Overview

Also Known As:p75^NGFR

Mice homozygous for the Ngfr^tm1Jae mutation display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Pineal glands lack sympathetic innervation, and innervation to sweat glands on foot pads is either reduced or absent. p75-deficient dorsal root ganglion and superior cervical ganglion neurons show a 2- to 3-fold decrease in sensitivity to nerve growth factor at embryonic day 15 and postnatal day 3, respectively.

Donating Investigator

Rudolf Jaenisch, Whitehead Institute, Massachusetts Institute of Technology

Genetic overview

Genetic Background	Generation

Ngfr^tm1Jae

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Ngfr	nerve growth factor receptor (TNFR superfamily, member 16)

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Research Applications

Sensorineural Research
Apoptosis Research
Neurobiology Research

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Base Price

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$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Mice homozygous for the Ngfr^tm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by 4 months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day 3, respectively. These ages coincide with the peak of naturally occurring cell death.

Development

The Ngfr^tm1Jae mutant strain was developed in the laboratory of Dr. Rudolf Jaenisch at the Whitehead Institute for Biomedical Research at the Massachusetts Institute of Technology. The 129/Sv-derived J1 ES cell line was used.

Control Suggestions

There are no appropriate physiological controls for this mutant strain. However, if you must have a control you may use either 129S3/SvImJ (Stock No. 002448) or BALB/cJ mice (Stock No. 000651) These strains also serve as DNA controls.

Approximate Controls

Additional Information

Considerations for Choosing Controls

Selected References

Lee KF; Li E; Huber LJ; Landis SC; Sharpe AH; Chao MV; Jaenisch R. 1992. Targeted mutation of the gene encoding the low affinity NGF receptor p75 leads to deficits in the peripheral sensory nervous system. Cell 69(5):737-49PubMed: 1317267 MGI: J:43748

View All References

Genetics

Ngfr^tm1Jae

Allele Symbol: Ngfr^tm1Jae

Allele Name	targeted mutation 1, Rudolf Jaenisch
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Ngfr^-; NGFR^tm1Jac; p75-; p75(III)^-; p75^exonIII-; p75^NGFR; p75^NTR-; p75^NTR KO; p75^NTRexon3-null; p75e3-; p75-KO; p75NTR-; p75NTR/ExonIII-
Gene Symbol and Name	Ngfr, nerve growth factor receptor (TNFR superfamily, member 16)
Gene Synonym(s)
Strain of Origin	129S4/SvJae
Chromosome	11
Molecular Note	A neomycin selection cassette was inserted into the third exon of the gene, disrupting the sequences encoding cysteine repeats 2, 3, and 4. Northern blot analysis revealed that the mutant gene did not yield a full length mRNA, however subsequent RT-PCR analysis, described in J:71955, detected an endogenous alternative transcript which lacks exon 3. Western blot analysis showed that the full length isoform was absent in homozygous mutant mice, but an isoform lacking cysteine repeats 2, 3, and 4 was present in both wild and mutant mice. In vitro experiments showed the persisting isoform to be a transmembrane protein that cannot bind neurotrophins but interacts with tyrosine kinase receptors.
Mutations Made By	Rudolf Jaenisch, Whitehead Institute, Massachusetts Institute of Technology

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Sensorineural Research
- Nociception

Genotype: Ngfr^tm1Jae related

Apoptosis Research
- Death Receptors
Neurobiology Research
- Neurotrophic Factor Defects
- Receptor Defects

Mammalian Phenotype Terms by Genotype

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

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
C;129S-Ngfr/J

cellular phenotype

abnormal neuron apoptosis
- reduced levels of neuronal cell death

nervous system phenotype

abnormal neuron apoptosis
- reduced levels of neuronal cell death

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
B6.129S4-Ngfr

cardiovascular system phenotype

abnormal Kupffer cell morphology
- after 3 weeks in culture hepatic stellate cells are in a quiescent state and are less differentiated than in wild-type mice

abnormal vascular wound healing
- apoptosis in neointimal lesions is decreased by 60% to 70%
- formation of neointimal lesions is enhanced 2 and 4 weeks after ligation compared to in wild-type mice such that there is a 2- to 4-fold increase in intimal to medial ratio at 500 um and 1.0 mm proximal to the ligation
- Normal - however, infiltration of inflammatory cells is normal

