Inbred Strains of Mice: SELH
SELHInbr. 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).
CharacteristicsHigh 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. INBRED STRAINS OF MICERetroSearch is an open source project built by @garambo | Open a GitHub Issue
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