Overview

Also Known As:Shh-

These Shh knock-out mice exhibit defects in the establishment and maintenance of midline structures.

Donating Investigator

Andrew P McMahon, University of Southern California

Genetic overview

Genetic Background	Generation

Shh^tm1Amc

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Shh	sonic hedgehog

View Genetics

Research Applications

Cancer Research
Dermatology Research
Developmental Biology Research
Neurobiology Research
Sensorineural Research
Cell Biology Research

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

View Price List

Details

Detailed Description

Mice homozygous for the Shh^tm1Amc targeted mutation display early defects in the establishment and maintenance of midline structures. These defects result from the critical role the Sonic hedgehog (Shh) gene plays in the patterning of vertebrate embryonic tissues, including the brain and spinal cord, the axial skeleton and the limbs. Defects are also observed in all tissues, confirming the proposed role of SHH proteins as an extracellular signal required for the tissue-organizing properties of several vertebrate patterning centers.

When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 004293) and a strain expressing Cre recombinase in the skin and dental epithelium (Stock No. 004782), this mutant mouse strain may be useful in studies of hedgehog signalling and cell proliferation in the dental epithelium.

When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 004293) and a strain expressing Cre recombinase in the mesonephric duct and its developmental derivatives (Stock No. 004692), this mutant mouse strain may be useful in studies of hedgehog signaling and cell proliferation/differentiation in mesenchymal cells of the kidney.

Control Suggestions

Wild-type from the colony

Additional Information

Considerations for Choosing Controls

Selected References

St-Jacques B; Dassule HR; Karavanova I; Botchkarev VA; Li J; Danielian PS; McMahon JA; Lewis PM; Paus R; McMahon AP. 1998. Sonic hedgehog signaling is essential for hair development. Curr Biol 8(19):1058-68PubMed: 9768360 MGI: J:50050

View All References

Genetics

Shh^tm1Amc

Allele Symbol: Shh^tm1Amc

Allele Name	targeted mutation 1, Andrew P McMahon
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Shh-; Shhⁿ
Gene Symbol and Name	Shh, sonic hedgehog
Gene Synonym(s)
Strain of Origin	(129X1/SvJ x 129S1/Sv)F1-Kitl⁺
Chromosome	5
Molecular Note	A neomycin cassette replaced exon 2 and portions of the flanking intronic sequences.
Mutations Made By	Dr. Paula Lewis, AstraZeneca, R&D Boston

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Genotype: Shh^tm1Amc related

Cancer Research
- Genes Regulating Growth and Proliferation
- Growth Factors/Receptors/Cytokines
- Oncogenes
Dermatology Research
- Skin and Hair Texture Defects
Developmental Biology Research
- Craniofacial and Palate Defects
- Embryonic Lethality (Homozygous)
- Postnatal Lethality
- Eye Defects
- Growth Defects
- Internal/Organ Defects
- Neural Tube Defects
- Neurodevelopmental Defects
- Skeletal Defects
Neurobiology Research
- Neural Tube Defects
- Neurodevelopmental Defects
Sensorineural Research
- Eye Defects
Cell Biology Research
- Genes Regulating Growth and Proliferation

Mammalian Phenotype Terms by Genotype

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

Genotype: Shh^tm1Amc/Shh^tm1Amc
Not Specified

digestive/alimentary phenotype

small stomach
- reduced stomach size, particularly in the fore-stomach, at E12.5

tracheoesophageal fistula
- a single tracheal-esophageal tube lacking any cartilaginous rings is seen
- this tube is lined with stratified squamous epithelium dorsally and columnar airway epithelium ventrally

skeleton phenotype

absent tracheal cartilage rings
- the cartilaginous rings that normally surround the trachea are absent

mortality/aging

neonatal lethality, complete penetrance
- homozygous mutants die shortly after birth

respiratory system phenotype

abnormal branching involved in lung morphogenesis
- branching morphogenesis is impaired with the single tracheal-esophageal tube connected to the proximal and peripheral lung structures

abnormal bronchus morphology
- peripheral tubules are absent

abnormal pharynx morphology
- the pharynx is closed anteriorly

absent tracheal cartilage rings
- the cartilaginous rings that normally surround the trachea are absent

pulmonary hypoplasia
- lungs are severely hypoplastic
- the anterior closed pharynx connects to a posteroir bilobed lung in which the central airway is surrounded only by rudimentary peripheral saccules

tracheoesophageal fistula
- a single tracheal-esophageal tube lacking any cartilaginous rings is seen
- this tube is lined with stratified squamous epithelium dorsally and columnar airway epithelium ventrally

