JAX Mouse Strain Datasheet - 004290

129-Ihh^tm1Amc/J

Stock No:: 004290 |; Ihh KO

Targeted Mutation

Cryo Recovery

Overview

Also Known As: Ihh KO

These Ihh knock-out mice exhibit embryonic lethality that may be due to circulatory abnormalities.

Donating Investigator

Andrew P McMahon, University of Southern California

Genetic overview

Genetic Background	Generation

Ihh^tm1Amc

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Ihh	Indian hedgehog

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Research Applications

Developmental Biology Research

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Base Price

Starting at:

$2,595.00 Domestic price Cryo Recovery

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Details

Detailed Description

Mice that are heterozygous for the targeted allele are viable and fertile. Mice homozygous for this mutation have a lethal phenotype. Half of homozygous null mice have an embryonic lethal phenotype, dying between 10.5 to 12.5 days post coitum. The cause of embryonic death may be due to circulatory abnormalities. Embryonic death also occurred in late gestation, with the remaining homozygous mutants dying at birth, due to respiratory failure. At 12.5 dpc, initial cartilaginous primordia of mutant embryos forelimbs are not abnormal, but by 13.5 dpc, mutant embryos display severe foreshortening of the forelimbs. At birth, the length of long bones of mutant animals are only one third the length of long bones of wildtype animals. Mutants have reduced chondrocyte proliferation, abnormal chondrocyte maturation and absence of mature osteoblasts in endochondral bones. Recent studies have linked mutations of Ihh to brachydactyly type A-1 St-Jacques. This mutant mouse strain represents a model that may be useful in studies of skeletal morphogenesis.

Development

A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to replace the entire first exon, encoding much of the signaling peptide, and approximately 1kb of flanking sequence. The construct was electroporated into 129 derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 derived blastocysts. The resulting chimeric animals were backcrossed to 129X1 mice.

Control Suggestions

Wild-type from the colony

Additional Information

Considerations for Choosing Controls

Selected References

St-Jacques B; Hammerschmidt M; McMahon AP. 1999. Indian hedgehog signaling regulates proliferation and differentiation of chondrocytes and is essential for bone formation [published erratum appears in Genes Dev 1999 Oct 1;13(19):2617]. In: . . MGI: J:57297

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Genetics

Ihh^tm1Amc

Allele Symbol: Ihh^tm1Amc

Allele Name	targeted mutation 1, Andrew P McMahon
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Ihh^-; Ihhⁿ
Gene Symbol and Name	Ihh, Indian hedgehog
Gene Synonym(s)	BDA1; HHG2
Strain of Origin	(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Chromosome	1
Molecular Note	A neomycin resistance cassette replaced the entire first exon, which encodes much of the signaling peptide, and approximately 1kb of flanking sequence.
Mutations Made By	Andrew McMahon, University of Southern California

Disease/Phenotype

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Genotype: Ihh^tm1Amc related

Developmental Biology Research
- Embryonic Lethality (Homozygous)
  - incomplete
- Perinatal Lethality
  - Homozygous

Mammalian Phenotype Terms by Genotype

Genotype: Ihh^tm1Amc/Ihh^tm1Amc
involves: 129S1/Sv * 129X1/SvJ

growth/size/body region phenotype

decreased body height
- at birth, homozygotes are consistently shorter than wild-type mice

disproportionate dwarf
- at birth mutants display severe short-limb dwarfism

short snout
- at birth, homozygotes show a foreshortened snout

skeleton phenotype

abnormal axial skeleton morphology

abnormal bone mineralization
- at 16.5 dpc, mutant humeri show ectopic initial calcification in the center of cartilage only, suggesting that mineralization occurs in cartilage and not in association with a bone collar
- by 18.5 dpc, ectopic calcification extends closer to the articular surfaces in mutant bones, including the humerus, sternum, vertebrae, and cartilaginous synchondroses of the base of the skull

abnormal bone ossification
- in homozygotes, appendicular skeletal elements fail to ossify

abnormal cartilage development
- although initial cartilage elements develop normally, 13.5-dpc mutant forelimbs show a slight reduction in each cartilage element relative to wild-type; this size difference is clearly visible at 14.5 dpc

abnormal chondrocyte morphology
- decrease in chondrocyte proliferation at E14.5
- homozygotes display ectopic maturation of chondrocytes: chondrocyte differentiation is initially delayed, but when it occurs, hypertrophic cells fail to exhibit a stacked columnar organization and occupy inappropriate positions close to articular surfaces
- premature chondrocyte hypertrophy, resulting in depletion of non-mineralized cartilage at articular ends of long bones

