| |||||||||||||||
- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
Description
The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.
Strain Information
Former Names 129/Sv-Nogtm1Amc/J (Changed: 29-JUN-05 ) Type Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Generation F?+3p Donating Investigator Andrew McMahon, Harvard University Description
Homozygous mice are born but die shortly after birth, exhibiting multiple defects, including an open neural tube, skeletal abnormalities, shortened body axis, and a small vestigial tail. Analysis of early gene expression has shown that the loss of Nog expression in the floorplate, notochord, and roofplate results in a progressive failure of ventral development in the CNS and somites. Nog is also expressed in condensing cartilage in the limb and in the sclerotome of somites so its loss results in defects in cartilage patterning and skeletal morphogenesis. Heterozygous embryos show lacZ reporter expression in pattern consistent with the endogenous gene.Development
A targeting vector containing neomycin resistance, herpes simplex virus thymidine kinase and lacZ genes was used to disrupt most of the Nog coding region and some 3' flanking sequence. The targeted allele consists of an in frame lacZ fusion to noggin's first 10 amino acids. The construct was electroporated into 129S1/Sv-derived CJ7 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric animals were backcrossed to 129/Sv mice.
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| 002448 129S1/SvImJ | ||
| Considerations for Choosing Controls | ||
Related Strains
lacZ Expression Strains
View lacZ Expression Strains (186 strains)
Additional Web Information
Fluorescent Proteins/lacZ Systems
New 129 Nomenclature Bulletin
Phenotype
Phenotype Information
Tracheoesophageal Fistula with or without Esophageal Atresia - 5
5 Conditionally targeted allele(s) assigned by genotype
Nogtm1Amc/Nogtm1Amc
involves: 129S1/Sv
- lethality-prenatal/perinatal
- perinatal lethality (MGI Ref ID J:110617)
- mice all die perinatally
- prenatal lethality (MGI Ref ID J:74136)
- time of death not specified
- nervous system phenotype
- abnormal neural plate morphology (MGI Ref ID J:110617)
- neural plate shows furrows and kinks in open cranial portion and closed spinal portion
- abnormal neural tube morphology/development (MGI Ref ID J:110617)
- neural tube at level of forelimbs is mildly affected
- between the limbs, flattened neural mass beneath edematous tissue replaces neural tube
- all homozygous embryos from heterozygous crosses where females injected with folate or myo-inositol still show neural tube defects (NTDs)
- defective neurulation is detected at E9.0
- at E10 and E11, development of the spinal cord shows severe disruption, with regions of the neural tube appearing ruptured
- abnormal neural tube closure (MGI Ref ID J:74136)
- abnormalities in neural tube closure, particularly in the brain vesicles between the diencephalons and myelencephalon
- walls of neural tube remain relatively flat or convex rather than bending to form concave walls
- incomplete cephalic closure (MGI Ref ID J:110617)
- all but most rostral portion of neural tube remains splayed open with no surface ectoderm covering open neural tissue at E9.0
- open neural tube (MGI Ref ID J:74136)
- spina bifida occulta (MGI Ref ID J:110617)
- all homozygotes have spina bifida; caudal to forelimb, dorsal neural arches are absent
- vertebral arches of axial skeleton are split in two, but surface ectoderm remains intact
- stillborn pups, spina bifida is restricted to the lumbar region between forelimb and hindlimb
- kinked neural tube (MGI Ref ID J:110617)
- observed in embryos at E8 or E9
- wavy neural tube (MGI Ref ID J:110617)
- observed in embryos at E8 or E9
- abnormal spinal cord morphology (MGI Ref ID J:110617)
- by E14, spinal cord is splayed open and dysmorphic in lumbar region, but remains closed at forelimb level
- exencephaly (MGI Ref ID J:74136)
- in mutants where the frontal, parietal and interparietal bones are absent, the brain is exposed at birth
- midbrain and hindbrain regions are directly exposed to extraembryonic environment
- large convoluted mass of brain tissue protrudes from head
- exencephaly is completely penetrant on 129/Sv background, but is almost never observed on C57BL/6 background and is variably observed on mixed or outbred backgrounds
- skeleton phenotype
- abnormal axial skeleton morphology (MGI Ref ID J:110617)
- all mutants show overgrowth and fusion of axial skeletal elements at birth
- at E14, axial skeleton supporting the spinal cord is malformed and deficient in lumbar region of embryo
- abnormal cranial base morphology (MGI Ref ID J:74136)
- fusion of presphenoid, basisphenoid, and basioccipital bones
- abnormal occipital bone morphology (MGI Ref ID J:74136)
- occipital condyles are loose, showing variability in the distance separating them
- abnormal frontal bone morphology (MGI Ref ID J:74136)
- frontal bone is loose or absent
- abnormal interparietal bone morphology (MGI Ref ID J:74136)
- interparietal bone is loose or absent
- abnormal parietal bone morphology (MGI Ref ID J:74136)
- parietal bone is loose or absent
- abnormal vertebral arch morphology (MGI Ref ID J:110617)
- vertebral arches of axial skeleton are split in two, but surface ectoderm remains intact
- absent vertebral arch (MGI Ref ID J:110617)
- caudal to forelimb, dorsal neural arches are absent
