All Phenotypes Rdh10<tm1c(KOMP)Wtsi> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Gt(ROSA)26Sor^{tm1(cre/ERT2)Tyj}/Gt(ROSA)26Sor⁺ Rdh10^{tm1c(KOMP)Wtsi}/Rdh10^{tm1d(KOMP)Wtsi}	involves: 129S4/SvJae * C57BL/6N * FVB/NJ	MGI:7382902
cn2	Gt(ROSA)26Sor^{tm1(cre/ERT2)Tyj}/Gt(ROSA)26Sor⁺ Rdh10^{tm1c(KOMP)Wtsi}/Rdh10^{tm1c(KOMP)Wtsi}	involves: 129S4/SvJae * C57BL/6N * FVB/NJ	MGI:7382903
cn3	Rdh10^{tm1c(KOMP)Wtsi}/Rdh10^{tm1c(KOMP)Wtsi} Tg(Amh-cre)8815Reb/0 Tg(RARE-Hspa1b/lacZ)12Jrt/0 Tg(Stra8-icre)1Reb/0	involves: C57BL/6 * C57BL/6N * CD-1 * FVB/N * SJL	MGI:5475537
cn4	Rdh10^{tm1c(KOMP)Wtsi}/Rdh10^{tm1c(KOMP)Wtsi} Tg(Stra8-icre)1Reb/0	involves: C57BL/6 * C57BL/6N * FVB/NJ * SJL	MGI:5475535
cn5	Rdh10^{tm1c(KOMP)Wtsi}/Rdh10^{tm1c(KOMP)Wtsi} Tg(Amh-cre)8815Reb/0	involves: C57BL/6 * C57BL/6N * FVB/N * SJL	MGI:5475534
cn6	Rdh10^{tm1c(KOMP)Wtsi}/Rdh10^{tm1c(KOMP)Wtsi} Tg(Amh-cre)8815Reb/0 Tg(Stra8-icre)1Reb/0	involves: C57BL/6 * C57BL/6N * FVB/N * SJL	MGI:5475536

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

craniofacial

craniofacial phenotype ( J:278485 )

N	• following tamoxifen treatment at E8.5 at E16.5 mandible size is not significantly different from controls, indicating this does not contribute to cleft palate

abnormal hyoid bone morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 variable morphological defects are seen

• in some cases the hyoid primordium is ectopically fused to the laryngeal prominence of the thyroid cartilage and the hyoid primordium has a gentle M shape

decreased palatine bone horizontal plate size ( J:278485 )

• feathery medial growth is lacking and ossified palatine bones do not approach the midline in 50% of embryos at E16.5 following tamoxifen treatment at E8.5

palatal shelves fail to meet at midline ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 in 40% of embryos the palatal shelves have elevated but fail to grow to the midline

• however, in maxillary explant cultures shelves elevate and make medial contact at a similar rate to controls

cleft secondary palate ( J:278485 )

• at E16.5 in 36% of embryos following tamoxifen treatment at E8.5

abnormal palatal shelf elevation ( J:278485 )

• following tamoxifen treatment at E8.5 at E14.5 only 33% of mutant embryos have both shelves elevated compared to 82% of controls

• following tamoxifen treatment at E8.5 at E14.5 palatal shelves appear to be obstructed by the arched tongue at the posterior end of the shelves

abnormal tongue muscle morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 tongue muscles lack apparent attachment to the hyoid primordium

abnormal tongue position ( J:278485 )

• following tamoxifen treatment at E8.5 at E14.5 the tongue is arched to the posterior rather than relatively flat as in controls

decreased tongue size ( J:278485 )

• following tamoxifen treatment at E8.5 at E14.5 tongue volume is slightly reduced compared to controls

• however, no defects in intrinsic muscle morphology are seen

skeleton

abnormal hyoid bone morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 variable morphological defects are seen

• in some cases the hyoid primordium is ectopically fused to the laryngeal prominence of the thyroid cartilage and the hyoid primordium has a gentle M shape

decreased palatine bone horizontal plate size ( J:278485 )

• feathery medial growth is lacking and ossified palatine bones do not approach the midline in 50% of embryos at E16.5 following tamoxifen treatment at E8.5

abnormal cricoid cartilage morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 variable morphological defects are seen

abnormal thyroid cartilage morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 variable morphological defects are seen

• in some cases the hyoid primordium is ectopically fused to the laryngeal prominence of the thyroid cartilage

nervous system

abnormal motor neuron morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E11.5 the C1 motor nerve fuses directly to the CN XII nerve in 50% of embryos but never seen in controls

abnormal hypoglossal nerve morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E11.5 the C1 motor nerve fuses directly to the CN XII nerve in 50% of embryos but never seen in controls

respiratory system

abnormal cricoid cartilage morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 variable morphological defects are seen

abnormal thyroid cartilage morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 variable morphological defects are seen

