombinant inbred strains but not in crosses between recombinant inbred strains with similar phenotypes. Cross fostering did not alter the phenotypes of the C57BL and BALB females or those of their reciprocal F1 hybrids. The findings are interpreted in terms of differential genomic imprinting of paternally inherited information. The possible general usefulness of patroclinous differences between reciprocal F1 females in revealing differences in imprinting is noted.

1972 ◽  
Vol 55 (2) ◽  
pp. 415-420 ◽  
Author(s):  
B. E. ELEFTHERIOU ◽  
D. W. BAILEY

SUMMARY Plasma corticosterone levels were determined fluorometrically in mice of two unrelated highly inbred strains, C57BL/6By and BALB/cBy, and in seven of their derived recombinant-inbred strains as well as their F1 hybrid and backcross generations necessary to arrive at a genetic model for plasma corticosterone levels. It was concluded that the simplest genetic model, and one which fits the experimental results, was one which assumed that plasma corticosterone levels are controlled genetically by two loci with the epistatic interaction indicating dependency of pathways of action for the two genes.


2018 ◽  
Vol 9 ◽  
Author(s):  
Megan K. Mulligan ◽  
Wenyuan Zhao ◽  
Morgan Dickerson ◽  
Danny Arends ◽  
Pjotr Prins ◽  
...  

1993 ◽  
Vol 4 (3) ◽  
pp. 148-152 ◽  
Author(s):  
Jian-Long Mu ◽  
J�rgen K. Naggert ◽  
Patsy M. Nishina ◽  
Yin-Chai Cheah ◽  
Beverly Paigen

1984 ◽  
Vol 159 (2) ◽  
pp. 355-364 ◽  
Author(s):  
J Van Snick ◽  
J P Coutelier ◽  
E Van Roost ◽  
J L Guénet

To examine the role of autologous IgG in the induction of murine rheumatoid factors (RF) we have analyzed the allotypic specificity of anti-IgG2a RF in recombinant inbred strains derived from 129/Sv (Igh-1a) and C57BL/6 (Igh-1b) mice. In five of six Igh-1a strains, anti-IgG2a RF reacted with IgG2aa but failed to react with IgG2ab. In contrast, isotype-specific RF, which reacted equally well with a and b allotypes of IgG2a, represented the major RF species in one Igh-1a and all five Igh-1b strains tested. An additional form of RF specific for IgG2ab and not reactive with IgG2aa was detected in one Igh-1b strain. RF specific for a give allotype was thus only found in the presence of that allotype, which strongly suggests the involvement of autologous IgG in the induction of mouse RF synthesis. The specificity of RF was apparently further controlled by genes linked to but different from the Igh-C locus, as indicated by the absence of IgG2aa-specific RF in one of the 6 Igh-1a strains tested. Because this strain, 129XBG, has been shown to express idiotypic markers characteristic of Igh-1b mice, it is likely that the genes, which in the presence of a given allotype induce the production of isotype rather than allotype-specific RF, are identical to those that control the expression of idiotypes. Evidence was also obtained to indicate that Igh-1-linked genes influence the isotypic specificity and the isotype of RF itself: IgA anti-IgG2a predominated in Igh-1a strains and IgM anti-IgG1 in Igh-1b strains. Interestingly enough, total IgA and IgG2a levels also were higher in Igh-1a than in Igh-1b strains.


Sign in / Sign up

Export Citation Format

Share Document