abnormal humerus morphology
- at 18.5 dpc, mutant humeri display no identifiable cortical bone, even in vascularized areas of the perichondrium
- at 18.5 dpc, the mutant humerus and ulna remain partly fused

abnormal joint morphology
- at 18.5 dpc, homozygotes show abnormal joint formation

abnormal long bone epiphyseal plate proliferative zone
- as early as 12.5 dpc, mutant humeri show a ~50% reduction in chondrocyte proliferation; in addition, the length of proliferative zone is severely reduced

abnormal long bone morphology
- depletion of non-mineralized cartilage at articular ends of long bones
- mutant long bones fail to show any signs of calcification at 14.5 dpc, as expected; instead, calcification is first noted at 16.5 dpc in mutant scapula and humerus, and slightly later in radius and ulna

abnormal rib morphology
- mutant ribs do not display excessive calcification

abnormal skeleton development
- skeletal growth retardation

abnormal skeleton morphology
- in homozygotes, most skeletal elements are present in the right position and in the right number; however, all elements of the axial and appendicular skeletons exhibit dwarfism

abnormal trabecular bone morphology
- 18.5 dpc, mutant humeri display no identifiable trabecular bone in the primary spongiosa

chondrodystrophy
- reduced chondrocyte proliferation and severe short-limb dwarfism are seen

decreased length of long bones
- at birth, mutant long bones are one-third the length of wild-type long bones

decreased osteoblast cell number
- at 18.5 dpc, homozygotes show no osteocalcin expression in endochondral bones of the appendicular or axial skeleton, indicating absence of mature osteoblasts in mutant long bones
- in contrast, mature osteoblasts are present in mutant bones formed by intramembranous ossification (e.g. flat bones of the skull, mandible, and clavicle)

decreased width of hypertrophic chondrocyte zone
- at 13.5 dpc, mutant humeri show absence of typical hypertrophic chondrocytes
- at 14.5 dpc, some hypertrophic cells are found in the center of mutant humeri but are neither as large nor as well-organized as those of wild-type bones
- such hypertrophic cells are surrounded by less mature chondrocytes and show no signs of vascularization or cortical bone formation

delayed endochondral bone ossification
- homozygotes exhibit absence of endochondral bone formation prior to birth
- in homozygous newborns, most endochondral bones are shorter and relatively malformed

domed cranium
- at birth, homozygotes show a rounded skull

fused carpal bones
- at 18.5 dpc, some of the wrist bones of homozygotes appear partly fused

short fibula

short humerus

short mandible
- at birth, homozygotes display a foreshortened mandible

short ribs
- homozygotes have significantly shortened ribs

short scapula
- length of scapula is shorter

short tibia
- growth retardation of tibia

short ulna

limbs/digits/tail phenotype

abnormal digit morphology
- failure of digit segmentation and ossification
- homozygotes display failure of digit segmentation: at 18.5 dpc, mutant digits remain unsegmented and uncalcified

abnormal forelimb morphology
- at 13.5 dpc, homozygotes display visibly shortened forelimbs

abnormal humerus morphology
- at 18.5 dpc, mutant humeri display no identifiable cortical bone, even in vascularized areas of the perichondrium
- at 18.5 dpc, the mutant humerus and ulna remain partly fused

fused carpal bones
- at 18.5 dpc, some of the wrist bones of homozygotes appear partly fused

short fibula

short humerus

short limbs
- 60-80% reduction in the length of the stylopod and the zeugopod at birth
- at 13.5 dpc, homozygotes display visibly shortened forelimbs
- at birth, homozygotes display significant dwarfism of the limbs

short tail

short tibia
- growth retardation of tibia

short ulna

vision/eye phenotype

vision/eye phenotype
- astrocyte precursor cells at the optic disc and in the optic nerve develop normally
- no rosettes are observed in the retina

mortality/aging

embryonic lethality during organogenesis, incomplete penetrance
- about 50% of homozygotes die at midgestation between 10.5 and 12.5 dpc, probably as a result of circulatory defects
- some lethality also occurs at later stages of gestation

neonatal lethality, complete penetrance
- homozygotes that develop to term die at birth due to respiratory failure

craniofacial phenotype

domed cranium
- at birth, homozygotes show a rounded skull

short mandible
- at birth, homozygotes display a foreshortened mandible

short snout
- at birth, homozygotes show a foreshortened snout

respiratory system phenotype

respiratory failure

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Ihh^tm1Amc/Ihh⁺
involves: 129S1/Sv * 129X1/SvJ * C57BL/6

skeleton phenotype

decreased long bone epiphyseal plate size
- modest shortening of the growth plate

