Mice heterozygous for the varitint-waddler spontaneous mutation (Mcoln3Va) are deaf and show circling behavior, head-tossing, and hyperactivity. Heterozygotes circle somewhat less than some of the other circling mutants. Their coats are variegated with patches of normal-colored, diluted, and white fur. Homozygotes show more intense behavioral abnormalities than heterozygotes, and their coats are white, except for small patches of unaltered color near the ears and base of the tail. The pathological changes in heterozygotes include degeneration of the organ of Corti, stria vascularis, spiral ganglion, saccular macula, cristae ampullares, and vestibular ganglion. In homozygotes the degenerative changes are more severe and also include the utricular macula. Viability of heterozygotes is nearly normal, but fertility is reduced. Mortality is very high in homozygotes, and very few of the survivors are fertile. Compound heterozygotes for the two alleles (Mcoln3Va-J
Mice heterozygous for the varitint-waddler spontaneous mutation (Mcoln3Va) are deaf and show circling behavior, head-tossing, and hyperactivity. Heterozygotes circle somewhat less than some of the other circling mutants. Their coats are variegated with patches of normal-colored, diluted, and white fur. Homozygotes show more intense behavioral abnormalities than heterozygotes, and their coats are white, except for small patches of unaltered color near the ears and base of the tail. The pathological changes in heterozygotes include degeneration of the organ of Corti, stria vascularis, spiral ganglion, saccular macula, cristae ampullares, and vestibular ganglion. In homozygotes the degenerative changes are more severe and also include the utricular macula. Viability of heterozygotes is nearly normal, but fertility is reduced. Mortality is very high in homozygotes, and very few of the survivors are fertile. Compound heterozygotes for the two alleles (Mcoln3Va-J/Mcoln3Va) are similar to Mcoln3Va-J/Mcoln3Va-J mice but are smaller with more white spotting and abnormal behavior. They are deaf and circle vigorously. Viability and fertility of Mcoln3Va-J/Mcoln3Va mice are considerably reduced.
The varitant waddler mutation arose spontaneously at The Jackson Laboratory in 1942 and was first identified in the backcross offspring of (C57 black x C57 brown)F1 female x C57 black male. Following the Bar Harbor fire of 1947 the veritant waddler mutation was returned to The Jackson Laboratory in 1950 from T. C. Carter at Edinburgh in a linkage testing stock called E1 and containing rex, Danforth's short tail, and varitint waddler. At some later timepoint this mutation was backcrossed onto the C57BL/6J background by Dr. Elizabeth Russell. This congenic strain reached N27 in 1968, N62 in 1978, and in 1980 embryos were generated for cryopreservation from C57BL/6J females bred to heterozygous males at generation N66. In 2008 the cryopreserved bankstock was replenished via in vitro fertilization using C57BL/6J females and cryo-recovered heterozygous males at generation N67p.
|Allele Name||varitint waddler|
|Allele Synonym(s)||TRPML3Va; Va|
|Gene Symbol and Name||Mcoln3, mucolipin 3|
|Gene Synonym(s)||6720490O21Rik; 6720490O21Rik; RIKEN cDNA 6720490O21 gene; TRP-ML3; TRPML3; Va; Va; varitint-waddler; varitint-waddler|
|Strain of Origin||(C57BL x C57BR)F1|
|Molecular Note||The mutation in the Va mouse is a G-to-C transversion at nucleotide 1255 within exon 10. This results in a change from alanine to proline at amino acid 419 which is in the fifth transmembrane domain.|
|Please inquire about possible genotypes.|
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided,
their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of
each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders
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