- spina bifida occulta (MGI Ref ID J:110617)
- all homozygotes have spina bifida; caudal to forelimb, dorsal neural arches are absent
- vertebral arches of axial skeleton are split in two, but surface ectoderm remains intact
- stillborn pups, spina bifida is restricted to the lumbar region between forelimb and hindlimb
- limbs/digits/tail phenotype
- absent tail (MGI Ref ID J:74136)
- short limbs (MGI Ref ID J:74136)
- truncated limbs
- respiratory system phenotype
- abnormal lung morphology (MGI Ref ID J:83697)
- at E15.5 all mice have abnormal lungs with malformed and truncated lobes
- fusions of the right lobes are seen in 78% of embryos
- blind-ended ectopic buds or diverticulum emerging near the junction of the main bronchi are present in 31% of embryos
- craniofacial phenotype
- abnormal cranial base morphology (MGI Ref ID J:74136)
- fusion of presphenoid, basisphenoid, and basioccipital bones
- abnormal occipital bone morphology (MGI Ref ID J:74136)
- occipital condyles are loose, showing variability in the distance separating them
- abnormal frontal bone morphology (MGI Ref ID J:74136)
- frontal bone is loose or absent
- abnormal interparietal bone morphology (MGI Ref ID J:74136)
- interparietal bone is loose or absent
- abnormal parietal bone morphology (MGI Ref ID J:74136)
- parietal bone is loose or absent
- cellular phenotype
- increased apoptosis (MGI Ref ID J:110617)
- embryogenesis phenotype
- abnormal neural tube morphology/development (MGI Ref ID J:110617)
- neural tube at level of forelimbs is mildly affected
- between the limbs, flattened neural mass beneath edematous tissue replaces neural tube
- all homozygous embryos from heterozygous crosses where females injected with folate or myo-inositol still show neural tube defects (NTDs)
- defective neurulation is detected at E9.0
- at E10 and E11, development of the spinal cord shows severe disruption, with regions of the neural tube appearing ruptured
- abnormal neural tube closure (MGI Ref ID J:74136)
- abnormalities in neural tube closure, particularly in the brain vesicles between the diencephalons and myelencephalon
- walls of neural tube remain relatively flat or convex rather than bending to form concave walls
- incomplete cephalic closure (MGI Ref ID J:110617)
- all but most rostral portion of neural tube remains splayed open with no surface ectoderm covering open neural tissue at E9.0
- open neural tube (MGI Ref ID J:74136)
- spina bifida occulta (MGI Ref ID J:110617)
- all homozygotes have spina bifida; caudal to forelimb, dorsal neural arches are absent
- vertebral arches of axial skeleton are split in two, but surface ectoderm remains intact
- stillborn pups, spina bifida is restricted to the lumbar region between forelimb and hindlimb
- kinked neural tube (MGI Ref ID J:110617)
- observed in embryos at E8 or E9
- wavy neural tube (MGI Ref ID J:110617)
- observed in embryos at E8 or E9
- abnormal somite development (MGI Ref ID J:110617)
- somite differentiation is disrupted in lumbar region of embryos at E9-10
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Nogtm1Amc/Nog+
D1.129S1-Nogtm1Amc
- skeleton phenotype
- abnormal middle ear ossicle morphology (MGI Ref ID J:132023)
- mice displaying hearing threshold shifts of >10 dB at two or more frequencies have an extra bone fragment between posterior crus of stapes and posterior wall of tympanium
- fragment is located where stapedius muscle is connected to temporal bone in wild-type ears
- no extra bone fragment associated with the malleus or incus was observed
- mice with threshold shifts >10 dB show rigid extra bone bridge in middle ear cavity; mice with less severe or unaffected threshold changes have bone fragments consisting of two unfused pieces that are found in the same location as in significantly affected ears
- bone bridges are not observed in unaffected or mildly affected ears
- abnormal stapes morphology (MGI Ref ID J:132023)
- in mice aged E15.5 to P4 the ectopic bone is located between the stapes and styloid process, likely due to failure of the stapes and styloid process to separate normally
- abnormal styloid process morphology (MGI Ref ID J:132023)
- in mice aged E15.5 to P4 the ectopic bone is located between the stapes and styloid process, likely due to failure of the stapes and styloid process to separate normally
- abnormal thoracic cage (MGI Ref ID J:108573)
- reduced rib cage due to malformed ribs
- abnormal rib morphology (MGI Ref ID J:108573)
- fused synovial joints (MGI Ref ID J:108573)
- carpal and tarsal fusions in 100% of mice in all backgrounds
- no additional fusions throughout life
- limbs/digits/tail phenotype
- kinked tail (MGI Ref ID J:108573)
- in embryos at E14.5
- craniofacial phenotype
- abnormal middle ear ossicle morphology (MGI Ref ID J:132023)
- mice displaying hearing threshold shifts of >10 dB at two or more frequencies have an extra bone fragment between posterior crus of stapes and posterior wall of tympanium
- fragment is located where stapedius muscle is connected to temporal bone in wild-type ears
- no extra bone fragment associated with the malleus or incus was observed
- mice with threshold shifts >10 dB show rigid extra bone bridge in middle ear cavity; mice with less severe or unaffected threshold changes have bone fragments consisting of two unfused pieces that are found in the same location as in significantly affected ears
- bone bridges are not observed in unaffected or mildly affected ears
