Phenotypes associated with this allele

• Allele Symbol: Tg(CAG-cre/ERT2)F34Fmr
• Allele Name: transgene insertion F34, Filippo M Rijli
• Allele ID: MGI:4415132
• Summary: 6 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Hoxa2^tm1.1Fmr/Hoxa2^tm1.1Fmr Tg(CAG-cre/ERT2)F34Fmr/0	involves: 129 * CD-1	MGI:5470404
cn2	Cdx2^tm1.1Lhn/Cdx2^tm1.1Lhn Tg(CAG-cre/ERT2)F34Fmr/0	involves: 129S1/Sv * 129X1/SvJ * CD-1	MGI:4415156
cn3	Cdx2^tm1.1Lhn/Cdx2^+ Tg(CAG-cre/ERT2)F34Fmr/0	involves: 129S1/Sv * 129X1/SvJ * CD-1	MGI:4415157
cn4	Hoxa2^tm1Ipc/Hoxa2^tm1.1Fmr Tg(CAG-cre/ERT2)F34Fmr/0	involves: 129/Sv * 129S2/SvPas * C57BL/6 * CD-1	MGI:4415144
cn5	Hoxa2^tm1.1Fmr/Hoxa2^tm1.1Fmr Tg(CAG-cre/ERT2)F34Fmr/0	involves: 129/Sv * C57BL/6 * CD-1	MGI:4415142
cx6	Hoxa2^tm1.1Fmr/Hoxa2^tm1.1Fmr Tg(CAG-cre/ERT2)F34Fmr/0	involves: 129/Sv * C57BL/6 * CD-1	MGI:4415140

Genotype
MGI:5470404

cn1

• Allelic Composition: Hoxa2^tm1.1Fmr/Hoxa2^tm1.1Fmr; Tg(CAG-cre/ERT2)F34Fmr/0
• Genetic Background: involves: 129 * CD-1

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

nervous system

abnormal brain development ( J:193058 )

• increased oligodendrogenesis in the prepontine (rhombomere 2- and 3-derived) and pontine territories (rhombomere 4-derived) at E13.5 5 in mice exposed to tamoxifen at E10.5

increased oligodendrocyte progenitor number ( J:193058 )

• in the basal plate of rhombomere 3-derived and pontine territory (rhombomere 4-d) at E13.5 in mice exposed to tamoxifen at E10.5 due to increased proliferation in the ventricular zone

• in the prepontine (rhombomere 2- and 3-derived) territory at E13.5 in mice exposed to tamoxifen at E10.5

cellular

increased oligodendrocyte progenitor number ( J:193058 )

• in the basal plate of rhombomere 3-derived and pontine territory (rhombomere 4-d) at E13.5 in mice exposed to tamoxifen at E10.5 due to increased proliferation in the ventricular zone

• in the prepontine (rhombomere 2- and 3-derived) territory at E13.5 in mice exposed to tamoxifen at E10.5

Genotype
MGI:4415156

cn2

• Allelic Composition: Cdx2^tm1.1Lhn/Cdx2^tm1.1Lhn; Tg(CAG-cre/ERT2)F34Fmr/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * CD-1

mortality/aging

embryonic lethality during organogenesis, complete penetrance ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5, mice die around E11.5

• however, mice exposed to tamoxifen beginning at E8.5 survive to term

embryo

abnormal mesoderm development ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5, mice lack presomitic and posterior mesoderm

short rostral-caudal axis ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5, mice exhibit a shortened anterior posterior axis by E8.5 compared with Cdx2^tm1.1Lhn homozygotes

• when mice are exposed to tamoxifen beginning at E8.5, mice exhibit axial truncation at the level of the sacral vertebrae at E18.5

abnormal presomitic mesoderm morphology ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5, mice lack presomitic mesoderm

absent hindlimb buds ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5, mice fail to develop hind limb buds

decreased somite size ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5, somites after the first 5 through 7 are progressively smaller than in Cdx2^tm1.1Lhn homozygotes

impaired somite development ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5, mice have fewer, more posteriorly located somites at E9.5 and E10.5 compared with Cdx2^tm1.1Lhn homozygotes

limbs/digits/tail

absent hindlimb buds ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5, mice fail to develop hind limb buds

Genotype
MGI:4415157

cn3

• Allelic Composition: Cdx2^tm1.1Lhn/Cdx2⁺; Tg(CAG-cre/ERT2)F34Fmr/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * CD-1

limbs/digits/tail

sirenomelia ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5 and 100 mg/kg body weight retinoic acid at E8.5

short tail ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5 and 10 mg/kg body weight retinoic acid at E8.5

absent tail ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5 and 100 mg/kg body weight retinoic acid at E8.5

embryo

sirenomelia ( J:154904 )

• when mice are exposed to tamoxifen beginning at E5.5 and 100 mg/kg body weight retinoic acid at E8.5

Genotype
MGI:4415144

cn4

• Allelic Composition: Hoxa2^tm1Ipc/Hoxa2^tm1.1Fmr; Tg(CAG-cre/ERT2)F34Fmr/0
• Genetic Background: involves: 129/Sv * 129S2/SvPas * C57BL/6 * CD-1

craniofacial

abnormal craniofacial bone morphology ( J:102845 )

