Overview

Also Known As:B6-staggerer

The cerebellar cortex of homozygous mutant staggerer (Rora^sg) mice show a deficiency of granule cells and Purkinje cells. They have a staggering gait, mild tremor, and hypotonia. These mice may be useful in studies of the composition and function of granule cells.

Genetic overview

Genetic Background	Generation
000664 C57BL/6J

Rora^sg

Allele Type	Gene Symbol	Gene Name
Spontaneous	Rora	RAR-related orphan receptor alpha

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Research Applications

Neurobiology Research

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Details

Detailed Description

Mice homozygous for the staggerer spontaneous mutation (Rora^sg) show a staggering gait, mild tremor, hypotonia, and small size. The cerebellar cortex of homozygous mutant mice is grossly underdeveloped with a deficiency of granule cells and Purkinje cells. The remaining granule cells migrate inward from the external layer prematurely and then degenerate. Purkinje cells are much delayed in postnatal differentiation and lack the dendritic spines on which synapses with the parallel fibers from the granule cells normally occur. Staggerer mutant mice have been used as a source of an agranulate cerebellum in a number of investigations of the composition and function of granule cells. Kopmels et al. have reported a hyperproduction of IL1 biological activity and mRNA from LPS stimulated spleen cells of Rora^sg/Rora^sg mice on the C57BL/6J background relative to wild type siblings. In addition, homozygous mice exhibit an enhanced susceptibility to LPS-induced lung inflammation, suggesting a role for Rora in LPS-induced inflammatory responses (Stapleton CM, et al., 2005).

Development

The first Rora^sg/Rora^sg mouse was observed in 1955 among the F2 progeny of a (BALB/cHm x C3H/HeJ)F1 female and a male of an obese(Lep^ob) stock of mixed background. The mutation was maintained for several generations by an intercross-backcross (within the same or a parallel lineage) mating scheme, then was backcrossed onto C57BL/6J for four generations. A Rora^sg/+ male from the fourth backcross was mated to a female C57BL/10-Myo5a^d Bmp5^se mouse to introduce the dilute and short-ear mutations into the stock in repulsion with Rora^{6 sg} ; this allowed the heterozygotes (Rora^sg + +/+ Myo5a^d Bmp5^se to be identified by a lack of either recessive phenotype. Brother-sister inbreeding was continued. At F55, Myo5a^d Bmp^se was backcrossed onto C57BL/6J seven times; at F58, Rora^sg was backcrossed onto C57BL/6J four times. The Rora^sg + +/+ Myo5a^d Bmp5^se stock was then reconstructed by crossing mice of the two independent stocks and maintained by brother-sister inbreeding. In early 1997, Myo5a^d and Bmp5^se were bred out of the stock by selective breeding assisted by PCR testing. Based on the alleles carried by this strain for 16 SSLPs mapping within 1 cM of Rora, it appears that the mutation occurred on a C3H chromosome (Hamilton et al. 1996).

Control Suggestions

Wild type mice from the colony are the preferred controls. Untyped mice from the colony may be used; however, heterozygotes exhibit "accelerated loss of Purkinje cells, granule cells, and inferior olivary neurons with age" (MLC; Zanjani et al.1992; Hadj-Sahraoui et al.1997).
Wild-type from the colony

Additional Information

Considerations for Choosing Controls

Selected References

Mamontova A; Seguret-Mace S; Esposito B; Chaniale C; Bouly M; Delhaye-Bouchaud N; Luc G; Staels B; Duverger N; Mariani J; Tedgui A. 1998. Severe atherosclerosis and hypoalphalipoproteinemia in the staggerer mouse, a mutant of the nuclear receptor RORalpha. Circulation 98(24):2738-43PubMed: 9851961 MGI: J:52105
SIDMAN RL; LANE PW; DICKIE MM. 1962. Staggerer, a new mutation in the mouse affecting the cerebellum. Science 137:610-2PubMed: 13912552 MGI: J:13140

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Genetics

Rora^sg

Allele Symbol: Rora^sg

Allele Name	staggerer
Allele Type	Spontaneous
Allele Synonym(s)	RORalpha^-; sg
Gene Symbol and Name	Rora, RAR-related orphan receptor alpha
Gene Synonym(s)
Strain of Origin	obese stock
Chromosome	9
Molecular Note	This allele contains a 6.5kb genomic deletion of an exon encoding part of the ligand binding domain. The deletion results in an exon-skipping event that introduces a shift in the reading frame. The resulting protein is predicted to be truncated due to introduction of a premature stop codon.