- abnormal stapes morphology (MGI Ref ID J:132023)
- in mice aged E15.5 to P4 the ectopic bone is located between the stapes and styloid process, likely due to failure of the stapes and styloid process to separate normally
- abnormal styloid process morphology (MGI Ref ID J:132023)
- in mice aged E15.5 to P4 the ectopic bone is located between the stapes and styloid process, likely due to failure of the stapes and styloid process to separate normally
- hearing/vestibular/ear phenotype
- abnormal middle ear morphology (MGI Ref ID J:132023)
- abnormal middle ear ossicle morphology (MGI Ref ID J:132023)
- mice displaying hearing threshold shifts of >10 dB at two or more frequencies have an extra bone fragment between posterior crus of stapes and posterior wall of tympanium
- fragment is located where stapedius muscle is connected to temporal bone in wild-type ears
- no extra bone fragment associated with the malleus or incus was observed
- mice with threshold shifts >10 dB show rigid extra bone bridge in middle ear cavity; mice with less severe or unaffected threshold changes have bone fragments consisting of two unfused pieces that are found in the same location as in significantly affected ears
- bone bridges are not observed in unaffected or mildly affected ears
- abnormal stapes morphology (MGI Ref ID J:132023)
- in mice aged E15.5 to P4 the ectopic bone is located between the stapes and styloid process, likely due to failure of the stapes and styloid process to separate normally
- decreased brainstem auditory evoked potential (MGI Ref ID J:132023)
- many animals on congenic backgrousnd show increased ABR thresholds relative to wild-type mice; these animals hearing threshold shifts >10dB at 2 or more different frequencies in one or both ears
- impaired hearing (MGI Ref ID J:132023)
- remaining mice do not show significant threshold differences from wild-type
- conductive hearing loss (MGI Ref ID J:132023)
Nogtm1Amc/Nog+
B6.129S1-Nogtm1Amc
- skeleton phenotype
- abnormal thoracic cage (MGI Ref ID J:108573)
- reduced rib cage due to malformed ribs
- abnormal rib morphology (MGI Ref ID J:108573)
- fused synovial joints (MGI Ref ID J:108573)
- carpal and tarsal fusions in 100% of mice in all backgrounds
- no additional fusions throughout life
- limbs/digits/tail phenotype
- kinked tail (MGI Ref ID J:108573)
- in embryos at E14.5
Nogtm1Amc/Nog+
involves: 129S1/Sv * CD1
- skeleton phenotype
- abnormal axial skeleton morphology (MGI Ref ID J:108573)
- abnormal thoracic cage (MGI Ref ID J:108573)
- reduced rib cage due to malformed ribs
- abnormal rib morphology (MGI Ref ID J:108573)
- kyphosis (MGI Ref ID J:108573)
- in 30% of mice
- fused synovial joints (MGI Ref ID J:108573)
- carpal and tarsal fusions in 100% of mice in all backgrounds
- no additional fusions throughout life
- limbs/digits/tail phenotype
- kinked tail (MGI Ref ID J:108573)
- in embryos at E14.5
Nogtm1Amc/Nog+
involves: 129S1/Sv * C57BL/6J * ICR
- endocrine/exocrine gland phenotype
- small prostate gland ventral lobe (MGI Ref ID J:130204)
- at P35 ventral prostate lobe weight is significantly lower than in wild-type males
- however, no differences in weights of dorsolateral prostate or coagulating gland weights or in numbers of main ducts, branch points or tips are observed relative to wild-type prostate lobes
- reproductive system phenotype
- small prostate gland ventral lobe (MGI Ref ID J:130204)
- at P35 ventral prostate lobe weight is significantly lower than in wild-type males
- however, no differences in weights of dorsolateral prostate or coagulating gland weights or in numbers of main ducts, branch points or tips are observed relative to wild-type prostate lobes
Nogtm1Amc/Nog+
involves: C57BL/6J * FVB
- hearing/vestibular/ear phenotype
- *normal* hearing/vestibular/ear phenotype (MGI Ref ID J:132023)
- no hearing impairment is observed in heterozygous mice on a mixed background
Nogtm1Amc/Nogtm1Amc
either: 129/Sv or (involves: 129S1/Sv * C57BL/6J)
- lethality-prenatal/perinatal
- perinatal lethality (MGI Ref ID J:47724)
- nervous system phenotype
- abnormal neural tube morphology/development (MGI Ref ID J:47724)
- reduced in size
- incomplete cephalic closure (MGI Ref ID J:47724)
- on a 129/Sv background the brain fails to close between the diencephalons and myelencephalon, sometimes remaining open all the way to the caudal limit
- neural folds flatten at the 8-9 somite stage on the 129/Sv background
- on a mixed background the brain closes
- abnormal spinal cord morphology (MGI Ref ID J:47724)
- becomes kinked on both backgrounds
- embryogenesis phenotype
- abnormal neural tube morphology/development (MGI Ref ID J:47724)
- reduced in size
- incomplete cephalic closure (MGI Ref ID J:47724)
- on a 129/Sv background the brain fails to close between the diencephalons and myelencephalon, sometimes remaining open all the way to the caudal limit
- neural folds flatten at the 8-9 somite stage on the 129/Sv background
- on a mixed background the brain closes
- abnormal notochord morphology (MGI Ref ID J:47724)
- occasional side branching and buckling at E10.5
- abnormal somite development (MGI Ref ID J:47724)
- abnormal rostral-caudal patterning of the somites (MGI Ref ID J:47724)
- abnormalities become increasingly severe in a caudal direction
- abnormal somite size (MGI Ref ID J:47724)
- reduced
- decreased embryo size (MGI Ref ID J:47724)
- skeleton phenotype
- abnormal axial skeleton morphology (MGI Ref ID J:47724)