Genotype: Ihh^tm1Amc/Ihh^tm1Amc
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J

digestive/alimentary phenotype

abnormal digestive organ placement
- at 18.5 dpc, all homozygotes display an obvious malrotation of the gut, in the absence of reversions in gut situs

abnormal digestive system morphology
- at 18.5 dpc, homozygotes display a smaller gastrointestinal tract relative to wild-type

abnormal duodenum morphology
- at 18.5 dpc, homozygotes show a 45% reduction in the number of cholecystokinin-producing cells of the duodenum
- at 18.5 dpc, no duodenal stenosis is observed

abnormal small intestine morphology
- at 18.5 dpc, homozygotes show a 34% reduction in thickness of the circular smooth muscle layer along the small intestine
- at 18.5 dpc, homozygotes show a significant dilation of the small intestine
- at this stage, the size of mutant villi is markedly reduced concomitant with a 54% decrease in epithelial stem cell proliferation between and at the base of villi

aganglionic megacolon
- at 18.5 dpc, 50% of homozygotes display an aganglionic megacolon

digestive/alimentary phenotype
- at 18.5 dpc, homozygotes exhibit no intestinal transformation of the stomach epithelium

megacolon
- at 18.5 dpc, homozygotes display a significant dilation of parts of the colon as well as a thin wall

growth/size/body region phenotype

decreased fetal size
- at 18.5 dpc, mutant embryos have an overall reduced size relative to wild-type embryos

nervous system phenotype

absent enteric neurons
- at 18.5 dpc, enteric neurons are completely absent along parts of the small intestine and in dilated portions of the colon

endocrine/exocrine gland phenotype

annular pancreas
- at 18.5 dpc, 43% of homozygotes exhibit an annular pancreas

muscle phenotype

abnormal smooth muscle morphology
- at 18.5 dpc, homozygotes show a 34% reduction in thickness of the circular smooth muscle layer along the small intestine

Genotype: Ihh^tm1Amc/Ihh^tm1Amc
involves: 129S1/Sv * 129X1/SvJ * C57BL/6

embryo phenotype

abnormal visceral yolk sac morphology

abnormal vitelline vasculature morphology
- yolk sacs have fewer and thinner blood vessels compared to wild-type at E9.5

cardiovascular system phenotype

abnormal vitelline vasculature morphology
- yolk sacs have fewer and thinner blood vessels compared to wild-type at E9.5

References

St-Jacques B; Hammerschmidt M; McMahon AP. 1999. Indian hedgehog signaling regulates proliferation and differentiation of chondrocytes and is essential for bone formation [published erratum appears in Genes Dev 1999 Oct 1;13(19):2617]. In: . . MGI: J:57297

