Phenotypes associated with this allele

• Allele Symbol: Tg(Atoh1-cre/Esr1*)14Fsh
• Allele Name: transgene insertion 14, Gordon Fishell
• Allele ID: MGI:3615691
• Summary: 10 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Cacna1a^tm1.1Ehess/Cacna1a^tm2.1Maag Tg(Atoh1-cre/Esr1*)14Fsh/0	involves: 129P2/OlaHsd * C57BL/6 * FVB/N	MGI:5707186
cn2	Ric8a^tm1Aks/Ric8a^tm1.1Zhua Tg(Atoh1-cre/Esr1*)14Fsh/0	involves: 129P2/OlaHsd * FVB/N	MGI:5467517
cn3	Eya1^tm2Px/Eya1^tm2Px Tg(Atoh1-cre/Esr1*)14Fsh/0	involves: 129S1/Sv * 129X1/SvJ * FVB/N	MGI:5316867
cn4	Ptch1^tm1Bjw/Ptch1^tm1Bjw Tg(Atoh1-cre/Esr1*)14Fsh/0	involves: 129T2/SvEms * FVB/N	MGI:5286071
cn5	Gt(ROSA)26Sor^tm1(Smo/EYFP)Amc/Gt(ROSA)26Sor^tm1(Smo/EYFP)Amc Tg(Atoh1-cre/Esr1*)14Fsh/0	involves: 129X1/SvJ * FVB/N	MGI:3810322
cn6	Bicd2^tm1Hgrd/Bicd2^tm1Hgrd Tg(Atoh1-cre/Esr1*)14Fsh/0	involves: C57BL/6 * FVB/N	MGI:5810139
cn7	Chd7^tm2c(EUCOMM)Wtsi/Chd7^tm2c(EUCOMM)Wtsi Tg(Atoh1-cre/Esr1*)14Fsh/0	involves: C57BL/6N	MGI:7518240
cn8	Ythdf1^tm1.1Sjj/Ythdf1^tm1.1Sjj Tg(Atoh1-cre/Esr1*)14Fsh/0	involves: FVB/N	MGI:6719337
cn9	Six1^tm1Px/Six1^tm1Px Tg(Atoh1-cre/Esr1*)14Fsh/0	involves: FVB/N	MGI:5316868
tg10	Tg(Atoh1-cre/Esr1*)14Fsh/0	involves: FVB/N * Swiss Webster	MGI:4452029

Genotype
MGI:5707186

cn1

• Allelic Composition: Cacna1a^tm1.1Ehess/Cacna1a^tm2.1Maag; Tg(Atoh1-cre/Esr1*)14Fsh/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * FVB/N

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

behavior/neurological

behavior/neurological phenotype ( J:217557 )

N • mice do not exhibit motor dysfunction on the rotarod

Genotype
MGI:5467517

cn2

• Allelic Composition: Ric8a^tm1Aks/Ric8a^tm1.1Zhua; Tg(Atoh1-cre/Esr1*)14Fsh/0
• Genetic Background: involves: 129P2/OlaHsd * FVB/N

nervous system

nervous system phenotype ( J:191222 )

N • granule cell precursors are normal in tamoxifen-treated mice

Genotype
MGI:5316867

cn3

• Allelic Composition: Eya1^tm2Px/Eya1^tm2Px; Tg(Atoh1-cre/Esr1*)14Fsh/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * FVB/N

hearing/vestibular/ear

abnormal cochlear hair cell morphology ( J:181471 )

• hair cells in the basal and medial turns of the cochlea from tamoxifen-treated mice exhibit abnormalities that disappear when cultured in vitro

decreased cochlear inner hair cell number ( J:181471 )

• tamoxifen-treated mice lack hair cells in the apical turn of the cochlea with outer rows more affected than inner rows

decreased cochlear outer hair cell number ( J:181471 )

• tamoxifen-treated mice lack hair cells in the apical turn of the cochlea with outer rows more affected than inner rows

nervous system

abnormal cochlear hair cell morphology ( J:181471 )

• hair cells in the basal and medial turns of the cochlea from tamoxifen-treated mice exhibit abnormalities that disappear when cultured in vitro

decreased cochlear inner hair cell number ( J:181471 )

• tamoxifen-treated mice lack hair cells in the apical turn of the cochlea with outer rows more affected than inner rows

decreased cochlear outer hair cell number ( J:181471 )

• tamoxifen-treated mice lack hair cells in the apical turn of the cochlea with outer rows more affected than inner rows

Genotype
MGI:5286071

cn4

• Allelic Composition: Ptch1^tm1Bjw/Ptch1^tm1Bjw; Tg(Atoh1-cre/Esr1*)14Fsh/0
• Genetic Background: involves: 129T2/SvEms * FVB/N

mortality/aging

premature death ( J:139573 )

• by 10 weeks, mice start becoming severely ill and must be sacrificed

• all mice die by 29 weeks of age

nervous system

abnormal neuronal precursor proliferation ( J:139573 )

• granule neuron precursors in mice treated with tamoxifen at P4 exhibit increased proliferation unlike in wild-type mice

increased medulloblastoma incidence ( J:139573 )

• in all mice treated with tamoxifen at E14.5 with a median age of tumor onset at 10 weeks

• in all mice treated with tamoxifen at P4 with a median age of tumor onset at 13 weeks

• in all mice treated with tamoxifen at P8 with a median age of tumor onset at 15.5 weeks

• in 29% of mice treated with tamoxifen at P10 with a median age of tumor onset at 19 weeks