- shortened axis between fore and hind limbs
- vision/eye phenotype
- abnormal eye development (MGI Ref ID J:47724)
- perturbed
- hearing/vestibular/ear phenotype
- abnormal ear development (MGI Ref ID J:47724)
- perturbed
- limbs/digits/tail phenotype
- short limbs (MGI Ref ID J:47724)
- broad club shaped limbs
- vestigial tail (MGI Ref ID J:47724)
- reduced at E12.5, absent later
- growth/size phenotype
- decreased embryo size (MGI Ref ID J:47724)
- skin/coat/nails phenotype
- abnormal hair follicle development (MGI Ref ID J:59676)
- significantly reduced numbers of hair follicles and fewer reach an advanced stage of morphogenesis than normal
- more apoptosis in hair placodes
Nogtm1Amc/Nogtm1Amc
D1.129S1-Nogtm1Amc
- lethality-prenatal/perinatal
- perinatal lethality (MGI Ref ID J:108573)
- nervous system phenotype
- exencephaly (MGI Ref ID J:108573)
- 25% penetrance, lower than on a CD-1 background
Nogtm1Amc/Nogtm1Amc
B6.129S1-Nogtm1Amc
- lethality-prenatal/perinatal
- lethality throughout fetal growth and development (MGI Ref ID J:108573)
- embryo death before E14.5 on a B6.129S1 background
- embryogenesis phenotype
- small limb buds (MGI Ref ID J:108573)
- reduction in limb buds is seen on the C57BL/6 background but not so much on a CD-1 background
- hearing/vestibular/ear phenotype
- abnormal incus morphology (MGI Ref ID J:132023)
- at E17.5 incus is malformed
- abnormal malleus morphology (MGI Ref ID J:132023)
- at E17.5 malleus is malformed
- fusion of middle ear ossicles (MGI Ref ID J:132023)
- at E17.5 embryos display overgrown and fused ossicles not identifiable as discrete entities
- craniofacial phenotype
- abnormal incus morphology (MGI Ref ID J:132023)
- at E17.5 incus is malformed
- abnormal malleus morphology (MGI Ref ID J:132023)
- at E17.5 malleus is malformed
- fusion of middle ear ossicles (MGI Ref ID J:132023)
- at E17.5 embryos display overgrown and fused ossicles not identifiable as discrete entities
- limbs/digits/tail phenotype
- small limb buds (MGI Ref ID J:108573)
- reduction in limb buds is seen on the C57BL/6 background but not so much on a CD-1 background
- skeleton phenotype
- abnormal incus morphology (MGI Ref ID J:132023)
- at E17.5 incus is malformed
- abnormal malleus morphology (MGI Ref ID J:132023)
- at E17.5 malleus is malformed
- fusion of middle ear ossicles (MGI Ref ID J:132023)
- at E17.5 embryos display overgrown and fused ossicles not identifiable as discrete entities
Nogtm1Amc/Nogtm1Amc
involves: 129S1/Sv * CD1
- lethality-prenatal/perinatal
- perinatal lethality (MGI Ref ID J:108573)
- skeleton phenotype
- abnormal bone mineralization (MGI Ref ID J:108573)
- highly variable throughout the skeleton but characteristic for each region
- fused synovial joints (MGI Ref ID J:108573)
- elbow fusion
- limbs/digits/tail phenotype
- abnormal limb bud morphology (MGI Ref ID J:108573)
- limb bud phenotype is much less pronounced, such that they almost appear normal, in the CD-1 background compared to the C57BL/6 background
- abnormal limb morphology (MGI Ref ID J:108573)
- newbrons exhibit stubby limbs
- abnormal tail morphology (MGI Ref ID J:108573)
- degeneration of the tail structure is seen at E12.5
- homeostasis/metabolism phenotype
- edema (MGI Ref ID J:108573)
- observed at E14.5
- muscle phenotype
- abnormal muscle morphology (MGI Ref ID J:108573)
- reduced muscle tissue in newborns
- abnormal muscle fiber morphology (MGI Ref ID J:108573)
- myofibers in loose structures rather than tightly packed
- skin/coat/nails phenotype
- abnormal hair follicle development (MGI Ref ID J:108573)
- rudimentary hair follicles at E18.5
- cardiovascular system phenotype
- hemorrhage (MGI Ref ID J:108573)
- a large hematoma is often seen in the degenerating tail at E12.5 and by E14.5, hematomas in other parts of the body are seen
- nervous system phenotype
- exencephaly (MGI Ref ID J:108573)
- 60% penetrance, higher than on a DBA/1 background
- growth/size phenotype
- decreased fetal size (MGI Ref ID J:108573)
- shorter along the rostral-caudal axis
- embryogenesis phenotype
- abnormal limb bud morphology (MGI Ref ID J:108573)
- limb bud phenotype is much less pronounced, such that they almost appear normal, in the CD-1 background compared to the C57BL/6 background
Nogtm1Amc/Nogtm1Amc
involves: C57BL/6
- lethality-prenatal/perinatal
- perinatal lethality (MGI Ref ID J:110617)
- mice all die perinatally
- nervous system phenotype
- abnormal neural tube morphology/development (MGI Ref ID J:110617)
- all homozygotes display spinal neural tube defects
- exencephaly (MGI Ref ID J:110617)
- never observed on C57BL/6 inbred background
- skeleton phenotype
- abnormal skeleton morphology (MGI Ref ID J:110617)
- all homozygotes display severe skeletal malformations
- craniofacial phenotype
- abnormal craniofacial morphology (MGI Ref ID J:110617)
- some mutants show severe craniofacial truncations
- abnormal facial morphology (MGI Ref ID J:110617)
- some mutants show mild facial truncations
- embryogenesis phenotype
- abnormal neural tube morphology/development (MGI Ref ID J:110617)
- all homozygotes display spinal neural tube defects
Nogtm1Amc/Nogtm1Amc
either: (involves: 129S1/Sv * C57BL/6) or (involves: 129S1/Sv * CD-1 * ICR)
- embryogenesis phenotype
- abnormal neural tube morphology/development (MGI Ref ID J:118341)
- incomplete cephalic closure (MGI Ref ID J:118341)
- at E11.5 embryos show open brain phenotype
