scholarly journals The susceptibility to cortisone-induced cleft palate of recombinant inbred strains of mice: lack of association with the H-2 haplotype

1981 ◽  
Vol 38 (3) ◽  
pp. 327-331 ◽  
Author(s):  
M. Vekemans ◽  
B. A. Taylor ◽  
F. C. Fraser

SUMMARYRecombinant-inbred (RI) strains of mice derived from the cross of strains C57BL/6J and DBA/2J were used to study the inheritance of susceptibility to cortisone-induced cleft palate. Most of the RI strains could be classified as either resistant, like C57BL/6J, or susceptible, like DBA/2J, suggesting the segregation of a major locus. An association with the phosphoglucomutase-1 locus (Pgm-1) on Chromosome 5 was observed. There was no association with the H-2 locus on Chromosome 17 as had been reported in previous studies utilizing different strains. We conclude that susceptibility to cortisone-induced cleft palate may be determined by different loci depending on the strains studied.

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 ◽  
...  

2008 ◽  
Vol 33 (8) ◽  
pp. 693-707 ◽  
Author(s):  
D. J. Reiner ◽  
T. A. Jan ◽  
J. D. Boughter ◽  
C.-X. Li ◽  
L. Lu ◽  
...  

1987 ◽  
Vol 49 (1) ◽  
pp. 43-49 ◽  
Author(s):  
I. Jill Karolyi ◽  
Sharon Liu ◽  
Robert P. Erickson

SummaryIn a search for genetic differences in susceptibility to cleft lip with or without cleft palate [CL(P)], congenic and recombinant inbred strains of mice were treated with phenytoin or control injections. Of six loci tested, five were found to affect susceptibility to phenytoin-induced and/or sporadic CL(P): (1) the major histocompatibility locus, H-2; (2) the locus controlling β2-microglobulin, B2m; (3) a locus controlling β-glucuronidase, Gus; (4) the locus controlling N-acetyl transferase, Nat; and (5) the locus for brown pigmentation, b. B2m and Gus only affected the sporadic incidence of CL(P), while the b locus only affected phenytoin-induced incidence of CL(P). Three of these loci are also known to affect glucocorticoid-induced isolated cleft palate (CP), but different alleles of the loci are involved. Phenytoin did not affect levels of adenosine 3′,5′-cyclic monophosphate (cAMP) in palates and tongues of day 15 fetuses. A comparison of glucocorticoid receptor parameters with the incidence of phenytoin-induced CL(P) found no correlation.


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