Curly tail arose at Glaxo Laboratories in 1950 on the GFF inbred background (which was Tyra/Tyra Tyrp1b/Tyrp1b p/p in coat color). A litter with 4 mutants was transferred to Hans Gruneberg who got one female curly tail to breed to a CBA/Gr male. He subsequently backcrossed her offspring to CBA/Gr for 2 more generations to reach N3 then maintained this colony through closed colony mating in which the curly tail phenotyped was maintained. On several occasions prior to 1991 this colony was re-derived through a small number of breeders ( Brook, FA et al. 1991. Development 113, p.671; Grunenberg H, 1954 J. Genet. 52, p. 52). Curly tail mice arrived at The Jackson Laboratory in 1990. According to Neumann et al. 1994, "The Oxford curly-tail colony was established from mice donated by Mary Seller (Guy s Hospital, London) in 1984. Subsequently, breeding pairs were sent from Oxford to Boston (1990), and from there, to The Jackson Laboratory." The Jackson Laboratory received these mice in 1990, expanded them by closed colony mating for 3 generations before passing through importation, and has maintained this strain by homozygous sibling matings ever since its passage through importation in 1991. The curly tail colony is considered homozygous for curly tail, however, incomplete penetrance and expressivity results in siblings displaying wildtype or mutant phenotypes of varying degrees.
|Allele Name||curly tail|
|Gene Symbol and Name||Grhl3, grainyhead like transcription factor 3|
|Strain of Origin||GFF|
|Molecular Note|| |
A novel C-to-T nucleotide substitution (G-to-A on forward strand) was identified at -21,350 downstream of the start codon at position 135,594,774 (GRCm38) in the promoter/enhancer region of mutant genomic DNA, compared with the partially congenic wild-type strain which carries a region of SWR encompassing the ct locus. The C to T nucleotide substitution is not a known polymorphism according to dbSNP. The wild-type sequence, corresponding to nucleotide C, was also present in C57/BL6 and four other strains.
A bacterial artificial chromosome (BAC), containing the complete Grhl3 gene together with 120 kb of upstream sequence that encompasses the site of the putative ct mutation, completely rescued the curly tail phenotype when expressed in mutant mice.
Grhl3 expression was examined in caudal regions isolated from ct/ct embryos and equivalent somite staged ct/ct embryos that were matched for genetic background. At the 28-29 and 30-31 somite stages, which correspond to the final stages of spinal neurulation, Grhl3 mRNA was reduced in abundance in ct/ct embryos compared with wild-type by 56 and 41%, respectively, whereas no difference was apparent at the 25-27 somite stage. These findings support the idea that insufficient expression of Grhl3, in the hindgut endoderm located ventrally to the PNP, could be causally related to spina bifida in curly tail embryos.
When using the curly tail mouse strain in a publication, please cite the originating article(s) and include JAX stock #001813 in your Materials and Methods section.
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