- open neural tube (MGI Ref ID J:118341)
- at E11.5 caudal neural tube is open
- abnormal notochord morphology (MGI Ref ID J:118341)
- abnormal at E8.5 and E9, indicating delayed detachment from dorsal foregut endoderm; appears hypertrophic compared to wild-type at E9
- no clear boundary between notochord and endoderm is detected at E8.5
- at E9.5, notochord has lateral branches close to or tethered to dorsal foregut in contrast to wild-type notochord
- increased apoptotic cell numbers are seen at E9.5-E9.75
- non-notochordal cells are observed within the notochord at E9.0
- digestive/alimentary phenotype
- abnormal esophagus morphology (MGI Ref ID J:118341)
- severe narrowing of the esophagus is seen by E9.5
- abnormal esophageal development (MGI Ref ID J:118341)
- at E10.5-11.5 most mutants display Type C esophageal atresia/tracheoesophageal fistula (EA/TEF); some embryos show milder phenotype indicative of esophageal stenosis
- esophageal atresia (MGI Ref ID J:118341)
- at E10.5-11.5, >80% of embryos display Type C esophageal atresia/tracheoesophageal fistula (EA/TEF)
- tracheoesophageal fistula (MGI Ref ID J:118341)
- at E10.5-11.5, >80% of embryos display Type C esophageal atresia/tracheoesophageal fistula (EA/TEF) with the upper esophagus ending in a blind pouch and the lower esophagus connects to the trachea via a fistula
- abnormal foregut morphology (MGI Ref ID J:118341)
- at E9.5, reduction in dorsoventral diameter of the foregut is observed; dorsal foregut endoderm is reduced in mutant embryos
- loosening or loss of dorsal foregut cells is consistently observed at E9; endodermal cells show basement membrane disruption
- nervous system phenotype
- abnormal neural tube morphology/development (MGI Ref ID J:118341)
- incomplete cephalic closure (MGI Ref ID J:118341)
- at E11.5 embryos show open brain phenotype
- open neural tube (MGI Ref ID J:118341)
- at E11.5 caudal neural tube is open
- respiratory system phenotype
- tracheoesophageal fistula (MGI Ref ID J:118341)
- at E10.5-11.5, >80% of embryos display Type C esophageal atresia/tracheoesophageal fistula (EA/TEF) with the upper esophagus ending in a blind pouch and the lower esophagus connects to the trachea via a fistula
Nogtm1Amc/Nogtm1Amc
either: (involves: 129S1/Sv * CD-1) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6)
- endocrine/exocrine gland phenotype
- abnormal pituitary gland development (MGI Ref ID J:121318)
- Rathke's pouch and anterior lobe development are severely affected
- however some cell specification appears to occur in pituitary tissue
- secondary pituitary tissue is found in some embryos examined at E11.5-14.5 with percentage of affected embryos decreasing when examined at later time point (E15.5-18.5)
- abnormal Rathke's pouch (MGI Ref ID J:121318)
- severely malformed at E10.5 with multiple invaginations within oral ectoderm; some embryos show duplication of Rathke's pouch with the two invaginations widely spaced or arising adjacent to each other
- commonly, Rathke's pouch is elongated and extend more rostrally than in wild-type; eventually cartilage plate surrounds mutant pituitary tissue
- some embryos don't appear to have a Rathke's pouch (about 14%) at E12.5
- domain of apoptosis normally observed on ventral side of pouch is absent in mutants at E10.5 and E11.5; apoptotic cells are not observed in mutants that do not achieve separation of Rathke's pouch
- abnormal pituitary gland physiology (MGI Ref ID J:121318)
- all normal pituitary hormones are detected in primary anterior lobe of mutants but levels are variable, dependent on number of terminally differentiated cells
- abnormal pituitary infundibular stalk (MGI Ref ID J:121318)
- morphologically distinct infundibulum is absent in most embryos examined between E12.5 and 16.5
- absent adenohypophysis (MGI Ref ID J:121318)
- in embryos with elongated, rostrally-positioned Rathke's pouch, developed anterior lobe is absent
- absent pituitary gland (MGI Ref ID J:121318)
- in some embryos an identifiable pituitary is not found at E12.5-16.5; normal position of pituitary is filled with mesenchyme in these embryos
- nervous system phenotype
- abnormal diencephalon morphology (MGI Ref ID J:121318)
- ventral diencephalon displays abnormalities
- a large domain of cell death is observed in ventral diencephalon of mutants but not in wild-type
- thickening of neuroepithelium in ventral diencephalon rostral to Rathke's pouch is decreased or absent in contrast to wild-type embryos
- abnormal pituitary gland development (MGI Ref ID J:121318)
- Rathke's pouch and anterior lobe development are severely affected
- however some cell specification appears to occur in pituitary tissue
- secondary pituitary tissue is found in some embryos examined at E11.5-14.5 with percentage of affected embryos decreasing when examined at later time point (E15.5-18.5)
- abnormal Rathke's pouch (MGI Ref ID J:121318)
- severely malformed at E10.5 with multiple invaginations within oral ectoderm; some embryos show duplication of Rathke's pouch with the two invaginations widely spaced or arising adjacent to each other
- commonly, Rathke's pouch is elongated and extend more rostrally than in wild-type; eventually cartilage plate surrounds mutant pituitary tissue
- some embryos don't appear to have a Rathke's pouch (about 14%) at E12.5
- domain of apoptosis normally observed on ventral side of pouch is absent in mutants at E10.5 and E11.5; apoptotic cells are not observed in mutants that do not achieve separation of Rathke's pouch