digestive/alimentary phenotype

abnormal circumvallate papillae morphology
- at P7 the vallate trench is only 60% as deep as in wild-type mice
- the vallate papilla is deformed and small in neonatal mutants

abnormal tongue epithelium morphology
- at P7 the gustatory epithelium of the vallate trench is thicker than normal blocking direct access of the ectopic tastse buds in the trench to taste solutions

growth/size/body region phenotype

abnormal circumvallate papillae morphology
- at P7 the vallate trench is only 60% as deep as in wild-type mice
- the vallate papilla is deformed and small in neonatal mutants

abnormal tongue epithelium morphology
- at P7 the gustatory epithelium of the vallate trench is thicker than normal blocking direct access of the ectopic tastse buds in the trench to taste solutions

hematopoietic system phenotype

abnormal Kupffer cell morphology
- after 3 weeks in culture hepatic stellate cells are in a quiescent state and are less differentiated than in wild-type mice

homeostasis/metabolism phenotype

abnormal vascular wound healing
- apoptosis in neointimal lesions is decreased by 60% to 70%
- formation of neointimal lesions is enhanced 2 and 4 weeks after ligation compared to in wild-type mice such that there is a 2- to 4-fold increase in intimal to medial ratio at 500 um and 1.0 mm proximal to the ligation
- Normal - however, infiltration of inflammatory cells is normal

immune system phenotype

abnormal Kupffer cell morphology
- after 3 weeks in culture hepatic stellate cells are in a quiescent state and are less differentiated than in wild-type mice

increased susceptibility to experimental autoimmune encephalomyelitis
- mice display considerable infiltration of fibronectin into the spinal cord parenchyma
- B220+ B cells make up 6% of cells in the inflammatory cuffs compared to 15% in wild-type mice immunized with MOG35-55
- Normal - however, the number of double-positive (monocyte) cells is normal
- mice have an increased risk of developing severe experimental autoimmune encephalomyelitis compared to wild-type mice
- microglial/macrophage and neutrophil numbers in the inflammatory infiltrate are reduced 68% to 40% while the size of the inflitratory cuffs is normal or even larger than in wild-type mice
- polymorphonuclear cells are reduced by half compared to in wild-type mice immunized with MOG35-55
- the population of Iba-1+ cells in the inflammatory cuffs is reduced by 10% compared to in wild-type mice immunized with MOG35-55

liver/biliary system phenotype

abnormal Kupffer cell morphology
- after 3 weeks in culture hepatic stellate cells are in a quiescent state and are less differentiated than in wild-type mice

nervous system phenotype

abnormal axon extension
- growth cones from dorsal root ganglion neurons are more sensitive to Sema3A repulsion than wild-type neurons
- Normal - however, increased sensitivity to Sema3A repulsion is alleviated in a double heterozygote cross of Ngfr and Sema3A
- when treated with 15 pM Sema3A outgrowth rate inhibition is increased (15 um per hour compared to 35 um per hour for wild-type neurons)

abnormal innervation pattern to muscle
- areas of the epithelium of the tongue lack innervation and the filiform papillae are sparsely innervated
- the axons in the tongue display reduced branching and smaller terminal arbors

abnormal neuron differentiation
- peripheral nerves in the hindlimb, forelimb, and trigeminal ganglia are severely stunted compared to in wild-type mice

abnormal neuron morphology
- at 60 weeks sympathetic neuron cell bodies are 25% smaller than in wild-type mice
- like wild-type neurons, cultured superior cervical ganglion neurons are resistant to apoptosis induced by pro-NGF and pro-BDNF
- the number of sympathetic neurons is increased 33% at P4 and 39% at P15 compared to in wild-type mice
- unlike in wild-type mice, superior cervical ganglion are protected from age-related apoptosis

abnormal sensory neuron innervation pattern
- at P0 there are 35% fewer geniculate ganglion neurons that supply taste neurons to the fungiform papillae in homozygotes compared to wild-type mice
- innervation of the fungiform papillae are reduced
- innervation of the somatosensory prominences is reduced

increased neuron number
- the number of sympathetic neurons is increased 33% at P4 and 39% at P15 compared to in wild-type mice