Genotype: Shh^tm1Amc/Shh^tm1Amc
involves: 129/Sv * C57BL/6J * CBA/J

cardiovascular system phenotype

abnormal lung vasculature morphology
- poorly vascularized airways

endocrine/exocrine gland phenotype

annular pancreas
- at 18.5 dpc, 85% of homozygotes exhibit an annular pancreas

growth/size/body region phenotype

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

integument phenotype

abnormal dermal layer morphology
- skin grafts of mutant skin transplanted onto nude mice exhibit a reduced dermal fat layer

abnormal dermis papillary layer morphology
- mutant skin displays only a rudimentary dermal papilla, indicating abnormal epithelial-mesenchymal interactions

abnormal hair follicle development
- at 18.5 dpc, mutant hair follicles at stage 1-2 show a 40% decline in keratinocyte proliferation relative to wild-type; no difference is observed in apoptosis
- homozygotes display delayed hair folliculoenesis: embryonic follicles are arrested shortly after induction and fail to progress beyond stage 2

abnormal hair follicle morphology
- at 15.5 dpc, mutant hair follicles form a smaller hair plug; however, epidermal expansion into the dermis and dermal condensation of mesenchyme at the base of the hair plug occur normally
- at 15.5 dpc, wild-type hair follicles have progressed to stage 2, whereas mutant follicles at still at stage 1 or 0
- skin grafts of mutant skin transplanted onto nude mice exhibit giant disorganized hair-bud-like structures, some with hair-shaft-like material, in the vicinity of epidermis

abnormal hair follicle orientation
- mutant hair buds fail to exhibit an obvious polarity; in contrast, wild-type follicles show a typical polarized development along the anterior-posterior axis

abnormal hair shaft morphology
- skin grafts of mutant skin transplanted onto nude mice show abnormal ingrowth of the epidermis and consequently aberrant morphogenesis of the hair shaft

absent hair follicle inner root sheath
- mutant hair follicles fail to initiate development of the inner root sheath from the hair matrix (stages 3-5)

absent hair follicles
- by 18.5 dpc, homozygotes show a severe reduction in the number of induced hair follicles relative to wild-type mice

alopecia
- skin grafts of mutant skin (epidermis and dermis) transplanted onto nude mice generate hairless, pigmented skin
- some keratinized pigmented material resembling hair matrix is present, but no hair is formed

decreased keratinocyte proliferation
- at 18.5 dpc, mutant hair follicles at stage 1-2 show a 40% decline in keratinocyte proliferation relative to wild-type, with no difference observed in apoptosis

epidermal hyperplasia
- skin grafts of mutant skin transplanted onto nude mice display hyperplasia and abnormal keratin expression in interfollicular epidermis

thick epidermis
- skin grafts of mutant skin transplanted onto nude mice exhibit a thickened epidermis with large disorganized ingrowths

cellular phenotype

decreased keratinocyte proliferation
- at 18.5 dpc, mutant hair follicles at stage 1-2 show a 40% decline in keratinocyte proliferation relative to wild-type, with no difference observed in apoptosis

digestive/alimentary phenotype

abnormal colon morphology
- at 18.5 dpc, the mutant colon ends in a blind dilation that is not fused to the surface ectoderm; however, no aganglionic colon is observed

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, 67% of homozygotes display occlusion of the duodenum by overgrown villi, resembling duodenal stenosis

abnormal esophagus morphology
- at 18.5 dpc, the mutant esophagus tissue is reduced and fused to the trachea

abnormal small intestine morphology
- at 18.5 dpc, homozygotes show a 21% reduction in thickness of the circular smooth muscle layer along the small intestine; however, no intestinal dilation is observed

abnormal stomach glandular epithelium morphology
- at 18.5 dpc, the mutant glandular epithelium displays histologic features that resemble intestinal metaplasia

anal atresia
- at 18.5 dpc, all homozygotes have an imperforate anus

gastric metaplasia
- at 18.5 dpc, all homozygotes exhibit intestinal transformation of the stomach epithelium