• in some cases the hyoid primordium is ectopically fused to the laryngeal prominence of the thyroid cartilage

muscle

abnormal tongue muscle morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 tongue muscles lack apparent attachment to the hyoid primordium

digestive/alimentary system

decreased palatine bone horizontal plate size ( J:278485 )

• feathery medial growth is lacking and ossified palatine bones do not approach the midline in 50% of embryos at E16.5 following tamoxifen treatment at E8.5

palatal shelves fail to meet at midline ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 in 40% of embryos the palatal shelves have elevated but fail to grow to the midline

• however, in maxillary explant cultures shelves elevate and make medial contact at a similar rate to controls

cleft secondary palate ( J:278485 )

• at E16.5 in 36% of embryos following tamoxifen treatment at E8.5

abnormal palatal shelf elevation ( J:278485 )

• following tamoxifen treatment at E8.5 at E14.5 only 33% of mutant embryos have both shelves elevated compared to 82% of controls

• following tamoxifen treatment at E8.5 at E14.5 palatal shelves appear to be obstructed by the arched tongue at the posterior end of the shelves

abnormal tongue muscle morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 tongue muscles lack apparent attachment to the hyoid primordium

abnormal tongue position ( J:278485 )

• following tamoxifen treatment at E8.5 at E14.5 the tongue is arched to the posterior rather than relatively flat as in controls

decreased tongue size ( J:278485 )

• following tamoxifen treatment at E8.5 at E14.5 tongue volume is slightly reduced compared to controls

• however, no defects in intrinsic muscle morphology are seen

growth/size/body

decreased palatine bone horizontal plate size ( J:278485 )

• feathery medial growth is lacking and ossified palatine bones do not approach the midline in 50% of embryos at E16.5 following tamoxifen treatment at E8.5

palatal shelves fail to meet at midline ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 in 40% of embryos the palatal shelves have elevated but fail to grow to the midline

• however, in maxillary explant cultures shelves elevate and make medial contact at a similar rate to controls

cleft secondary palate ( J:278485 )

• at E16.5 in 36% of embryos following tamoxifen treatment at E8.5

abnormal palatal shelf elevation ( J:278485 )

• following tamoxifen treatment at E8.5 at E14.5 only 33% of mutant embryos have both shelves elevated compared to 82% of controls

• following tamoxifen treatment at E8.5 at E14.5 palatal shelves appear to be obstructed by the arched tongue at the posterior end of the shelves

abnormal tongue muscle morphology ( J:278485 )

• following tamoxifen treatment at E8.5 at E16.5 tongue muscles lack apparent attachment to the hyoid primordium

abnormal tongue position ( J:278485 )

• following tamoxifen treatment at E8.5 at E14.5 the tongue is arched to the posterior rather than relatively flat as in controls

decreased tongue size ( J:278485 )

• following tamoxifen treatment at E8.5 at E14.5 tongue volume is slightly reduced compared to controls

• however, no defects in intrinsic muscle morphology are seen

Allelic Composition	Gt(ROSA)26Sor^{tm1(cre/ERT2)Tyj}/Gt(ROSA)26Sor⁺ Rdh10^{tm1c(KOMP)Wtsi}/Rdh10^{tm1c(KOMP)Wtsi}
Genetic Background	involves: 129S4/SvJae * C57BL/6N * FVB/NJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm1(cre/ERT2)Tyj} mutation (3 available); any Gt(ROSA)26Sor mutation (993 available)
Rdh10^{tm1c(KOMP)Wtsi} mutation (0 available); any Rdh10 mutation (20 available)

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

behavior/neurological

abnormal spontaneous fetal mouth movement ( J:278485 )

• following tamoxifen treatment at E8.5 at E14.5, head movements are not accompanied by detectable mouth opening or tongue movement unlike in controls

Allelic Composition	Rdh10^{tm1c(KOMP)Wtsi}/Rdh10^{tm1c(KOMP)Wtsi} Tg(Amh-cre)8815Reb/0 Tg(RARE-Hspa1b/lacZ)12Jrt/0 Tg(Stra8-icre)1Reb/0
Genetic Background	involves: C57BL/6 * C57BL/6N * CD-1 * FVB/N * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rdh10^{tm1c(KOMP)Wtsi} mutation (0 available); any Rdh10 mutation (20 available)
Tg(Amh-cre)8815Reb mutation (2 available)
Tg(RARE-Hspa1b/lacZ)12Jrt mutation (2 available)
Tg(Stra8-icre)1Reb mutation (2 available)

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

reproductive system

small testis ( J:193281 )

abnormal male reproductive system physiology ( J:193281 )