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Genotype: Rora^sg related

Neurobiology Research
- Ataxia (Movement) Defects
- Receptor Defects
- Tremor Defects
- Cerebellar Defects
  - Purkinje cell defect

Mammalian Phenotype Terms by Genotype

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

Genotype: Rora^sg/Rora^sg
involves: obese stock

growth/size/body region phenotype

decreased body size
- mutants are smaller than littermates

homeostasis/metabolism phenotype

abnormal hormone level
- prothyrotropin releasing hormone levels are elevated in the thalamus, cerebellum, brainstem, and spinal cord

behavior/neurological phenotype

abnormal gait
- gait is shuffling and hesitant, interrupted every few steps by lurching motions side-to-side
- abnormal gait is apparent at ~2 weeks of age

abnormal motor learning
- mice hang onto the rod as opposed the walking strategy WT mice exclusively use
- mice have an impaired ability to learn how to hang onto a rotating rod
- scores do not improve with 10 days of training

ataxia
- treatment with a thyrotropin releasing hormone analog improves ataxia (fewer falls in a given distance travelled)

decreased grip strength
- mice have a mean hanging time of 12 seconds compared to over 3 minutes for WT mice

impaired coordination
- mice fall off an elevated rod on average of 13 seconds compared to over 3 minutes for WT mice
- mice fall off an elevated rod on average of 13 seconds compared to over 3 minutes for WT mice

abnormal limb posture
- some animals have hindlimbs held abducted and everted at 45 degrees at rest

hypoactivity
- mutants remain stationary much more than littermates

abnormal motor capabilities/coordination/movement

limb grasping
- is observed in all mice

tremors
- mild tremors accompany initiation of movement

mortality/aging

postnatal lethality, incomplete penetrance
- about 50% of mutants die by weaning

nervous system phenotype

abnormal cerebellar granule cell morphology
- conspicuous differences in the internal granule layer at 10 days of age
- reduced rate of cell proliferation at 1 and 5 days of age
- external granule layer less developed at birth
- cells migrate prematurely from the external granule layer having undergone fewer cell divisions

abnormal cerebellum morphology
- cerebellum is less than one-third the size of wild-type littermates
- cells agglutinable with wheat germ agglutinin but not wit h Con-A
- cerebellum of adults shows tiny folia with indistinct fissures
- adult cerebellar cell surface with embryonic characteristics

abnormal cochlear VIII nucleus morphology
- dendritic spines are rare on cartwheel cells at 1 month of age
- cartwheel cells are rarely seen in adults
- cochlear nuclei are reduced in volume and severely malformed

small cerebellum
- weight is significantly less than controls even before neurological symptoms appear
- less than half of control weight at 5 days of age

abnormal olfactory bulb glomerular layer morphology
- reduced cell number and intercellular space
- reduced number of interneuronal relays
- thinner than controls
- glomerular surface reduced about 15%

abnormal olfactory bulb mitral cell layer morphology
- somewhat discontinuous

abnormal Purkinje cell morphology
- cells are randomly oriented
- poorly elaborated dendritic trees

abnormal olfactory bulb internal plexiform layer morphology
- less distinct
- thinner than controls

decreased cerebellar granule cell number
- 25% reduction in granule cells in the internal granule cell layer

abnormal olfactory bulb external plexiform layer morphology
- thinner than controls
- large, empty, intercellular spaces
- lower density of secondary dendrites

abnormal olfactory bulb granule cell layer morphology
- composed of several layers of anaxonal interneurons with smaller than normal cell bodies
- nuclear size is smaller than controls

abnormal olfactory bulb outer nerve layer morphology
- glial cells with more processes ensheathing axons in the nerve layer

abnormal brain morphology

abnormal cerebellar granule layer morphology
- granular cell layer displays a paucity of cells in mutants

abnormal olfactory bulb granule cell morphology
- vacuolations and ruptured membranes
- pycnotic nuclei