• when tamoxifen is administered beginning at E11.5 or E12.5, mice exhibit similar craniofacial defects as observed in Hoxa2^tm1.1Fmr Tg(CAG-cre/ERT2)F34Fmr homozygotes

small ears ( J:102845 )

• when tamoxifen is administered beginning at E12.5 or E13.5

hearing/vestibular/ear

small ears ( J:102845 )

• when tamoxifen is administered beginning at E12.5 or E13.5

skeleton

abnormal craniofacial bone morphology ( J:102845 )

• when tamoxifen is administered beginning at E11.5 or E12.5, mice exhibit similar craniofacial defects as observed in Hoxa2^tm1.1Fmr Tg(CAG-cre/ERT2)F34Fmr homozygotes

growth/size/body

small ears ( J:102845 )

• when tamoxifen is administered beginning at E12.5 or E13.5

Genotype
MGI:4415142

cn5

• Allelic Composition: Hoxa2^tm1.1Fmr/Hoxa2^tm1.1Fmr; Tg(CAG-cre/ERT2)F34Fmr/0
• Genetic Background: involves: 129/Sv * C57BL/6 * CD-1

mortality/aging

perinatal lethality, complete penetrance ( J:102845 )

• when tamoxifen is administered beginning at E7.0

craniofacial

abnormal craniofacial bone morphology ( J:102845 )

• when tamoxifen is administered beginning at E7.0 or E9.5, second arch structures are replaced with a mirror duplication of first arch structures

• when tamoxifen is administered beginning at E11.5, second arch cartilaginous derivatives are abnormal

• when tamoxifen is administered beginning at E12.5, second arch skeletal elements are only mildly affected

abnormal styloid process morphology ( J:102845 )

• when tamoxifen is administered beginning at E11.5, the styloid process is malformed and associated with ectopic cartilage

absent hyoid bone lesser horns ( J:102845 )

• when tamoxifen is administered beginning at E9.5, E10.5, E11.0 or E11.5, mice lack the lesser horns of the hyoid bone

abnormal gonial bone morphology ( J:102845 )

• when tamoxifen is administered beginning at E7.0, the gonial bone appears transformed such that it is enlarged and stretches across, bridging over the two halves of the mirror duplication

• when tamoxifen is administered beginning at E8.0, gonial bone phenotype is variable, ranging from a malformed gonial bone to complete transformation

• however, the gonial bone is normal when mice are treated with tamoxifen beginning at E9.5 or later

abnormal stapes morphology ( J:102845 )

• when tamoxifen is administered beginning at E11.5, the stapes is malformed and associated with ectopic cartilage

absent outer ear ( J:102845 )

• when tamoxifen is administered beginning up to E11.5

hearing/vestibular/ear

absent outer ear ( J:102845 )

• when tamoxifen is administered beginning up to E11.5

abnormal middle ear morphology ( J:102845 )

• when tamoxifen is administered beginning at E9.5, E10.5, or E11.5, middle ear elements are duplicated, with the exception of the gonial bone

abnormal gonial bone morphology ( J:102845 )

• when tamoxifen is administered beginning at E7.0, the gonial bone appears transformed such that it is enlarged and stretches across, bridging over the two halves of the mirror duplication

• when tamoxifen is administered beginning at E8.0, gonial bone phenotype is variable, ranging from a malformed gonial bone to complete transformation

• however, the gonial bone is normal when mice are treated with tamoxifen beginning at E9.5 or later

abnormal stapes morphology ( J:102845 )

• when tamoxifen is administered beginning at E11.5, the stapes is malformed and associated with ectopic cartilage

skeleton

abnormal craniofacial bone morphology ( J:102845 )

• when tamoxifen is administered beginning at E7.0 or E9.5, second arch structures are replaced with a mirror duplication of first arch structures

• when tamoxifen is administered beginning at E11.5, second arch cartilaginous derivatives are abnormal

• when tamoxifen is administered beginning at E12.5, second arch skeletal elements are only mildly affected

abnormal styloid process morphology ( J:102845 )

• when tamoxifen is administered beginning at E11.5, the styloid process is malformed and associated with ectopic cartilage

absent hyoid bone lesser horns ( J:102845 )

• when tamoxifen is administered beginning at E9.5, E10.5, E11.0 or E11.5, mice lack the lesser horns of the hyoid bone

abnormal gonial bone morphology ( J:102845 )

• when tamoxifen is administered beginning at E7.0, the gonial bone appears transformed such that it is enlarged and stretches across, bridging over the two halves of the mirror duplication

• when tamoxifen is administered beginning at E8.0, gonial bone phenotype is variable, ranging from a malformed gonial bone to complete transformation

• however, the gonial bone is normal when mice are treated with tamoxifen beginning at E9.5 or later

abnormal stapes morphology ( J:102845 )

• when tamoxifen is administered beginning at E11.5, the stapes is malformed and associated with ectopic cartilage

growth/size/body

absent outer ear ( J:102845 )

• when tamoxifen is administered beginning up to E11.5

Genotype
MGI:4415140

cx6

• Allelic Composition: Hoxa2^tm1.1Fmr/Hoxa2^tm1.1Fmr; Tg(CAG-cre/ERT2)F34Fmr/0
• Genetic Background: involves: 129/Sv * C57BL/6 * CD-1

normal phenotype

no abnormal phenotype detected ( J:102845 )

• newborn mice are normal