STOCK Tg(Atoh1-cre/Esr1*)14Fsh/J

Stock number: 007684
Product name: Math1-CreER^T2
Research areas: Neurobiology Research, Research Tools

Description

These knock-in mice express a tamoxifen-inducible cre recombinase from the endogenous promoter/enhancer elements of the atonal homolog 1 (Drosophila) (Atoh1, also referred to as Math1) gene. When induced, cre activity is observed in neural progenitors of the cerebellar rhombic lip, dorsal hindbrain and spinal cord, as well as in inner-ear primordial. These mice may be useful in studying cerebellum development and fate mapping of Math1/Atoh1 cells.

Detailed description

Mice hemizygous for this Math1-CreER^T2 transgene are viable and fertile. Under control of the Math1 (Atoh1) enhancer, tamoxifen-inducible cre activity is observed in neural progenitors of the cerebellar rhombic lip, dorsal hindbrain and spinal cord, as well as in inner-ear primordia (with a limited amount of ectopic expression in the primordium of the hippocampus but not the cortex). The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered. When these Math1-CreER^T2 mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the flanked sequences in Math1 expressing cells (the entire dorsal neural tube from posterior rhombomere 1 to the spinal cord); making them useful in studying cerebellum development and fate mapping of Math1/Atoh1 cells.

Development

The Math1-CreER^T2 transgene was designed with a 1.4 kb mouse Math1 (Atoh1) 3' enhancer (and a β-globin minimal promoter) sequence upstream of a CreER^T2 fusion gene (Cre recombinase fused to a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain). The transgene was microinjected into FVB/N embryos. Founder mice were bred to mice on a mixed outbred background to test transgene efficacy. Mice found to exhibit appropriate expression levels and patterns (founder line 14) were selected and bred to Swiss Webster outbred mice. Transgenic mice were bred to Swiss Webster for several generations prior to arrival at The Jackson Laboratory. Upon arrival, mice were bred to FVB/NJ for at least one generation to establish the colony.

Allele

Symbol: Tg(Atoh1-cre/Esr1*)14Fsh
Name: transgene insertion 14, Gordon Fishell
MGI accession ID: MGI:3615691
Generation method: Transgenic
Attributes: Recombinase-expressing; Inducible
Synonyms: Atoh1-cre; Math1-cre; Math1-CreER^T2; Tg(Atoh1-cre/ESR1)1Fsh; Tg(HBB-cre)1Fsh
Marker symbol: Tg(Atoh1-cre/Esr1*)14Fsh
Marker name: transgene insertion 14, Gordon Fishell
Marker synonyms: Math1-CreER^T2; Tg(Atoh1-cre/ESR1)1Fsh; Tg(Atoh1-creESR1)14Fsh; Tg(HBB-cre)1Fsh
Chromosome: UN
Strain of origin: FVB/N
Expressed genes: cre/Esr1,Cre recombinase and estrogen receptor 1 fusion gene,
Site of expression: tamoxifen-inducible cre activity is observed in neural progenitors of the cerebellar rhombic lip, dorsal hindbrain and spinal cord, as well as in inner-ear primordia (with a limited amount of ectopic expression in the primordium of the hippocampus but not the cortex)
Molecular note: The transgene was designed with a 1.4 kb mouse Math1 (Atoh1) 3' enhancer (and a beta-globin minimal promoter) sequence upstream of a CreERT2 fusion gene (Cre recombinase fused to a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain). Tamoxifen-inducible cre activity is observed in neural progenitors of the cerebellar rhombic lip, dorsal hindbrain and spinal cord, as well as in inner-ear primordia (with a limited amount of ectopic expression in the primordium of the hippocampus but not the cortex).