stomach epithelial hyperplasia
- at 18.5 dpc, all homozygotes display a significant overgrowth of stomach epithelium, in spite of normal rates of cell proliferation in the stomach

tracheoesophageal fistula
- at 18.5 dpc, the mutant trachea and esophagus are fused to form a fistula-like fusion of the alimentary and respiratory tract

mortality/aging

perinatal lethality, complete penetrance
- none of the homozygotes surviving to term live beyond this time

prenatal lethality, incomplete penetrance
- only ~50% of homozygotes survive to term

muscle phenotype

abnormal smooth muscle morphology
- at 18.5 dpc, homozygotes show a 21% reduction in thickness of the circular smooth muscle layer along the small intestine

abnormal tracheal smooth muscle morphology
- in mutant trachea, the layer of smooth muscle that normally lines the proximal epithelium is absent

nervous system phenotype

abnormal enteric neuron morphology
- at 18.5 dpc, homozygotes show excessive and abnormally located neurons that differentiate under the epithelium and into the villi

respiratory system phenotype

abnormal lung development
- although left and right buds form, mutant lungs fail to undergo lobation or subsequent extensive branching

abnormal lung saccule morphology
- by 18.5 dpc, only a few air sacs are present

abnormal lung vasculature morphology
- poorly vascularized airways

abnormal tracheal cartilage morphology
- in mutant trachea, cartilaginous rings are present but appear disorganized

abnormal tracheal smooth muscle morphology
- in mutant trachea, the layer of smooth muscle that normally lines the proximal epithelium is absent

impaired branching involved in bronchus morphogenesis
- at 12.5 dpc, mutant lungs fail to branch or display one abnormally positioned branch point
- in organ culture, mutant lungs fail to grow or branch extensively; bronchial mesenchyme cells detach from the endodermal epithelium

impaired lung lobe morphogenesis
- mutant lungs fail to undergo lobation

pulmonary hypoplasia
- at 18.5 dpc, homozygotes display a rudimentary respiratory organ with a few large, poorly vascularized airways

tracheoesophageal fistula
- at 18.5 dpc, the mutant trachea and esophagus are fused to form a fistula-like fusion of the alimentary and respiratory tract

skeleton phenotype

abnormal tracheal cartilage morphology
- in mutant trachea, cartilaginous rings are present but appear disorganized

Genotype: Shh^tm1Amc/Shh^tm2Amc Tg(KRT14-cre)1Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

craniofacial phenotype

abnormal ameloblast morphology
- at birth, functional ameloblast layers are present but display abnormal polarity and cellular architecture
- when early tooth rudiments (13.5-15.5 dpc) are transplanted under kidney capsules of nude mice, enamel and dentin matrices are deposited in spite of absent ameloblast elongation and odontoblast disorganization

abnormal cranium morphology
- at birth, mutant pups display flattened skulls

abnormal dentin morphology
- in grafts of early tooth rudiments (13.5-15.5 dpc), dentin deposits are deposited but crown formation is incomplete and resulting teeth are small and abnormally shaped

abnormal enamel morphology
- at 14.5 dpc, the outer enamel epithelium of the lingual side is severely reduced and the lingual inner enamel epithelium has not invaginated, suggesting impaired crown formation
- when early tooth rudiments (13.5-15.5 dpc) are transplanted under kidney capsules of nude mice, enamel matrix is secreted but crown formation is incomplete and resulting teeth are small and abnormally shaped

abnormal incisor morphology
- at birth, mutant pups display small (only 5% of normal size) and abnormally shaped incisors in both the mandible and maxilla

abnormal lower incisor morphology
- mandibular incisors display a single cusp with two symmetrical cervical loops; additional cusp formation is disrupted

abnormal molar cusp morphology
- mandibular molars display a single irregular cusp; additional cusp formation is disrupted

abnormal nasal bone morphology
- at birth, mutant pups display a small frontal nasal process; nasal passageways are severely reduced

abnormal odontoblast morphology
- at birth, functional odontoblast layers are present but display abnormal polarity and cellular architecture

abnormal palatal shelf fusion at midline
- the rudimentary palatal shelves are spaced widely apart

