Steel 23 Jackson (KitlSl-23J); a new remutation in the Kitl gene.

Richard M. Samples, Patricia F. Ward-Bailey, Son Yon Karst, 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-23J

Mutation (allele) name: Steel 23 Jackson

Gene symbol: Kitl

Strain of origin: B6Smn.C3H-Faslgld/J

Current strain name: B6Smn(C3)-Fasl<?>KitlSl-23J/J

Stock #:006961 (view JAX® Mice Data Sheet for additional information including Price and Supply Information) NOTE: after 3-2408 available as cryo and DNA only.

Phenotype categories: coat color

Abstract

A spontaneous, dominant coat color mutation that maps to the same region of Chromosome 10 as Kitl has been characterized and named Steel 23 Jackson (KitlSl-23J).

Origin and Description

Mice carrying the new steel 23 Jackson (KitlSl-23J) mutation were discovered by Karrie Willey in a production colony of B6Smn.C3H-Faslgld/J mice (Stock #001021) at the Jackson Laboratory in January 2003. This dominant mutation causes no noticeable difference between heterozygous and homozygous mice. The KitlSl-23J mutation affects the black pigment by diluting the coat color (See Photo) and causes white belly spots, the degree of which varies greatly from mouse to mouse. There may also be white hairs appearing throughout the rest of the coat of KitlSl-23J mice. The colony is at N2 as of August 2, 2007. The two backcrosses may have removed the gld mutation from this strain. The phenotype remains, but gld genotype has not been confirmed.

 

Genetic Analysis

In order to determine the mode of inheritance for this new mutation, a mouse carrying the KitlSl-23J mutation was mated to an unrelated +/+ C57BL/6J mouse. This mating produced 7 litters of which 19 of the progeny were affected by the mutant phenotype and 19 were unaffected, proving that the mutation is dominant.

Using our standard mapping procedures  two female mice carrying the KitlSl-23J mutation were mated to a CAST/Ei male mouse. The progeny from this previous cross were then backcrossed to 5 +/+ mice and they produced 53 offspring that were utilized for linkage analysis. The new KitlSl-23J mutation was mapped to Chromosome 10 and is distal to D10Mit291 (NCBIm36 position 95.7Mb), proximal to D10Mit163 (NCBIm36 position107 Mb), and non-recombinant with D10Mit290 (NCBIm36 position 98.3 Mb), D10Mit96 (NCBIm36 position 98.9 Mb), and D10Mit178 (NCBIm36 position 99.6 Mb). The previously described KitlSl is at (NCBIm36) position 99.4 Mb.

Pathology

A routine pathological screen  of two mice carrying the KitlSl-23J mutation and one littermate control at 7 weeks of age revealed no gross lesions.

Hearing as assessed by auditory brainstem response (ABR)  on one 6-month old mutant mouse was normal.

The eyes of mice carrying the KitlSl-23J mutation were examined with an opthalamascope and revealed no abnormalities.

Discussion

Based on phenotype and map position, this new mutation was determined to be an allele of the Kitl gene. A direct test for allelism was not performed as both Kitl and the new KitlSl-23J have dominant inheritance.

Acknowledgements

The authors would like to thank Norm Hawes for the eye examinations, Chantal Longo-Guess for hearing assessment, Coleen Marden for histological techniques, and Leona Gagnon for photographic assistance.