abnormal olfactory bulb layer morphology

abnormal olfactory bulb morphology
- dendro-dendritic asymmetrical synapses are abundant
- fewer astrocytes found

small olfactory bulb
- volume slightly reduced

abnormal cerebellar layer morphology

abnormal cerebellar foliation

abnormal cerebellar molecular layer

abnormal nervous system physiology
- immunoreactive somatostatin is significantly elevated in both the cerebrum and in the cerebellum

thin cerebellar molecular layer

Genotype: Rora^sg/Rora⁺
involves: C57BL

nervous system phenotype

abnormal inferior olivary complex morphology
- neuron counts are 60% of controls at 1 year of age

abnormal cerebellar granule layer morphology
- cell density is reduced
- granule cell layer decreases with age

abnormal cerebellum morphology

decreased cerebellar granule cell number
- cell numbers are about 35% of controls

small cerebellum
- decreased cross-sectional area of the cerebellum at 1 year of age

decreased Purkinje cell number
- significant loss of Purkinje cells at 1 year of age

abnormal cerebellar layer morphology

Genotype: Rora^sg/Rora^sg
involves: C57BL/6

cardiovascular system phenotype

decreased mean systemic arterial blood pressure
- 80mmHg vs 87mmHg for controls
- phenylephrine causes less blood pressure increase than in controls
- acetyl choline causes less blood pressure decrease than in controls

abnormal vasodilation
- endothelium-dependent and independent dilation is reduced
- blood flow induced dilation of the mesenteric artery is less than for controls

increased susceptibility to atherosclerosis
- Although homozygotes fed a normal diet do not display abnormal atherosclerotic lesions, 9 weeks of an atherosclerotic diet induces exaggerated altherosclerotic lesions compared with wild-type controls on the atherosclerotic diet

increased angiogenesis
- significantly increased in the ischemic leg 28 days after femoral artery ligature
- 3 fold increase in capillary density relative to controls
- 80% rise in vascular density relative to controls

abnormal vasoconstriction
- contractions of the mesenteric artery induced by phenylephrin or serotonin are less than in controls

atherosclerotic lesions
- the atherosclerotic lesions induced in homozygotes by 9 weeks of an atherosclerotic diet have a 6 fold greater area in female homozygotes and a 7.5 fold greater area in male homozygotes than those in wild-type controls on the same diet

endocrine/exocrine gland phenotype

thymus atrophy

hematopoietic system phenotype

increased IgE level
- OVA sensitization causes an additional elevation in IgE levels
- levels are elevated in unsensitized mice
- OVA challenge of sensitized mice causes a very great increase in IgE levels

thymus atrophy

abnormal macrophage physiology
- LPS stimulated macrophage produce 2 fold more IL-1 relative to macrophage of controls

spleen atrophy

homeostasis/metabolism phenotype

abnormal lipid homeostasis
- plasma APOA1 and APOA2 concentrations are approximately 2 fold lower than in wild-type controls on a normal diet, and the Apoa1 mRNA level in intestine is diminished relative to wild-type, although liver expression of Apoa1 is comparable with wild-type
- the production rate of APOA1 is diminished, but the fractional catabolic rate is comparable to wild-type

decreased circulating HDL cholesterol level
- plasma HDL cholesterol level is significantly lower in both male and female homozygotes than in wild-type controls, and females have significantly lower plasma HDL level than males both for the homozygous and wild-type data sets. This is true even on an atherogenic diet.
- therogenic diet.

decreased circulating cholesterol level
- plasma total cholesterol levels are significantly lower in both male and female homozygotes than in wild-type controls
- although cholesterol levels increase on an atherosclerotic diet, homozygotes still have lower plasma cholesterol than wild-type controls also fed this diet

immune system phenotype

lung inflammation
- less alveolar infiltration as well
- less increase of inflammatory cells in bronchoalveolar lavage
- less increase of IL-4, IL-5, and IL-13
- OVA sensitized and challenged mice experience less infiltration of lymphocytes and polymorphonuclear cells into peribronchiolar and perivascular regions of the lungs

spleen atrophy

abnormal immune system physiology
- abnormal immune responses

abnormal macrophage physiology
- LPS stimulated macrophage produce 2 fold more IL-1 relative to macrophage of controls