• lack of retinoic acid

endocrine/exocrine glands

small testis ( J:193281 )

Allelic Composition	Rdh10^{tm1c(KOMP)Wtsi}/Rdh10^{tm1c(KOMP)Wtsi} Tg(Stra8-icre)1Reb/0
Genetic Background	involves: C57BL/6 * C57BL/6N * FVB/NJ * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rdh10^{tm1c(KOMP)Wtsi} mutation (0 available); any Rdh10 mutation (20 available)
Tg(Stra8-icre)1Reb mutation (2 available)

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

reproductive system

reproductive system phenotype ( J:193281 )

N	• testes weight and morphology are indistinguishable from controls at 2 and 3 weeks of age

Allelic Composition	Rdh10^{tm1c(KOMP)Wtsi}/Rdh10^{tm1c(KOMP)Wtsi} Tg(Amh-cre)8815Reb/0
Genetic Background	involves: C57BL/6 * C57BL/6N * FVB/N * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rdh10^{tm1c(KOMP)Wtsi} mutation (0 available); any Rdh10 mutation (20 available)
Tg(Amh-cre)8815Reb mutation (2 available)

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

reproductive system

seminiferous tubule degeneration ( J:193281 )

• about 45% of the tubules are degenerated at 2 and 3 weeks of age

decreased testis weight ( J:193281 )

• at 2 and 3 weeks of age

abnormal male reproductive system physiology ( J:193281 )

• numerous degenerated germ cells are present in the testes

endocrine/exocrine glands

seminiferous tubule degeneration ( J:193281 )

• about 45% of the tubules are degenerated at 2 and 3 weeks of age

decreased testis weight ( J:193281 )

• at 2 and 3 weeks of age

Allelic Composition	Rdh10^{tm1c(KOMP)Wtsi}/Rdh10^{tm1c(KOMP)Wtsi} Tg(Amh-cre)8815Reb/0 Tg(Stra8-icre)1Reb/0
Genetic Background	involves: C57BL/6 * C57BL/6N * FVB/N * SJL

Find Mice

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

reproductive system

abnormal spermatogonia morphology ( J:193281 )

• block of differentiation of Aal spermatogonia into A1 spermatogonia at 2 and 3 weeks of age

abnormal seminiferous tubule morphology ( J:193281 )

• most tubules are devoid of meiotic cells at 2 and 3 weeks of age, retaining only undifferentiated spermatogonia-like cells and Sertoli cells

• however, by 9 weeks of age, tubules contain the expected spermatogonia, spermatocytes, and spermatids

seminiferous tubule degeneration ( J:193281 )

• over 85% of tubules are degenerated at 2 and 3 weeks of age

small testis ( J:193281 )

• at 2 and 3 weeks of age

decreased testis weight ( J:193281 )

• dramatically lower at 2 and 3 weeks of age compared to wild-type controls and homozygous mice carrying only one of the cre transgenes

abnormal spermatogenesis ( J:193281 )

• most tubules are devoid of meiotic cells at 2 and 3 weeks of age, retaining only undifferentiated spermatogonia-like cells and Sertoli cells

• treatment with retinoic acid enhances synchrony of spermatogenesis

• however, by 9 weeks of age, spermatogenesis is similar to controls

• in adults only 1 of 48 males shows spermatogenesis with an altered stage frequency

arrest of male meiosis ( J:193281 )

• fail to initiate meiosis at 2 and 3 weeks of age

abnormal male reproductive system physiology ( J:193281 )

• numerous degenerated germ cells are present in the testes at 2 and 3 weeks of age

reduced male fertility ( J:193281 )

• males under 7 weeks of age are infertile or subfertile

• however, mice over 9 weeks of age are fertile and produce litters similar in size to controls

endocrine/exocrine glands

abnormal seminiferous tubule morphology ( J:193281 )

• most tubules are devoid of meiotic cells at 2 and 3 weeks of age, retaining only undifferentiated spermatogonia-like cells and Sertoli cells

• however, by 9 weeks of age, tubules contain the expected spermatogonia, spermatocytes, and spermatids

seminiferous tubule degeneration ( J:193281 )

• over 85% of tubules are degenerated at 2 and 3 weeks of age

small testis ( J:193281 )

• at 2 and 3 weeks of age

decreased testis weight ( J:193281 )

• dramatically lower at 2 and 3 weeks of age compared to wild-type controls and homozygous mice carrying only one of the cre transgenes

cellular

abnormal spermatogonia morphology ( J:193281 )

• block of differentiation of Aal spermatogonia into A1 spermatogonia at 2 and 3 weeks of age

arrest of male meiosis ( J:193281 )

• fail to initiate meiosis at 2 and 3 weeks of age

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