absent alveolar process
- mutant mandibular molars are fused with the oral ectoderm and the alveolar bone is absent

absent enamel cord
- the dental cord is absent in mandibular molars

arrest of tooth development
- at birth, mutant pups show absence of obvious teeth: manidbular molars and incisors exhibit a cap stage tooth rudiment of abnormal morphology

cleft secondary palate
- 85% exhibit a cleft palate with rudimentary palatal shelves spaced widely apart

growth retardation of incisors
- at birth, mandibular incisors are more developmentally advanced relative to mandibular molars

growth retardation of molars
- at birth, mandibular molars are less developmentally advanced relative to mandibular incisors

palatal shelf hypoplasia
- the palatal shelves fail to develop beyond rudimentary processes

small incisors
- at birth, incisors are only 5% of normal size

small molars
- although cervical loops, dental papilla, inner enamel epithelium, predentin, and stellate reticulum are present, no dental cord is formed
- at birth, mutant pups display small and abnormally shaped first molars in both the mandible and maxilla
- maxillary molars are less affected than mandibular molars which are 25% of normal size

digestive/alimentary phenotype

abnormal palatal shelf fusion at midline
- the rudimentary palatal shelves are spaced widely apart

cleft secondary palate
- 85% exhibit a cleft palate with rudimentary palatal shelves spaced widely apart

palatal shelf hypoplasia
- the palatal shelves fail to develop beyond rudimentary processes

growth/size/body region phenotype

abnormal ameloblast morphology
- at birth, functional ameloblast layers are present but display abnormal polarity and cellular architecture
- when early tooth rudiments (13.5-15.5 dpc) are transplanted under kidney capsules of nude mice, enamel and dentin matrices are deposited in spite of absent ameloblast elongation and odontoblast disorganization

abnormal dentin morphology
- in grafts of early tooth rudiments (13.5-15.5 dpc), dentin deposits are deposited but crown formation is incomplete and resulting teeth are small and abnormally shaped

abnormal enamel morphology
- at 14.5 dpc, the outer enamel epithelium of the lingual side is severely reduced and the lingual inner enamel epithelium has not invaginated, suggesting impaired crown formation
- when early tooth rudiments (13.5-15.5 dpc) are transplanted under kidney capsules of nude mice, enamel matrix is secreted but crown formation is incomplete and resulting teeth are small and abnormally shaped

abnormal incisor morphology
- at birth, mutant pups display small (only 5% of normal size) and abnormally shaped incisors in both the mandible and maxilla

abnormal lower incisor morphology
- mandibular incisors display a single cusp with two symmetrical cervical loops; additional cusp formation is disrupted

abnormal molar cusp morphology
- mandibular molars display a single irregular cusp; additional cusp formation is disrupted

abnormal odontoblast morphology
- at birth, functional odontoblast layers are present but display abnormal polarity and cellular architecture

abnormal palatal shelf fusion at midline
- the rudimentary palatal shelves are spaced widely apart

absent alveolar process
- mutant mandibular molars are fused with the oral ectoderm and the alveolar bone is absent

absent enamel cord
- the dental cord is absent in mandibular molars

arrest of tooth development
- at birth, mutant pups show absence of obvious teeth: manidbular molars and incisors exhibit a cap stage tooth rudiment of abnormal morphology

cleft secondary palate
- 85% exhibit a cleft palate with rudimentary palatal shelves spaced widely apart

growth retardation of incisors
- at birth, mandibular incisors are more developmentally advanced relative to mandibular molars

growth retardation of molars
- at birth, mandibular molars are less developmentally advanced relative to mandibular incisors

palatal shelf hypoplasia
- the palatal shelves fail to develop beyond rudimentary processes

small incisors
- at birth, incisors are only 5% of normal size

small molars
- although cervical loops, dental papilla, inner enamel epithelium, predentin, and stellate reticulum are present, no dental cord is formed
- at birth, mutant pups display small and abnormally shaped first molars in both the mandible and maxilla
- maxillary molars are less affected than mandibular molars which are 25% of normal size

integument phenotype

absent vibrissae

mammalian phenotype

skeleton phenotype
- Normal - at birth, mutant pups possess normal skeletal elements; the upper and lower jaws are of normal length

mortality/aging

neonatal lethality, complete penetrance
- mutant newborns die within a day after birth

