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Inbred Strains of Mice: SELH


Inbr. F20+. Non-agouti, black, chinchilla (aaBBcchcch ). Origin: A partially inbred stock of mixed background, including BALB/cGa, 129/- and CBA/- and homozygous for the lidgap-Gates (lgGa ) was backcrossed to N3 in 1977 with outbred BLU:Ha(ICR) mice from Arbor Scientific Company, Ontario, Canada. A new recessive mutation spherocytosis-British Columbia (sph2Bc ) appeared at the second intercross (N3xN3), and was selected for during brother x sister mating with the elimination of the lidgap-Gates mutation. Exencephaly was observed in 1981 at F5. Exencephaly producing parents were selected in subsequent generations, and all animals trace back to a single breeding pair at F6. The strain has been typed at 28 polymorphic loci (Juriloff et al, 1989). See also Gunn et al (1992).


High incidence of exencephaly at birth which has been attributed to two or three additive genetic loci which differ between SELH and the closely-related normal strain ICR/Bc. Defects may be related to abnormal cranial neural tube closure mechanism with a lack of the initiation of contact and fusion of the cranial neural tube at the prosencephalon/mesencephalon boundary (Closure 2). SELH mice undergo closure by extension of a more rostral site of fusion (Gunn et al, 1995) leading to 10-20% exencephaly, cleft cerebellum and 5-10% ataxia in young adults, which all appear to be causally related (Juriloff et al, 1993, Gunn et al, 1995, Harris et al, 1994). More sensitive to retinoic acid (Tom et al, 1991) and valproic acid-induced (Hall et al, 1997) exencephaly than SWV/Bc and ICR/Bc. The strain appears to have a high incidence of spontaneous mutations, including three at the albino locus (Juriloff et al, 1994).

Gunn T. M., Juriloff D. M., and Harris M. J. (1992) Further genetic studies of the cause of exencephaly in SELH mice. Teratology 45, 679-686. \par

Gunn T. M., Juriloff D. M., and Harris M. J. (1995) Genetically-determined absence of an initiation site of cranial neural-tube closure is causally related to exencephaly in SELH/Bc mouse embryos. Teratology 52, 101-108. \par

Hall J. L., Harris M. J., and Juriloff D. M. (1997) Effect of multifactorial genetic liability to exencephaly on the teratogenic effect of valproic acid in mice. Teratology 55, 306-313. \par

Harris M. J., Juriloff D. M., Gunn T. M., and Miller J. E. (1994) Development of the cerebellar defect in ataxic SELH/Bc mice. Teratology 50, 63-73. \par

Juriloff D. M., MacDonald K. B., and Harris M. J. (1989) Genetic analysis of the cause of exencephaly in the SELH/Bc mouse stock. Teratology 40, 395-405. \par

Juriloff D. M., Harris M. J., Harrod M. L., Gunn T. M., and Miller J. E. (1993) Ataxia and a cerebellar defect in the exencephaly-prone SELH/Bc mouse stock. Teratology 47, 333-340. \par

Juriloff D. M., Porter S. D., and Harris M. J. (1994) 3 spontaneous mutations at the albino locus in SELH/Bc mice. Genome 37, 190-197. \par

Tom C., Juriloff D. M., and Harris M. J. (1991) Studies of the effect of retinoic acid on anterior neural-tube closure in mice genetically liable to exencephaly. Teratology 43, 27-40. \par

Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK

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