Additional - Ihh^tm1Amc related

Astorga J; Carlsson P. 2007. Hedgehog induction of murine vasculogenesis is mediated by Foxf1 and Bmp4.. In: . . MGI: J:128367
Bondurand N; Southard-Smith EM. 2016. Mouse models of Hirschsprung disease and other developmental disorders of the enteric nervous system: Old and new players.. In: . . MGI: J:235629
Bren-Mattison Y; Hausburg M; Olwin BB. 2011. Growth of limb muscle is dependent on skeletal-derived Indian hedgehog.. In: . . MGI: J:175458
Capurro MI; Li F; Filmus J. 2009. Overgrowth of a mouse model of Simpson-Golabi-Behmel syndrome is partly mediated by Indian hedgehog.. In: . . MGI: J:157333
Chen MH; Li YJ; Kawakami T; Xu SM; Chuang PT. 2004. Palmitoylation is required for the production of a soluble multimeric Hedgehog protein complex and long-range signaling in vertebrates.. In: . . MGI: J:89228
Colnot C; de la Fuente L; Huang S; Hu D; Lu C; St-Jacques B; Helms JA. 2005. Indian hedgehog synchronizes skeletal angiogenesis and perichondrial maturation with cartilage development.. In: . . MGI: J:97179
Dakubo GD; Mazerolle C; Furimsky M; Yu C; St-Jacques B; McMahon AP; Wallace VA. 2008. Indian hedgehog signaling from endothelial cells is required for sclera and retinal pigment epithelium development in the mouse eye.. In: . . MGI: J:139168
Dakubo GD; Wang YP; Mazerolle C; Campsall K; McMahon AP; Wallace VA. 2003. Retinal ganglion cell-derived sonic hedgehog signaling is required for optic disc and stalk neuroepithelial cell development.. In: . . MGI: J:83530
Ehlen H. 2013. Inactivation of anoctamin-6/Tmem16f, a regulator of phosphatidylserine scrambling in osteoblasts, leads to decreased mineral deposition in skeletal tissues. In: . . MGI: J:195901
Gao B; Hu J; Stricker S; Cheung M; Ma G; Law KF; Witte F; Briscoe J; Mundlos S; He L; Cheah KS; Chan D. 2009. A mutation in Ihh that causes digit abnormalities alters its signalling capacity and range.. In: . . MGI: J:147878
Hebrok M; Kim SK; St Jacques B; McMahon AP; Melton DA. 2000. Regulation of pancreas development by hedgehog signaling.. In: . . MGI: J:65293
Hojo H; Ohba S; Taniguchi K; Shirai M; Yano F; Saito T; Ikeda T; Nakajima K; Komiyama Y; Nakagata N; Suzuki K; Mishina Y; Yamada M; Konno T; Takato T; Kawaguchi H; Kambara H; Chung UI. 2013. Hedgehog-Gli activators direct osteo-chondrogenic function of bone morphogenetic protein toward osteogenesis in the perichondrium.. In: . . MGI: J:197832
Hojo H; Ohba S; Yano F; Saito T; Ikeda T; Nakajima K; Komiyama Y; Nakagata N; Suzuki K; Takato T; Kawaguchi H; Chung UI. 2012. Gli1 protein participates in Hedgehog-mediated specification of osteoblast lineage during endochondral ossification.. In: . . MGI: J:185618
Hu H; Hilton MJ; Tu X; Yu K; Ornitz DM; Long F. 2005. Sequential roles of Hedgehog and Wnt signaling in osteoblast development.. In: . . MGI: J:94274
Huang AH; Riordan TJ; Pryce B; Weibel JL; Watson SS; Long F; Lefebvre V; Harfe BD; Stadler HS; Akiyama H; Tufa SF; Keene DR; Schweitzer R. 2015. Musculoskeletal integration at the wrist underlies the modular development of limb tendons.. In: . . MGI: J:224077
Joeng KS; Long F. 2009. The Gli2 transcriptional activator is a crucial effector for Ihh signaling in osteoblast development and cartilage vascularization.. In: . . MGI: J:154905
Karp SJ; Schipani E; St-Jacques B; Hunzelman J; Kronenberg H; McMahon AP. 2000. Indian hedgehog coordinates endochondral bone growth and morphogenesis via parathyroid hormone related-protein-dependent and -independent pathways.. In: . . MGI: J:59287
Kesper DA; Didt-Koziel L; Vortkamp A. 2010. Gli2 activator function in preosteoblasts is sufficient to mediate Ihh-dependent osteoblast differentiation, whereas the repressor function of Gli2 is dispensable for endochondral ossification.. In: . . MGI: J:160585
Kobayashi T; Soegiarto DW; Yang Y; Lanske B; Schipani E; McMahon AP; Kronenberg HM. 2005. Indian hedgehog stimulates periarticular chondrocyte differentiation to regulate growth plate length independently of PTHrP.. In: . . MGI: J:99641
Koyama E; Ochiai T; Rountree RB; Kingsley DM; Enomoto-Iwamoto M; Iwamoto M; Pacifici M. 2007. Synovial joint formation during mouse limb skeletogenesis: roles of Indian hedgehog signaling.. In: . . MGI: J:133905
Koziel L; Wuelling M; Schneider S; Vortkamp A. 2005. Gli3 acts as a repressor downstream of Ihh in regulating two distinct steps of chondrocyte differentiation.. In: . . MGI: J:102948
Lenton K; James AW; Manu A; Brugmann SA; Birker D; Nelson ER; Leucht P; Helms JA; Longaker MT. 2011. Indian hedgehog positively regulates calvarial ossification and modulates bone morphogenetic protein signaling.. In: . . MGI: J:178364
Levi B; James AW; Nelson ER; Brugmann SA; Sorkin M; Manu A; Longaker MT. 2011. Role of Indian hedgehog signaling in palatal osteogenesis.. In: . . MGI: J:182649
Li X; Blagden CS; Bildsoe H; Bonnin MA; Duprez D; Hughes SM. 2004. Hedgehog can drive terminal differentiation of amniote slow skeletal muscle.. In: . . MGI: J:107621
Liu C; Peng J; Matzuk MM; Yao HH. 2015. Lineage specification of ovarian theca cells requires multicellular interactions via oocyte and granulosa cells.. In: . . MGI: J:222787
Long F; Joeng KS; Xuan S; Efstratiadis A; McMahon AP. 2006. Independent regulation of skeletal growth by Ihh and IGF signaling.. In: . . MGI: J:119575
Long F; Zhang XM; Karp S; Yang Y; McMahon AP. 2001. Genetic manipulation of hedgehog signaling in the endochondral skeleton reveals a direct role in the regulation of chondrocyte proliferation.. In: . . MGI: J:73071
Mao J; Kim BM; Rajurkar M; Shivdasani RA; McMahon AP. 2010. Hedgehog signaling controls mesenchymal growth in the developing mammalian digestive tract.. In: . . MGI: J:160363
Nelson ER; Levi B; Sorkin M; James AW; Liu KJ; Quarto N; Longaker MT. 2011. Role of GSK-3beta in the osteogenic differentiation of palatal mesenchyme.. In: . . MGI: J:179587
Outram SV; Hager-Theodorides AL; Shah DK; Rowbotham NJ; Drakopoulou E; Ross SE; Lanske B; Dessens JT; Crompton T. 2009. Indian hedgehog (Ihh) both promotes and restricts thymocyte differentiation.. In: . . MGI: J:145997
Ramalho-Santos M; Melton DA; McMahon AP. 2000. Hedgehog signals regulate multiple aspects of gastrointestinal development.. In: . . MGI: J:62158
Shibukawa Y; Young B; Wu C; Yamada S; Long F; Pacifici M; Koyama E. 2007. Temporomandibular joint formation and condyle growth require Indian hedgehog signaling.. In: . . MGI: J:117221
Tu X; Joeng KS; Long F. 2012. Indian hedgehog requires additional effectors besides Runx2 to induce osteoblast differentiation.. In: . . MGI: J:180304
Wang YP; Dakubo G; Howley P; Campsall KD; Mazarolle CJ; Shiga SA; Lewis PM; McMahon AP; Wallace VA. 2002. Development of normal retinal organization depends on Sonic hedgehog signaling from ganglion cells.. In: . . MGI: J:78708
Witte F; Chan D; Economides AN; Mundlos S; Stricker S. 2010. Receptor tyrosine kinase-like orphan receptor 2 (ROR2) and Indian hedgehog regulate digit outgrowth mediated by the phalanx-forming region.. In: . . MGI: J:163602
Young B; Minugh-Purvis N; Shimo T; St-Jacques B; Iwamoto M; Enomoto-Iwamoto M; Koyama E; Pacifici M. 2006. Indian and sonic hedgehogs regulate synchondrosis growth plate and cranial base development and function.. In: . . MGI: J:171806
Zhang XM; Ramalho-Santos M; McMahon AP. 2001. Smoothened mutants reveal redundant roles for Shh and Ihh signaling including regulation of L/R symmetry by the mouse node.. In: . . MGI: J:175111
Zhang XQ; Afink GB; Hu XR; Nister M; Forsberg-Nilsson K. 2005. Gli1 is not required for Pdgfralpha expression during mouse embryonic development.. In: . . MGI: J:97242