increased retinal photoreceptor cell number
- after 2 weeks of light exposure, the number of rows of photoreceptors is 4.6+/-0.31 rows compared to 2.3+/-0.25 in wild-type mice and 21.2+/-0.25 in homozygous mice
- after 3 weeks of light exposure, the number of rows of photoreceptors is 3.0+/-0.41 rows compared to 1.5+/-0.24 in wild-type mice and 0.9+/-0.28 in homozygous mice

taste/olfaction phenotype

abnormal gustatory papillae taste bud morphology
- at P7 homozygous mice have 26% fewer vallate taste buds than wild-type mice
- homozygous mice have fewer fungiform taste buds than wild-type mice

vision/eye phenotype

increased retinal photoreceptor cell number
- after 2 weeks of light exposure, the number of rows of photoreceptors is 4.6+/-0.31 rows compared to 2.3+/-0.25 in wild-type mice and 21.2+/-0.25 in homozygous mice
- after 3 weeks of light exposure, the number of rows of photoreceptors is 3.0+/-0.41 rows compared to 1.5+/-0.24 in wild-type mice and 0.9+/-0.28 in homozygous mice

cellular phenotype

abnormal axon extension
- growth cones from dorsal root ganglion neurons are more sensitive to Sema3A repulsion than wild-type neurons
- Normal - however, increased sensitivity to Sema3A repulsion is alleviated in a double heterozygote cross of Ngfr and Sema3A
- when treated with 15 pM Sema3A outgrowth rate inhibition is increased (15 um per hour compared to 35 um per hour for wild-type neurons)

abnormal neuron differentiation
- peripheral nerves in the hindlimb, forelimb, and trigeminal ganglia are severely stunted compared to in wild-type mice

craniofacial phenotype

abnormal circumvallate papillae morphology
- at P7 the vallate trench is only 60% as deep as in wild-type mice
- the vallate papilla is deformed and small in neonatal mutants

abnormal tongue epithelium morphology
- at P7 the gustatory epithelium of the vallate trench is thicker than normal blocking direct access of the ectopic tastse buds in the trench to taste solutions

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
B6.129S4-Ngfr/J

cardiovascular system phenotype

decreased myocardial infarction size
- 10 days after myocardial ischemic/reperfusion injury

homeostasis/metabolism phenotype

decreased myocardial infarction size
- 10 days after myocardial ischemic/reperfusion injury

nervous system phenotype

cochlear ganglion degeneration
- at 4 months, male homozygotes display significant SGN degeneration in the basal cochlear turn and swelling of the afferent dendrites below IHCs in the middle turns
- by 6 months, the density of SGNs is significantly reduced in the middle and basal turns, with a 59.8% loss of SGNs in the most basal turns
- starting at 1 month, male homozygotes show a slight (15.7%) but progressive loss of SGNs from the basal to the apical cochlear turns

cochlear hair cell degeneration
- by 6 months, male homozygotes exhibit absence or damage of cochlear HCs in both the basal and upper turns
- Normal - however, IHCs are still present and morphologically normal at 4 months, suggesting that SGN's dendrites connecting the IHCs are damaged earlier than IHCs

hearing/vestibular/ear phenotype

cochlear hair cell degeneration
- by 6 months, male homozygotes exhibit absence or damage of cochlear HCs in both the basal and upper turns
- Normal - however, IHCs are still present and morphologically normal at 4 months, suggesting that SGN's dendrites connecting the IHCs are damaged earlier than IHCs

increased or absent threshold for auditory brainstem response
- at 4 months of age, male homozygotes exhibit a significant elevation (>33 dB SPL) in click-evoked ABR thresholds relative to wild-type males
- at 6 months and 1 year, male homozygotes continue to display significant increases in ABR thresholds relative to age-matched wild-type males (100 and 126 dB SPL, respectively)
- however, no significant differences in click-evoked ABR thresholds are observed at 1 month, consistent with a normal cochlear structure at this age

increased susceptibility to age-related hearing loss
- by 1 year of age, homozygotes are unresponsive to click stimuli at the maximum level (136 dB SPL)
- starting at 4 months, male homozygotes display an age-related progressive hearing loss relative to age-matched wild-type males

organ of Corti degeneration
- at 1 month of age, male homozygotes exhibit a grossly normal organ of the Corti, except for a slight reduction in the number of SGNs
- by 6 months, male homozygotes show complete degeneration of the organ of Corti in the basal turns

sensorineural hearing loss
- male homozygotes show progressive hearing loss at 4 months, when both SGN degeneration and hair cell loss are observed in the basal cochlear turn