- abnormal pituitary infundibular stalk (MGI Ref ID J:121318)
- morphologically distinct infundibulum is absent in most embryos examined between E12.5 and 16.5
- absent adenohypophysis (MGI Ref ID J:121318)
- in embryos with elongated, rostrally-positioned Rathke's pouch, developed anterior lobe is absent
- absent pituitary gland (MGI Ref ID J:121318)
- in some embryos an identifiable pituitary is not found at E12.5-16.5; normal position of pituitary is filled with mesenchyme in these embryos
- abnormal neural tube morphology/development (MGI Ref ID J:121318)
- severe neural tube defect is occasionally observed
- abnormal pituitary gland physiology (MGI Ref ID J:121318)
- all normal pituitary hormones are detected in primary anterior lobe of mutants but levels are variable, dependent on number of terminally differentiated cells
- craniofacial phenotype
- abnormal head morphology (MGI Ref ID J:121318)
- with severe neural tube defect gross head morphology is altered, being split down anterior midline at E15.5
- embryogenesis phenotype
- abnormal neural tube morphology/development (MGI Ref ID J:121318)
- severe neural tube defect is occasionally observed
Nogtm1Amc/Nogtm1Amc
involves: 129S1/Sv * C57BL/6J * ICR
- embryogenesis phenotype
- abnormal embryogenesis/ development (MGI Ref ID J:130204)
- incomplete separation of the hindgut from the urogenital sinus (UGS) is observed in some embryos
- at E17 males have a fistulous connection between hindgut and dorsal surface of UGS; females show similar defects at E17
- at E14 ventral mesenchymal cell density of UGS is reduced relative to E14 wild-type embryos indicating defective development of the ventral mesenchyme pad; this reduced cell density occurs along with decreased epithelial cell proliferation in the ventral UGS
- at P1 this is observed as reduction in ventral mesenchyme pad thickness and density
- reproductive system phenotype
- abnormal male reproductive system morphology (MGI Ref ID J:130204)
- UGS is smaller at E17 in males
- dorsal ridges are absent or reduced in size; dorsal sulcus is missing and ejaculatory duct connection is exposed
- abnormal prostate gland morphology (MGI Ref ID J:130204)
- dorsal and lateral buds are reduced in number but a degree of ductal branching is observed in all embryos
- abnormal prostate gland development (MGI Ref ID J:130204)
- in developing embryos the ventral prostate (VP) bud is absent
- absent prostate gland anterior lobe (MGI Ref ID J:130204)
- in developing prostate the coagulating gland bud is absent
- absent bulbourethral gland (MGI Ref ID J:130204)
- some males show agenesis of the bulbourethral gland
- cryptorchism (MGI Ref ID J:130204)
- varying degrees of cryptorchism ranging from high intra-abdominal position to complete descent
- renal/urinary system phenotype
- abnormal urethra morphology (MGI Ref ID J:130204)
- some males exhibit agenesis of the membranous (pelvic) urethra while others develop a preursor urethral epithelial tube
- angle between bladder neck and urethra in urogenital sinus (UGS) is much larger than the approximate 90 degrees seen in wild-type embryos
- abnormal urinary system development (MGI Ref ID J:130204)
- ectopic kidney (MGI Ref ID J:130204)
- occasionally an ectopic kidney is observed in the pelvic cavity (pelvic kidney)
- digestive/alimentary phenotype
- anal atresia (MGI Ref ID J:130204)
- fistulous connection between hindgut and dorsal UGS surface is typically associated with anal atresia in males and females
- endocrine/exocrine gland phenotype
- abnormal prostate gland morphology (MGI Ref ID J:130204)
- dorsal and lateral buds are reduced in number but a degree of ductal branching is observed in all embryos
- abnormal prostate gland development (MGI Ref ID J:130204)
- in developing embryos the ventral prostate (VP) bud is absent
- absent prostate gland anterior lobe (MGI Ref ID J:130204)
- in developing prostate the coagulating gland bud is absent
- absent bulbourethral gland (MGI Ref ID J:130204)
- some males show agenesis of the bulbourethral gland
- cryptorchism (MGI Ref ID J:130204)
- varying degrees of cryptorchism ranging from high intra-abdominal position to complete descent
- limbs/digits/tail phenotype
- abnormal tail development (MGI Ref ID J:130204)
- some embryos exhibit agenesis of the tail
This mouse can be used to support research in many areas including:
Nogtm1Amc relatedDevelopmental Biology Research
Neurodevelopmental Defects
Perinatal Lethality
Homozygous
Neurobiology Research
Neurodevelopmental Defects
Research Tools
lacZ Expression
Developmental Biology Research
Developmental Biology Research
Embryonic Lethality (Homozygous)
Neural Tube Defects
Neurodevelopmental Defects
Postnatal Mortality
Skeletal Defects
Neurobiology Research
Neural Tube Defects
Neurodevelopmental Defects
Genes & Alleles
Gene & Allele Information
| Allele Symbol | Nogtm1Amc | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Andrew P McMahon | ||
| Allele Type | Targeted (Reporter) | ||
| Common Name(s) | Nog-; Nog9E; NogginlacZ; noggin-; | ||
| Mutation Made By | Andrew McMahon, Harvard University | ||
| Strain of Origin | 129S1/Sv-Oca2<+> Tyr<+> Kitl<+> | ||
| ES Cell Line Name | CJ7 | ||
| ES Cell Line Strain | 129S1/Sv-Oca2<+> Tyr<+> Kitl<+> | ||
| Site of Expression | Expression of the lacZ reporter is consistent with the expression pattern of the endogenous gene. | ||