Service	Genotype	Price
	Heterozygous or Wild-type for Ihh<tm1Amc>

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Also Known As: Ihh KO

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Ihhtm1Amc

Allele Symbol: Ihhtm1Amc

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Genotype: Ihhtm1Amc related

Mammalian Phenotype Terms by Genotype

Genotype: Ihhtm1Amc/Ihhtm1Amcinvolves: 129S1/Sv * 129X1/SvJ

growth/size/body region phenotype

skeleton phenotype

limbs/digits/tail phenotype

vision/eye phenotype

mortality/aging

craniofacial phenotype

respiratory system phenotype

Genotype: Ihhtm1Amc/Ihh+involves: 129S1/Sv * 129X1/SvJ * C57BL/6

skeleton phenotype

Genotype: Ihhtm1Amc/Ihhtm1Amcinvolves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J

digestive/alimentary phenotype

growth/size/body region phenotype

nervous system phenotype

endocrine/exocrine gland phenotype

muscle phenotype

Genotype: Ihhtm1Amc/Ihhtm1Amcinvolves: 129S1/Sv * 129X1/SvJ * C57BL/6

embryo phenotype

cardiovascular system phenotype

References

Additional - Ihhtm1Amc related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Ihh^tm1Amc

Allele Symbol: Ihh^tm1Amc

Genotype: Ihh^tm1Amc related

Genotype: Ihh^tm1Amc/Ihh^tm1Amc
involves: 129S1/Sv * 129X1/SvJ

Genotype: Ihh^tm1Amc/Ihh⁺
involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Genotype: Ihh^tm1Amc/Ihh^tm1Amc
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * CBA/J

Genotype: Ihh^tm1Amc/Ihh^tm1Amc
involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Additional - Ihh^tm1Amc related