These mice carry a spontaneous mutation at the Dnah11 locus characterized by inverse placement of the visceral and thoracic organs, anomalous positioning and interactions of blood vessels, and abnormal shape of organs and blood vessels.Read More +
DNAHC11 is important for developmental control of organ positioning in the left-right axis such that homozygosity for the situs inversus viscerum (iv) mutant allele can result not only in inverse placement of the visceral and thoracic organs, but also in anomalous positioning and interactions of blood vessels (including the hepatic portal, inferior vena cava, and azygos vein) and modified shape of organs and blood vessels, including abnormal lobation of lungs or liver. Approximately 50% of mice homozygous for Dnah11iv have situs inversus, and the likelihood of situs inversus is not impacted by whether the homozygous parent has situs inversus. This indicates that wild type Dnah11 instructs left-right asymmetry, and in the absence of functional Dnah11 the direction of this asymmetry is random. Heterotaxia is found in less than half of homozygotes and occurs equally in those that do and do not have situs inversus. While heterotaxia may be impacted by genetic background, the incidence of situs inversus has not shown this variation. Situs inversus can be identified shortly after birth, until the skin thickens at approximately day 5, by viewing the location of the milk-filled stomach through the skin. Homozygotes are generally viable and do breed, although poorreproductive performance with a high rate of resorption has been reported by Brown et al. (Development 1989). Some premature death has been reported and may be caused by deformities of the cardiac loop. (Hummel and Chapman, 1959; Layton 1976; Brown et al., 1989; Icardo and Colvee, 2001.)
In 1956 Katherine Hummel reported finding situs inversus viscerum (iv) in 6 out of 42 mice in the F3 generation from a cross of a C3H/e female with an my/my male. This my/my male was likely from the line that was then being inbred to become My/Hu (see stock#000265). The my mutation was bred out of this new mutant stock and in 1972 the iv-bearing stock was transferred from Katherine Hummel to Robert Collins, both at The Jackson Laboratory. Collins began inbreeding from the outbred stock in 1975 and this generated the strain SI/Col which is homozygous for Dnah11iv, a, and Tyrp1b. SI/Col reached F62 in 1994 and F88 in 2004. Embryos were generated for cyropreservation from homozygous parents in 1997, when the strain was at generation F73, and again in 2007, when the strain was at generation F94.
|Gene Symbol and Name||Tyrp1, tyrosinase-related protein 1|
|Strain of Origin||old mutant of the mouse fancy|
|Molecular Note||A G-to-A transition point mutation at position 329 was shown by revertant analysis to be responsible for the mutant phenotype seen in the brown mutant. This mutation changes cysteine to tyrosine at position 110 (p.C110Y) in the encoded protein. Three other point mutations in the brown sequence were identified, but do not contribute to the mutant phenotype.|
|Allele Name||situs inversus viscerum|
|Gene Symbol and Name||Dnah11, dynein, axonemal, heavy chain 11|
|Strain of Origin||(C3HeB/Fe x STOCK Frem2my)F3|
|Molecular Note||A G-to-A transition mutation led to a substitution of glutamate with lysine at position 2271 (p.E2271K)in the encoded protein. This residue is located between the second and third P-loop motifs, a highly conserved region that constitutes the motor domain.|
When using the situs inversus viscerum mouse strain in a publication, please include JAX stock #001045 in your Materials and Methods section.
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