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129S4/SvJae * C57BL/6J

nervous system phenotype

abnormal peripheral nervous system regeneration
- motor axonal regeneration is increased in the tibial nerve cross-suture

decreased motor neuron number
- the number of motor neurons in tibial nerve is reduced

Genotype: Ngfr^tm1Jae/Ngfr⁺
B6.129S4-Ngfr

cellular phenotype

abnormal axon extension
- neurons exhibit an intermediate effect to Sema3a repulsion that is more sensitive than wild-type neurons but not as sensitive as Ngfr^tm1Jae homozygotes

abnormal neuron differentiation
- nerve coverage is less than in wild-type mice but not as severely reduced as in Ngfr^tm1Jae homozygotes

nervous system phenotype

abnormal axon extension
- neurons exhibit an intermediate effect to Sema3a repulsion that is more sensitive than wild-type neurons but not as sensitive as Ngfr^tm1Jae homozygotes

abnormal neuron differentiation
- nerve coverage is less than in wild-type mice but not as severely reduced as in Ngfr^tm1Jae homozygotes

respiratory system phenotype

decreased airway responsiveness
- for wild-type mice)
- Normal - however, interferon-gamma production following exposure to provocation agent is normal
- total leukocytes, eosinophils and lymphocytes do not increase as in wild-type following exposure to provocation agent
- unlike in exposed wild-type mice IL-4 and IL-5 production is not increased
- unlike in exposed wild-type mice, no pulmonary eosinophilic inflammation is observed
- unlike in wild-type mice, no airway hyper-responsiveness was observed following exposure to Ach and ovalbumin (50% brionchiorestriction occurs at 580 ug per kg for Ach and 586 ug per kg ovalbulmin compared to 552 ug per kg Ach and 62.5 ug per kg ovalbumin for wild-type mice)
- while IgE levels increase following exposure to provocation they do not increase as much as in wild-type mice

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129S4/SvJae

behavior/neurological phenotype

abnormal spatial learning
- spatial learning is improved compared to in wild-type mice without deterioration with age

cellular phenotype

abnormal axon guidance
- Normal - however, avoidance of stripes with EPHA5-Fc is normal
- when given the choice between strips that contain Eph47-Fc or Fc, retinal axons fail to avoid EPHA7-Fc stripes or exhibit a preference for the Fc stripes unlike wild-type axons

decreased neuron apoptosis
- at E12 and E14, neuron apoptosis is reduced 72% and 70%, respectively, compared to in wild-type mice
- nearly all neurons cultured with NT4 survive unlike wild-type neurons

vision/eye phenotype

abnormal eye physiology
- mice subjected to intraocular injection of the pro form of nerve growth factor are protected from induced retinal ganglion cell death

abnormal retinal ganglion cell morphology
- 50% of mice exhibit ectopic branches and arbors along the anterior posterior length of the nasal RGC axons in the superior colliculus unlike in wild-type mice
- at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice
- the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice

homeostasis/metabolism phenotype

abnormal tumor necrosis factor level
- the pro form of nerve growth factor fails to induce TNF expression in retinas

immune system phenotype

abnormal tumor necrosis factor level
- the pro form of nerve growth factor fails to induce TNF expression in retinas

nervous system phenotype

abnormal axon guidance
- Normal - however, avoidance of stripes with EPHA5-Fc is normal
- when given the choice between strips that contain Eph47-Fc or Fc, retinal axons fail to avoid EPHA7-Fc stripes or exhibit a preference for the Fc stripes unlike wild-type axons

abnormal cholinergic neuron morphology
- increased size of cholinergic forebrain neurons

abnormal retinal ganglion cell morphology
- 50% of mice exhibit ectopic branches and arbors along the anterior posterior length of the nasal RGC axons in the superior colliculus unlike in wild-type mice
- at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice
- the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice

abnormal sensory neuron innervation pattern
- absence of sensory innervation to pineal and sweat glands

abnormal superior colliculus morphology
- at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice
- Normal - however, total area of the superior colliculus is normal
- the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice

abnormal trigeminal ganglion morphology
- ophthalmic branch of the trigeminal ganglion is severely truncated at E12.5

decreased neuron apoptosis
- at E12 and E14, neuron apoptosis is reduced 72% and 70%, respectively, compared to in wild-type mice
- nearly all neurons cultured with NT4 survive unlike wild-type neurons