respiratory system phenotype

aerophagia
- at birth, mutant pups are observed gulping air

skeleton phenotype

abnormal ameloblast morphology
- at birth, functional ameloblast layers are present but display abnormal polarity and cellular architecture
- when early tooth rudiments (13.5-15.5 dpc) are transplanted under kidney capsules of nude mice, enamel and dentin matrices are deposited in spite of absent ameloblast elongation and odontoblast disorganization

abnormal cranium morphology
- at birth, mutant pups display flattened skulls

abnormal dentin morphology
- in grafts of early tooth rudiments (13.5-15.5 dpc), dentin deposits are deposited but crown formation is incomplete and resulting teeth are small and abnormally shaped

abnormal enamel morphology
- at 14.5 dpc, the outer enamel epithelium of the lingual side is severely reduced and the lingual inner enamel epithelium has not invaginated, suggesting impaired crown formation
- when early tooth rudiments (13.5-15.5 dpc) are transplanted under kidney capsules of nude mice, enamel matrix is secreted but crown formation is incomplete and resulting teeth are small and abnormally shaped

abnormal incisor morphology
- at birth, mutant pups display small (only 5% of normal size) and abnormally shaped incisors in both the mandible and maxilla

abnormal lower incisor morphology
- mandibular incisors display a single cusp with two symmetrical cervical loops; additional cusp formation is disrupted

abnormal molar cusp morphology
- mandibular molars display a single irregular cusp; additional cusp formation is disrupted

abnormal nasal bone morphology
- at birth, mutant pups display a small frontal nasal process; nasal passageways are severely reduced

abnormal odontoblast morphology
- at birth, functional odontoblast layers are present but display abnormal polarity and cellular architecture

absent alveolar process
- mutant mandibular molars are fused with the oral ectoderm and the alveolar bone is absent

absent enamel cord
- the dental cord is absent in mandibular molars

arrest of tooth development
- at birth, mutant pups show absence of obvious teeth: manidbular molars and incisors exhibit a cap stage tooth rudiment of abnormal morphology

growth retardation of incisors
- at birth, mandibular incisors are more developmentally advanced relative to mandibular molars

growth retardation of molars
- at birth, mandibular molars are less developmentally advanced relative to mandibular incisors

small incisors
- at birth, incisors are only 5% of normal size

small molars
- although cervical loops, dental papilla, inner enamel epithelium, predentin, and stellate reticulum are present, no dental cord is formed
- at birth, mutant pups display small and abnormally shaped first molars in both the mandible and maxilla
- maxillary molars are less affected than mandibular molars which are 25% of normal size

vision/eye phenotype

eyelids open at birth

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

embryo phenotype

notochord degeneration
- at E9.5

nervous system phenotype

holoprosencephaly

skeleton phenotype

abnormal vertebrae morphology
- all ventral vertebral components are absent

Genotype: Shh^tm1Amc/Shh^tm2Amc Tg(Hoxb7-cre)13Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6

renal/urinary system phenotype

abnormal kidney inner medulla morphology
- at 4 months of age, most of the inner medulla is lost in hydronephric kidneys

abnormal kidney outer medulla inner stripe morphology
- at 4 months of age, most of the inner stripe of the outer medulla is lost in hydronephric kidneys

abnormal renal glomerulus morphology
- at the newborn stage, cortical glomerular density is increased by 24% while glomerular density of the whole kidney is increased by 26% relative to that in wild-type controls
- Normal - however, no gross differences in glomerular size are observed

abnormal ureter development
- at E14.5, fewer mesenchymal cells line the ureteral epithelium relative to wild-type controls
- at E14.5, the mitotic index of the proximal and distal ureter mesenchyme is ~50% of that in wild-type controls, indicating reduced cell proliferation
- Normal - however, no differences in ureteral mesenchyme apoptosis are observed by TUNEL analysis

abnormal ureter smooth muscle morphology
- a delay in smooth muscle differentiation is observed along the proximodistal axis of the ureter
- at E15.0, no smooth muscle alpha-actin protein (SMA), an early marker of smooth muscle differentiation, is detected at any axial level of the ureter, unlike in wild-type embryos where SMA is detected in the proximal ureter
- at the newborn stage, SMA is detected in the proximal ureter but, in contrast to wild-type controls, almost no SMA is detected in the distal-most part of the ureter, closest to the bladder
- in addition, mesenchymal cells in the distal ureter are not as condensed as those in wild-type controls