| Gene Symbol and Name | Nog, noggin | ||
| Chromosome | 11 | ||
| Gene Common Name(s) | SYM1; SYNS1; | ||
| Molecular Note | Gene targeting generated a null allele by fusing the first 10 amino acids of coding sequence in-frame to the lacZ gene. The remainder of the coding sequence and some of the 3' flanking sequence of the gene were deleted. Ectopic expression of the resulting transcript was noted. [MGI Ref ID J:47724] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Nogtm1Amc, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References
Selected Reference(s)
McMahon JA; Takada S; Zimmerman LB; Fan CM; Harland RM; McMahon AP. 1998. Noggin-mediated antagonism of BMP signaling is required for growth and patterning of the neural tube and somite. Genes Dev 12(10):1438-52. [PubMed: 9585504] [MGI Ref ID J:47724]
Additional References
Brunet LJ; McMahon JA; McMahon AP; Harland RM. 1998. Noggin, cartilage morphogenesis, and joint formation in the mammalian skeleton [see comments] Science 280(5368):1455-7. [PubMed: 9603738] [MGI Ref ID J:48000]
Nogtm1Amc relatedAnderson RM; Lawrence AR; Stottmann RW; Bachiller D; Klingensmith J. 2002. Chordin and noggin promote organizing centers of forebrain development in the mouse. Development 129(21):4975-87. [PubMed: 12397106] [MGI Ref ID J:79855]
Anderson RM; Stottmann RW; Choi M; Klingensmith J. 2006. Endogenous bone morphogenetic protein antagonists regulate mammalian neural crest generation and survival. Dev Dyn 235(9):2507-2520. [PubMed: 16894609] [MGI Ref ID J:111609]
Bachiller D; Klingensmith J; Kemp C; Belo JA; Anderson RM; May SR; McMahon JA; McMahon AP; Harland RM; Rossant J; De Robertis EM. 2000. The organizer factors Chordin and Noggin are required for mouse forebrain development. Nature 403(6770):658-61. [PubMed: 10688202] [MGI Ref ID J:60303]
Bok J; Brunet LJ; Howard O; Burton Q; Wu DK. 2007. Role of hindbrain in inner ear morphogenesis: Analysis of Noggin knockout mice. Dev Biol 311(1):69-78. [PubMed: 17900554] [MGI Ref ID J:126342]
Borges AC; Marques S; Belo JA. 2001. The BMP antagonists cerberus-like and noggin do not interact during mouse forebrain development. Int J Dev Biol 45(2):441-4. [PubMed: 11330864] [MGI Ref ID J:74136]
Botchkarev VA; Botchkareva NV; Nakamura M; Huber O; Funa K; Lauster R; Paus R; Gilchrest BA. 2001. Noggin is required for induction of the hair follicle growth phase in postnatal skin. FASEB J 15(12):2205-14. [PubMed: 11641247] [MGI Ref ID J:71952]
Botchkarev VA; Botchkareva NV; Roth W; Nakamura M; Chen LH; Herzog W; Lindner G; McMahon JA; Peters C; Lauster R; McMahon AP; Paus R. 1999. Noggin is a mesenchymally derived stimulator of hair-follicle induction. Nat Cell Biol 1(3):158-64. [PubMed: 10559902] [MGI Ref ID J:59676]
Brunet LJ; McMahon JA; McMahon AP; Harland RM. 1998. Noggin, cartilage morphogenesis, and joint formation in the mammalian skeleton [see comments] Science 280(5368):1455-7. [PubMed: 9603738] [MGI Ref ID J:48000]
Choi M; Stottmann RW; Yang YP; Meyers EN; Klingensmith J. 2007. The bone morphogenetic protein antagonist noggin regulates mammalian cardiac morphogenesis. Circ Res 100(2):220-8. [PubMed: 17218603] [MGI Ref ID J:133691]
Cook C; Vezina CM; Allgeier SH; Shaw A; Yu M; Peterson RE; Bushman W. 2007. Noggin is required for normal lobe patterning and ductal budding in the mouse prostate. Dev Biol 312(1):217-30. [PubMed: 18028901] [MGI Ref ID J:130204]
Davis SW; Camper SA. 2007. Noggin regulates Bmp4 activity during pituitary induction. Dev Biol 305(1):145-60. [PubMed: 17359964] [MGI Ref ID J:121318]
Dionne MS; Brunet LJ; Eimon PM; Harland RM. 2002. Noggin is required for correct guidance of dorsal root ganglion axons. Dev Biol 251(2):283-93. [PubMed: 12435358] [MGI Ref ID J:111207]
Dionne MS; Skarnes WC; Harland RM. 2001. Mutation and analysis of Dan, the founding member of the Dan family of transforming growth factor beta antagonists. Mol Cell Biol 21(2):636-43. [PubMed: 11134349] [MGI Ref ID J:67351]
He XC; Zhang J; Tong WG; Tawfik O; Ross J; Scoville DH; Tian Q; Zeng X; He X; Wiedemann LM; Mishina Y; Li L. 2004. BMP signaling inhibits intestinal stem cell self-renewal through suppression of Wnt-beta-catenin signaling. Nat Genet 36(10):1117-21. [PubMed: 15378062] [MGI Ref ID J:93850]
Hwang CH; Wu DK. 2008. Noggin heterozygous mice: an animal model for congenital conductive hearing loss in humans. Hum Mol Genet 17(6):844-53. [PubMed: 18096605] [MGI Ref ID J:132023]
Kulessa H; Turk G; Hogan BL. 2000. Inhibition of Bmp signaling affects growth and differentiation in the anagen hair follicle. EMBO J 19(24):6664-74. [PubMed: 11118201] [MGI Ref ID J:140021]
Li Y; Litingtung Y; Ten Dijke P; Chiang C. 2007. Aberrant Bmp signaling and notochord delamination in the pathogenesis of esophageal atresia. Dev Dyn 236(3):746-54. [PubMed: 17260385] [MGI Ref ID J:118341]
Liu Z; Yu S; Manley NR. 2007. Gcm2 is required for the differentiation and survival of parathyroid precursor cells in the parathyroid/thymus primordia. Dev Biol 305(1):333-46. [PubMed: 17382312] [MGI Ref ID J:121311]
Mayer JA; Foley J; De La Cruz D; Chuong CM; Widelitz R. 2008. Conversion of the nipple to hair-bearing epithelia by lowering bone morphogenetic protein pathway activity at the dermal-epidermal interface. Am J Pathol 173(5):1339-48. [PubMed: 18832580] [MGI Ref ID J:143432]
Mine N; Anderson RM; Klingensmith J. 2008. BMP antagonism is required in both the node and lateral plate mesoderm for mammalian left-right axis establishment. Development 135(14):2425-34. [PubMed: 18550712] [MGI Ref ID J:137629]