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129S4/SvJae * C57BL/6

cellular phenotype

abnormal axon extension
- axons of mutant neurons grown in vitro in the presence of NGF grow equally well regardless if they are stimulated or not in contrast to wild-type neurons where stimulated axons out compete non-stimulated axons
- this lack of growth disadvantage in non-stimulated axons is due to less axon degeneration than occurs to wild-type neurons

abnormal axon pruning
- at p35 where SCG neurons are actively pruning exons in wild-type mice, mutant mice have significantly less degenerating SCG axons than in wild-type mice
- mutant mice have a similar percentage of SCG neurons that connect to both eyes at P20 but this percentage does not decrease with age
- SCG neurons in wild-type mice reduce through axon pruning the number of neurons projecting to both eyes from 78% at p20 to 20% at p50
- sympathetic neurons of the superior cervical ganglion (SCG) have improper pruning of axons from neurons that reach into both eye compartments

nervous system phenotype

abnormal axon extension
- axons of mutant neurons grown in vitro in the presence of NGF grow equally well regardless if they are stimulated or not in contrast to wild-type neurons where stimulated axons out compete non-stimulated axons
- this lack of growth disadvantage in non-stimulated axons is due to less axon degeneration than occurs to wild-type neurons

abnormal axon pruning
- at p35 where SCG neurons are actively pruning exons in wild-type mice, mutant mice have significantly less degenerating SCG axons than in wild-type mice
- mutant mice have a similar percentage of SCG neurons that connect to both eyes at P20 but this percentage does not decrease with age
- SCG neurons in wild-type mice reduce through axon pruning the number of neurons projecting to both eyes from 78% at p20 to 20% at p50
- sympathetic neurons of the superior cervical ganglion (SCG) have improper pruning of axons from neurons that reach into both eye compartments

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129S1/Sv * 129S4/SvJae

nervous system phenotype

abnormal retinal ganglion cell morphology
- at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice
- the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice

abnormal superior colliculus morphology
- at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice
- the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice

vision/eye phenotype

abnormal retinal ganglion cell morphology
- at P8, the termination zone of retinal ganglion cell axons in the superior colliculus is shifted anteriorly compared to in wild-type mice
- the nasal domain of retinal axon termination zone is expanded anteriorly and in some cases evidence of ectopic arborization in non-labelled axons unlike in wild-type mice

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

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129 * BALB/c

cellular phenotype

abnormal axon extension
- dorsal hemisection
- reduced inhibition by myelin of neurite outgrowth from dorsal root ganglion neurons, but not cerebellar neurons, compared to heterozygous controls, indicating that mutant neurons are much less sensitive to myelin
- reduced inhibition by Nogo-66 (Rtn4) peptide of neurite outgrowth from P7 cerebellar neurons compared with heterozygous controls, however homozygotes did not show enhanced regeneration of corticospinal tract axons in comparison with wild-type after spinal dorsal hemisection

nervous system phenotype

abnormal axon extension
- dorsal hemisection
- reduced inhibition by myelin of neurite outgrowth from dorsal root ganglion neurons, but not cerebellar neurons, compared to heterozygous controls, indicating that mutant neurons are much less sensitive to myelin
- reduced inhibition by Nogo-66 (Rtn4) peptide of neurite outgrowth from P7 cerebellar neurons compared with heterozygous controls, however homozygotes did not show enhanced regeneration of corticospinal tract axons in comparison with wild-type after spinal dorsal hemisection