decreased renal glomerulus number
- newborn mice exhibit a 40% reduction in glomerular number

hydronephrosis
- at 4 months of age, 50% of mice exhibit hydronephrosis
- Normal - however, no hydronephrosis is detected in newborn pups

hydroureter
- newborn mice exhibit prominent hydroureter, usually more severe in the proximal region

kidney cortex hypoplasia
- at the newborn stage, cortical volume is reduced by 51%

kidney medulla hypoplasia
- at the newborn stage, medullary volume is reduced by 46%

renal hypoplasia

short ureter
- at E14.5, ureter length is ~21% shorter than in wild-type controls

small kidney
- neonatal kidneys are 52% smaller than wild-type kidneys

The following phenotype relates to a compound genotype created using this strain

Genotype: Shh^tm1Amc/Shh^tm1Amc
STOCK Shh/J

digestive/alimentary phenotype

abnormal submandibular gland morphology
- in vitro, Pseudoglandular (E14) stage SMG primordia cultured in the presence of Shh show a ~2-fold increase in epithelial branching compared with Initial Bud (E13) stage primordia, indicating a stage-specific difference in Shh-stimulated branching
- at E13.5 and E15.5, homozygotes show a severely reduced, dysplastic remnant of the submandibular salivary gland (SMG)
- at E18.5, homozygotes display a slightly larger but severely pedomorphic dysplastic SMG consisting of largely undifferentiated epithelium with very few branches surrounded by undifferentiated mesenchyme (reminiscent of the Pseudoglandular stage at ~E14)
- cyclopamine-treated explants show a marked reduction in branching and epithelial cell proliferation; notably FGF8-supplemented explants exhibit a significant 58% increase in branching morphogenesis compared with cyclopamine treatment alone

endocrine/exocrine gland phenotype

abnormal submandibular gland morphology
- in vitro, Pseudoglandular (E14) stage SMG primordia cultured in the presence of Shh show a ~2-fold increase in epithelial branching compared with Initial Bud (E13) stage primordia, indicating a stage-specific difference in Shh-stimulated branching
- at E13.5 and E15.5, homozygotes show a severely reduced, dysplastic remnant of the submandibular salivary gland (SMG)
- at E18.5, homozygotes display a slightly larger but severely pedomorphic dysplastic SMG consisting of largely undifferentiated epithelium with very few branches surrounded by undifferentiated mesenchyme (reminiscent of the Pseudoglandular stage at ~E14)
- cyclopamine-treated explants show a marked reduction in branching and epithelial cell proliferation; notably FGF8-supplemented explants exhibit a significant 58% increase in branching morphogenesis compared with cyclopamine treatment alone

References

St-Jacques B; Dassule HR; Karavanova I; Botchkarev VA; Li J; Danielian PS; McMahon JA; Lewis PM; Paus R; McMahon AP. 1998. Sonic hedgehog signaling is essential for hair development. Curr Biol 8(19):1058-68PubMed: 9768360 MGI: J:50050

Additional References

Chiang C; Litingtung Y; Lee E; Young KE; Corden JL; Westphal H; Beachy PA. 1996. Cyclopia and defective axial patterning in mice lacking Sonic hedgehog gene function. Nature 383(6599):407-13PubMed: 8837770 MGI: J:35802
Fedtsova N; Perris R; Turner EE. 2003. Sonic hedgehog regulates the position of the trigeminal ganglia. Dev Biol 261(2):456-69PubMed: 14499653 MGI: J:85580
Jaskoll T; Leo T; Witcher D; Ormestad M; Astorga J; Bringas P Jr; Carlsson P; Melnick M. 2004. Sonic hedgehog signaling plays an essential role during embryonic salivary gland epithelial branching morphogenesis. Dev Dyn 229(4):722-32PubMed: 15042696 MGI: J:89200

Additional - Shh^tm1Amc related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Shh
- Genotyping resources and troubleshooting
Breeding Considerations

Homozygotes are not viable. The strain is maintained by mating heterozygotes. The expected coat color from breeding is Black, White Bellied Agouti.
- Additional Breeding and Husbandry Support
Appearance
- agouti
  Related Genotype: A/?
  