Ohta S; Suzuki K; Tachibana K; Tanaka H; Yamada G. 2007. Cessation of gastrulation is mediated by suppression of epithelial-mesenchymal transition at the ventral ectodermal ridge. Development 134(24):4315-24. [PubMed: 18003744] [MGI Ref ID J:130130]
Patel SR; Gordon J; Mahbub F; Blackburn CC; Manley NR. 2006. Bmp4 and Noggin expression during early thymus and parathyroid organogenesis. Gene Expr Patterns 6(8):794-9. [PubMed: 16517216] [MGI Ref ID J:112219]
Plikus MV; Mayer JA; de la Cruz D; Baker RE; Maini PK; Maxson R; Chuong CM. 2008. Cyclic dermal BMP signalling regulates stem cell activation during hair regeneration. Nature 451(7176):340-4. [PubMed: 18202659] [MGI Ref ID J:131404]
Stottmann RW; Anderson RM; Klingensmith J. 2001. The BMP antagonists Chordin and Noggin have essential but redundant roles in mouse mandibular outgrowth. Dev Biol 240(2):457-73. [PubMed: 11784076] [MGI Ref ID J:73669]
Stottmann RW; Berrong M; Matta K; Choi M; Klingensmith J. 2006. The BMP antagonist Noggin promotes cranial and spinal neurulation by distinct mechanisms. Dev Biol 295(2):647-63. [PubMed: 16712836] [MGI Ref ID J:110617]
Suzuki K; Bachiller D; Chen YP; Kamikawa M; Ogi H; Haraguchi R; Ogino Y; Minami Y; Mishina Y; Ahn K; Crenshaw EB rd; Yamada G. 2003. Regulation of outgrowth and apoptosis for the terminal appendage: external genitalia: development by concerted actions of BMP signaling. (Erratum) Development 130(25):6209-20. [PubMed: 14602679] [MGI Ref ID J:87225]
Tylzanowski P; Mebis L; Luyten FP. 2006. The Noggin null mouse phenotype is strain dependent and haploinsufficiency leads to skeletal defects. Dev Dyn 235(6):1599-607. [PubMed: 16598734] [MGI Ref ID J:108573]
Weaver M; Batts L; Hogan BL. 2003. Tissue interactions pattern the mesenchyme of the embryonic mouse lung. Dev Biol 258(1):169-84. [PubMed: 12781691] [MGI Ref ID J:83697]
Wijgerde M; Karp S; McMahon J; McMahon AP. 2005. Noggin antagonism of BMP4 signaling controls development of the axial skeleton in the mouse. Dev Biol 286(1):149-57. [PubMed: 16122729] [MGI Ref ID J:103548]
Wu XB; Li Y; Schneider A; Yu W; Rajendren G; Iqbal J; Yamamoto M; Alam M; Brunet LJ; Blair HC; Zaidi M; Abe E. 2003. Impaired osteoblastic differentiation, reduced bone formation, and severe osteoporosis in noggin-overexpressing mice. J Clin Invest 112(6):924-34. [PubMed: 12975477] [MGI Ref ID J:85541]
Ybot-Gonzalez P; Gaston-Massuet C; Girdler G; Klingensmith J; Arkell R; Greene ND; Copp AJ. 2007. Neural plate morphogenesis during mouse neurulation is regulated by antagonism of Bmp signalling. Development 134(17):3203-11. [PubMed: 17693602] [MGI Ref ID J:124256]
Yi L; Domyan ET; Lewandoski M; Sun X. 2008. Fibroblast growth factor 9 signaling inhibits airway smooth muscle differentiation in mouse lung. Dev Dyn 238(1):123-137. [PubMed: 19097117] [MGI Ref ID J:142646]
Zhu J; Nakamura E; Nguyen MT; Bao X; Akiyama H; Mackem S. 2008. Uncoupling Sonic hedgehog control of pattern and expansion of the developing limb bud. Dev Cell 14(4):624-32. [PubMed: 18410737] [MGI Ref ID J:135157]
del Barco Barrantes I; Davidson G; Grone HJ; Westphal H; Niehrs C. 2003. Dkk1 and noggin cooperate in mammalian head induction. Genes Dev 17(18):2239-44. [PubMed: 12952897] [MGI Ref ID J:85554]
Health & husbandry
The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.
Health & Colony Maintenance Information
Colony Maintenance
Breeding & Husbandry The strain originated on and is currently on a 129/Sv background. Homozygotes are not viable. The investigator maintains the strain by breeding heterozygotes or heterozygous males with 129/SvJ females.
Purchasing information
Pricing, Supply Level & Notes, Controls, General Terms & Conditions
Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $1900.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Additional Supply Details
| Pricing for International shipping destinations |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $2470.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Additional Supply Details
|
|
|
Supply Details
| Standard Supply | Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information. |
|---|---|
| Supply Notes |
|
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| 002448 129S1/SvImJ | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| International - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
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.
See Terms of Use tab for General Terms and Conditions
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.Ordering and Purchasing Information
Purchasing Information
JAX® Mice Orders
Surgical Services
Contact Information
Orders & Technical Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form
Terms of Use
Terms of Use
General Terms and Conditions
For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.
Contact information
General inquiries
Contracts Administration
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "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 the 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 or PRODUCTS 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.
In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.
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. 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 and PRODUCTS 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.