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129S4/SvJae * BALB/c

behavior/neurological phenotype

abnormal sensory capabilities/reflexes/nociception
- prolonged latency in hot plate test

homeostasis/metabolism phenotype

extremity edema
- at 4 months of age, mice exbihit edema in the fore- and hindlimb paws

integument phenotype

absent hair follicles
- loss of follicles, at distal extremities, progressive to more proximal regions

limbs/digits/tail phenotype

ulcerated paws
- at 4 months of age, fore- and hindlimb paws become edematous and develop severe ulcers
- epidermis and epidermal structures are lost from areas affected by ulcers
- excessive epidermal proliferation is present at the edges of ulcers
- ulcers are complicated by secondary infections that result in the lose of toenails and hair
- ulcers progress more proximally

mammalian phenotype

renal/urinary system phenotype
- Normal - unlike in studies using p75^NGFR oligonucleotide knockdown, kidney function is normal

craniofacial phenotype

abnormal molar crown morphology
- Normal - however, full height of teeth is normal
- maxillary molar crown height is reduced by 15%

abnormal molar morphology
- mandibular molar occlusal facets are longer than in wild-type mice

abnormal mouth morphology
- the height of the oral cavity is reduced

abnormal tooth morphology
- increased signs of wear on molars

muscle phenotype

abnormal muscle morphology
- muscles exhibit fewer myelinated fibers than in wild-type mice (36+/-2 compared to 76+/-2 in wild-type mice)

decreased muscle spindle number
- spindle density in the soleus, but no the medial gastrocnemius, plantaris and lumbrical muscles, is reduced 50% compared to in wild-type mice

nervous system phenotype

abnormal dorsal root ganglion morphology
- mice exhibit a loss of myelinated fibers in the dorsal root ganglion

abnormal proprioceptive neuron morphology
- mice exhibit a 50% loss of proprioreceptive neurons in L4 of the dorsal root ganglion

abnormal sensory neuron innervation pattern
- at 3 to 5 months, Pde6a+ pulpal neurons are decreased
- Normal - however, sympathetic innervation of the iris and salivary glands is normal
- only a few single fibers are present in the subepidermis and none are detected in the epidermis of fore- and hindlimb paws
- reduced innervation is not restricted to hairless patches
- the dermis of fore- and hindlimb paws either lacks or have reduced numbers of Pde6a+ sensory fibers and small-diameter nerves are absent

decreased muscle spindle number
- spindle density in the soleus, but no the medial gastrocnemius, plantaris and lumbrical muscles, is reduced 50% compared to in wild-type mice

small L4 dorsal root ganglion
- at E14.5, L4 is smaller than in wild-type mice due to a 7.5-fold increase in apoptosis

skeleton phenotype

abnormal molar crown morphology
- Normal - however, full height of teeth is normal
- maxillary molar crown height is reduced by 15%

abnormal molar morphology
- mandibular molar occlusal facets are longer than in wild-type mice

abnormal tooth morphology
- increased signs of wear on molars

growth/size/body region phenotype

abnormal molar crown morphology
- Normal - however, full height of teeth is normal
- maxillary molar crown height is reduced by 15%

abnormal molar morphology
- mandibular molar occlusal facets are longer than in wild-type mice

abnormal mouth morphology
- the height of the oral cavity is reduced

abnormal tooth morphology
- increased signs of wear on molars

References

Lee KF; Li E; Huber LJ; Landis SC; Sharpe AH; Chao MV; Jaenisch R. 1992. Targeted mutation of the gene encoding the low affinity NGF receptor p75 leads to deficits in the peripheral sensory nervous system. Cell 69(5):737-49PubMed: 1317267 MGI: J:43748

Additional References

Lee KF; Bachman K; Landis S; Jaenisch R. 1994. Dependence on p75 for innervation of some sympathetic targets. Science 263(5152):1447-9PubMed: 8128229 MGI: J:43749
Lee KF; Davies AM; Jaenisch R. 1994. p75-deficient embryonic dorsal root sensory and neonatal sympathetic neurons display a decreased sensitivity to NGF. Development 120(4):1027-33PubMed: 7600951 MGI: J:43751
McQuillen PS; DeFreitas MF; Zada G; Shatz CJ. 2002. A novel role for p75NTR in subplate growth cone complexity and visual thalamocortical innervation. J Neurosci 22(9):3580-93PubMed: 11978834 MGI: J:76254
Ward NL; Stanford LE; Brown RE; Hagg T. 2000. Cholinergic medial septum neurons do not degenerate in aged 129/Sv control or p75(NGFR)-/-mice(*) Neurobiol Aging 21(1):125-34PubMed: 10794857 MGI: J:62452