  black
  Related Genotype: a/a
Citation
When using the Shh- mouse strain in a publication, please cite the originating article(s) and include JAX stock #003318 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or Wild-type for Shh<tm1Amc>

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

Terms Of Use

General Terms and Conditions

Questions about Terms of Use

Additional Use Restrictions Apply

Use of MICE by companies or for-profit entities requires a license prior to shipping.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCT(S)" means biological materials supplied by JACKSON, and their derivatives. "SERVICES" means projects conducted by JACKSON for other parties that may include but are not limited to the use of MICE or PRODUCTS. "RECIPIENT" means each recipient of MICE, PRODUCTS, or SERVICES provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE, PRODUCTS or SERVICES from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON’s prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED "AS IS". JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

Credit for PRODUCTS or SERVICES

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of, PRODUCTS or SERVICES, JACKSON will, at its option, provide credit or replacement for the PRODUCT received or the SERVICES provided; JACKSON makes no other representations and this shall be the exclusive remedy of the purchaser. Please note specific policy for live mice.

Animal Care and Use for SERVICES

Consistent with the requirement for a written understanding regarding animal care and use, the JACKSON Animal Care and Use Committee will review the animal care and use protocol(s) associated with any SERVICES to be performed at JACKSON, and JACKSON shall have ultimate responsibility and authority for the care of animals while on site or in JACKSON custody.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS, or SERVICES, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS, or SERVICES from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE, PRODUCTS or SERVICES are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or SERVICES. In addition, special terms and conditions of sale of certain MICE, PRODUCTS, or SERVICES may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and SERVICES by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or SERVICES shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or SERVICES by JACKSON.

Also Known As:Shh-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Control Suggestions

Additional Information

Selected References

Shhtm1Amc

Allele Symbol: Shhtm1Amc

Disease Terms

Research Areas By Phenotype

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

Genotype: Shhtm1Amc related

Mammalian Phenotype Terms by Genotype

Genotype: Shhtm1Amc/Shhtm1AmcNot Specified

digestive/alimentary phenotype

skeleton phenotype

mortality/aging

respiratory system phenotype

Genotype: Shhtm1Amc/Shhtm1Amcinvolves: 129/Sv * C57BL/6J * CBA/J

cardiovascular system phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

integument phenotype

cellular phenotype

digestive/alimentary phenotype

mortality/aging

muscle phenotype

nervous system phenotype

respiratory system phenotype

skeleton phenotype

Genotype: Shhtm1Amc/Shhtm2Amc Tg(KRT14-cre)1Amc/0involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

craniofacial phenotype

digestive/alimentary phenotype

growth/size/body region phenotype

integument phenotype

mammalian phenotype

mortality/aging

respiratory system phenotype

skeleton phenotype

vision/eye phenotype

Genotype: Shhtm1Amc/Shhtm1Amcinvolves: 129S1/Sv * 129X1/SvJ

embryo phenotype

nervous system phenotype

skeleton phenotype

Genotype: Shhtm1Amc/Shhtm2Amc Tg(Hoxb7-cre)13Amc/0involves: 129S1/Sv * 129X1/SvJ * C57BL/6

renal/urinary system phenotype

Genotype: Shhtm1Amc/Shhtm1AmcSTOCK Shh/J

digestive/alimentary phenotype

endocrine/exocrine gland phenotype

References

Additional References

Additional - Shhtm1Amc related

Genotyping Protocols

Breeding Considerations

Appearance

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

Shh^tm1Amc

Allele Symbol: Shh^tm1Amc

Genotype: Shh^tm1Amc related

Genotype: Shh^tm1Amc/Shh^tm1Amc
Not Specified

Genotype: Shh^tm1Amc/Shh^tm1Amc
involves: 129/Sv * C57BL/6J * CBA/J

Genotype: Shh^tm1Amc/Shh^tm2Amc Tg(KRT14-cre)1Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

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

Genotype: Shh^tm1Amc/Shh^tm2Amc Tg(Hoxb7-cre)13Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Genotype: Shh^tm1Amc/Shh^tm1Amc
STOCK Shh/J

Additional - Shh^tm1Amc related