Steel 21 Jackson: a remutation of the KitlSl gene

Richard M. Samples, Patricia F. Ward-Bailey, Leah Rae Donahue, Roderick T. Bronson, and Muriel T. Davisson

Source of Support: The research was supported by NIH/NCRR grant RR01183 to the Mouse Mutant Resources (M.T.Davisson, PI) and Cancer Center Core Grant CA34196.

Mutation (allele) symbol: KitlSl-21J

Mutation (allele) name: steel 21 Jackson

Gene symbol: Kitl

Strain of origin: B10.BR-H2k H2-T18a/SgSnJ

Current strain name: B10.BR-H2k-T18a/SgSnJ- KitlSl-21J/J

Stock #: 006108 (Available as DNA only from the Jackson Laboratory DNA Resource)

Phenotype categories: coat color and belly spotting

Abstract

A spontaneous, dominant coat color mutation that maps to the same region as Kitlsl on Chr 10 has been characterized and named steel 21 Jackson (KitlSl-21J).

Origin and Description

The steel 21 Jackson ( KitlSl-21J) mutation was discovered by Patricia Anne Mosley in a production colony of B10.BR-H2K-T18a/SgSnJ mice (Stock # 000465) on June 20, 2001. Mice heterozygous for this spontaneous, dominant mutation are recognizable by a slightly diluted coat color that also lightens the ears, tail and feet. (See Photo) All affected animals have a belly spot of variable size. (See Photo)

Genetic Analysis

In order to determine the mode of inheritance for this new remutation, two mice carrying the KitlSl-21J mutation were mated to an unrelated C57BL/6J mouse. These matings produced 25 progeny in 3 litters in which 13 were affected and 12 were unaffected, proving that the new mutation is dominant.

Using our standard mapping procedures   a female B10.BR-H2k-T18a/SgSnJ- KitlSl-21J/J mouse was mated to a CAST/Ei male. Three male F1 progeny from this mating were then backcrossed to three +/+ females.These matings produced 25 affected animals of which 21 were used for linkage analysis.

This new Kitl Sl-21J remutation was mapped to Chromosome 10 distal to D10Mit65 at 46 cM (NCBIm34 position 84.1 Mb) showing 9.5% recombination and proximal to D10Mit203 at 60 cM (NCBIm34 position 109.3 Mb) showing 4.7% recombination. KitlSl is positioned at 57 cM (NCBIm34 position 99.9-100.0 Mb) on Chromosome 10. A direct test for allelism was not set up because homozygotes of KitlSl are generally lethal.

Pathology

A routine pathological screen  of 2 homozygous mutant mice and 1 control at 11weeks of age revealed no lesions. Hearing as assessed by auditory brainstem response (ABR)  testing of two homozygous mutants and 2 controls at 4 weeks of age revealed no hearing loss.

The eyes of 2 homozygous mutant mice at 4 weeks of age were tested with an opthalmascope and were determined to be normal.

Acknowledgements

The authors wish to thank Patricia Anne Mosley for the discovery of the mutant, Heping Yu for hearing tests, Norm Hawes for eye examinations, and Coleen Marden for her excellent technical assistance