Additional - Ngfr^tm1Jae related

Technical Support

CONTACT TECHNICAL SUPPORT

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

The Ngfr^tm1Jae strain is maintained by mating homozygous siblings. Homozygous mice may be ordered. The feet of these mice tend to become sore and to bleed because of the loss of sensory nerves. They need to be handled very carefully to minimize these problems. The lifespan is normal. Expected coat color from breeding:White Bellied Agouti
- Additional Breeding and Husbandry Support
Appearance
- white-bellied agouti
  Related Genotype: A^w/A^w
Citation
When using the p75^NGFR mouse strain in a publication, please cite the originating article(s) and include JAX stock #002124 in your Materials and Methods section.

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

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	Heterozygous for Ngfr<tm1Jae>

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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:p75NGFR

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Ngfrtm1Jae

Allele Symbol: Ngfrtm1Jae

Disease Terms

Research Areas By Phenotype

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

Genotype: Ngfrtm1Jae related

Mammalian Phenotype Terms by Genotype

Genotype: Ngfrtm1Jae/Ngfrtm1JaeC;129S-Ngfr/J

cellular phenotype

nervous system phenotype

Genotype: Ngfrtm1Jae/Ngfrtm1JaeB6.129S4-Ngfr

cardiovascular system phenotype

digestive/alimentary phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

liver/biliary system phenotype

nervous system phenotype

taste/olfaction phenotype

vision/eye phenotype

cellular phenotype

craniofacial phenotype

Genotype: Ngfrtm1Jae/Ngfrtm1JaeB6.129S4-Ngfr/J

cardiovascular system phenotype

homeostasis/metabolism phenotype

nervous system phenotype

hearing/vestibular/ear phenotype

Genotype: Ngfrtm1Jae/Ngfrtm1Jaeinvolves: 129S4/SvJae * C57BL/6J

nervous system phenotype

Genotype: Ngfrtm1Jae/Ngfr+B6.129S4-Ngfr

cellular phenotype

nervous system phenotype

respiratory system phenotype

Genotype: Ngfrtm1Jae/Ngfrtm1Jaeinvolves: 129S4/SvJae

behavior/neurological phenotype

cellular phenotype

vision/eye phenotype

homeostasis/metabolism phenotype

immune system phenotype

nervous system phenotype

Genotype: Ngfrtm1Jae/Ngfrtm1Jaeinvolves: 129S4/SvJae * C57BL/6

cellular phenotype

nervous system phenotype

Genotype: Ngfrtm1Jae/Ngfrtm1Jaeinvolves: 129S1/Sv * 129S4/SvJae

nervous system phenotype

vision/eye phenotype

Genotype: Ngfrtm1Jae/Ngfrtm1Jaeinvolves: 129 * BALB/c

cellular phenotype

nervous system phenotype

Genotype: Ngfrtm1Jae/Ngfrtm1Jaeinvolves: 129S4/SvJae * BALB/c

behavior/neurological phenotype

homeostasis/metabolism phenotype

integument phenotype

limbs/digits/tail phenotype

mammalian phenotype

craniofacial phenotype

muscle phenotype

nervous system phenotype

skeleton phenotype

growth/size/body region phenotype

References

Additional References

Additional - Ngfrtm1Jae related

Genotyping Protocols

Breeding Considerations

Appearance

Citation

Animal Health Reports

Also Known As:p75^NGFR

Ngfr^tm1Jae

Allele Symbol: Ngfr^tm1Jae

Genotype: Ngfr^tm1Jae related

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
C;129S-Ngfr/J

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
B6.129S4-Ngfr

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
B6.129S4-Ngfr/J

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129S4/SvJae * C57BL/6J

Genotype: Ngfr^tm1Jae/Ngfr⁺
B6.129S4-Ngfr

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129S4/SvJae

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129S4/SvJae * C57BL/6

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129S1/Sv * 129S4/SvJae

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129 * BALB/c

Genotype: Ngfr^tm1Jae/Ngfr^tm1Jae
involves: 129S4/SvJae * BALB/c

Additional - Ngfr^tm1Jae related