• however, mice treated with tamoxifen at E10.5, at P12, or later than P12 do not develop tumors

abnormal cerebellum external granule cell layer morphology ( J:139573 )

• at P21 in mice treated with tamoxifen at P4

enlarged cerebellum ( J:139573 )

• cerebellar hyperplasia at 10 weeks of age

neoplasm

increased medulloblastoma incidence ( J:139573 )

• in all mice treated with tamoxifen at E14.5 with a median age of tumor onset at 10 weeks

• in all mice treated with tamoxifen at P4 with a median age of tumor onset at 13 weeks

• in all mice treated with tamoxifen at P8 with a median age of tumor onset at 15.5 weeks

• in 29% of mice treated with tamoxifen at P10 with a median age of tumor onset at 19 weeks

• however, mice treated with tamoxifen at E10.5, at P12, or later than P12 do not develop tumors

cellular

abnormal neuronal precursor proliferation ( J:139573 )

• granule neuron precursors in mice treated with tamoxifen at P4 exhibit increased proliferation unlike in wild-type mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
medulloblastoma		DOID:0050902	OMIM:155255	J:139573

Genotype
MGI:3810322

cn5

• Allelic Composition: Gt(ROSA)26Sor^{tm1(Smo/EYFP)Amc}/Gt(ROSA)26Sor^{tm1(Smo/EYFP)Amc}; Tg(Atoh1-cre/Esr1*)14Fsh/0
• Genetic Background: involves: 129X1/SvJ * FVB/N

mortality/aging

premature death ( J:139574 )

• mice survive 41 days

nervous system

increased medulloblastoma incidence ( J:139574 )

• all mice develop diffuse medulloblastomas and have a mean survival of 41 days

abnormal cerebellum external granule cell layer morphology ( J:139574 )

• mice exhibit hyperplasia on the external granule cell layer beginning at P0 and more prominently at P7

neoplasm

increased medulloblastoma incidence ( J:139574 )

• all mice develop diffuse medulloblastomas and have a mean survival of 41 days

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
medulloblastoma		DOID:0050902	OMIM:155255	J:139574

Genotype
MGI:5810139

cn6

• Allelic Composition: Bicd2^tm1Hgrd/Bicd2^tm1Hgrd; Tg(Atoh1-cre/Esr1*)14Fsh/0
• Genetic Background: involves: C57BL/6 * FVB/N

normal phenotype

no abnormal phenotype detected ( J:210236 )

• tamoxifen-treated mice survive to >8 weeks (when they are sacrificed) and do not exhibit hydrocephalus or disrupted laminar organization in the cerebral cortex, cerebellum or hippocampus

• at P25, all post-migratory granule cells are found in the cerebellar internal granule cell layer, indicating that cerebellar granule cell migration is normal

Genotype
MGI:7518240

cn7

• Allelic Composition: Chd7^{tm2c(EUCOMM)Wtsi}/Chd7^{tm2c(EUCOMM)Wtsi}; Tg(Atoh1-cre/Esr1*)14Fsh/0
• Genetic Background: involves: C57BL/6N
• Cell Lines: EPD0019_1_D07

hearing/vestibular/ear

hearing/vestibular/ear phenotype ( J:314588 )

N • tamoxifen treatment at E16 does not result in postnatal hair cell degeneration unlike in mice where recombinase is active in the early embryonic period

Genotype
MGI:6719337

cn8

• Allelic Composition: Ythdf1^tm1.1Sjj/Ythdf1^tm1.1Sjj; Tg(Atoh1-cre/Esr1*)14Fsh/0
• Genetic Background: involves: FVB/N

nervous system

abnormal axon guidance ( J:276416 )

• embryos exhibit defects in pre-crossing commissural axon guidance, with significantly more commissural axons misprojecting into motor columns at E11.5

• pre-crossing axon guidance defects include stalling and pre-crossing turning phenotypes

• however, patterning of the spinal cord and development of dI1 commissural neurons is normal

homeostasis/metabolism

abnormal protein level ( J:276416 )

• however, Robo3.1 mRNA level is not affected in the spinal cord

• when dorsal spinal cord (DSC) explants are dissected from pre-crossing E10.5 spinal cord and cultured in vitro, dorsal commissural axons show a dramatic reduction in Robo3.1 protein level relative to controls

cellular

abnormal axon guidance ( J:276416 )

• embryos exhibit defects in pre-crossing commissural axon guidance, with significantly more commissural axons misprojecting into motor columns at E11.5

• pre-crossing axon guidance defects include stalling and pre-crossing turning phenotypes

• however, patterning of the spinal cord and development of dI1 commissural neurons is normal

Genotype
MGI:5316868

cn9

• Allelic Composition: Six1^tm1Px/Six1^tm1Px; Tg(Atoh1-cre/Esr1*)14Fsh/0
• Genetic Background: involves: FVB/N

hearing/vestibular/ear

abnormal cochlear hair cell morphology ( J:181471 )

• authors state that tamoxifen-treated mice exhibit the same phenotype as in Eya1^tm2Px/Eya1^tm2Px Tg(Atoh1-cre/Esr1*)14Fsh mice

nervous system

abnormal cochlear hair cell morphology ( J:181471 )

• authors state that tamoxifen-treated mice exhibit the same phenotype as in Eya1^tm2Px/Eya1^tm2Px Tg(Atoh1-cre/Esr1*)14Fsh mice

Genotype
MGI:4452029

tg10

• Allelic Composition: Tg(Atoh1-cre/Esr1*)14Fsh/0
• Genetic Background: involves: FVB/N * Swiss Webster

normal phenotype

no abnormal phenotype detected ( J:105186 )