increased IgE level
- levels are elevated in unsensitized mice
- OVA challenge of sensitized mice causes a very great increase in IgE levels
- OVA sensitization causes an additional elevation in IgE levels

thymus atrophy

increased interleukin-1 secretion
- LPS stimulated macrophage produce 2 fold more IL-1 relative to macrophage of controls

abnormal immune system organ morphology

mammalian phenotype

immune system phenotype
- white blood cell, lymphocyte, and neutrophil counts are not significantly different between homozygotes and wild-type controls

taste/olfaction phenotype
- Normal - male mice are able to distinguish between the vaginal secretions of estrus and non-estrus females

muscle phenotype

abnormal vasodilation
- endothelium-dependent and independent dilation is reduced
- blood flow induced dilation of the mesenteric artery is less than for controls

abnormal vasoconstriction
- contractions of the mesenteric artery induced by phenylephrin or serotonin are less than in controls

nervous system phenotype

abnormal inferior olivary complex morphology
- decreased cell density
- inferior olive extends further dorsally in the midline
- individual olivary subnuclei are poorly defined relative to controls
- number of neurons in adults is decreased 60% relative to newborns
- olivary dendrites tend to be multipolar and well branched
- adult cell bodies are smaller than in newborns
- definition of subnuclei is better in 21 day old mice but regresses in adults
- number of neurons drops 30% within 3 days of birth and continues to decline for 2 months

abnormal cerebellum morphology
- embryonic, high sialic acid forms of N-CAM persist on cell surfaces to 14 and 21 days of age

behavior/neurological phenotype

abnormal spatial learning
- higher latency to escape at all time tested using two types of water maze
- less age related degradation in latency to escape although it is always greater than in controls

abnormal sexual interaction
- vestibular stimulation improves the ability of males to mate with experienced females
- successful mating occurs from 35-160 days after the end of male isolation
- one to two months of social isolation results in increased mounting behavior when a receptive female is encountered

abnormal maternal nurturing
- females from selected homozygous lineages sometimes (9/14) raise pups to weaning although growth rate of pups is lower than normal
- females from heterozygous parents fail to nurture pups to weaning

reproductive system phenotype

abnormal female reproductive system physiology

abnormal fertility/fecundity
- no unstimulated couples mated
- some couples receiving vestibular stimulation mated between the ages of 36 and 89 days of age

reduced female fertility
- no females mate before 2.5 months of age
- only one of 10 females still mating at 6 months of age
- females sexual activity decreases after 4.5 months

abnormal estrous cycle
- irregular cycles

abnormal external female genitalia morphology
- vaginal opening averaged 35 days (never earlier than 31 days) while controls averaged 28 days (earliest 26 days)

prolonged metestrus

delayed estrous cycle
- onset of estrus at 45 days vs 40 days for controls

prolonged estrus
- prolonged vaginal estrus relative to controls

respiratory system phenotype

abnormal lung compliance
- lung resistance in response to methacholine challenge of OVA exposed mice fails to increase

lung inflammation
- OVA sensitized and challenged mice experience less infiltration of lymphocytes and polymorphonuclear cells into peribronchiolar and perivascular regions of the lungs
- less increase of inflammatory cells in bronchoalveolar lavage
- less alveolar infiltration as well
- less increase of IL-4, IL-5, and IL-13

abnormal respiratory mucosa morphology
- less mucous cell hyperplasia in airways after OVA exposure of sensitized mice

taste/olfaction phenotype

abnormal olfaction
- amyl alchohol odor induced evoked field potential shows an increased latency preceding the functional response of mitral cells in the olfactory bulb
- attractive threshold concentration for vanillin is increased
- aversive threshold concentration for butanol is increased
- N1 and N2 response amplitudes of the evoked field potential are significantly reduced

Genotype: Rora^sg/Rora^sg
involves: C57BL

cellular phenotype

abnormal Purkinje cell differentiation
- retarded

homeostasis/metabolism phenotype

decreased aspartic acid level
- aspartate levels decline between 7 and 10 days; low levels persist

increased noradrenaline level
- measurably increased in the spinal cord
- significantly elevated in cerebellum
- significantly elevated in cerebral cortex

decreased gamma-aminobutyric acid level
- GABA levels in deep cerebellar nuclei are reduced at all ages examined
- GABA levels are 52% of controls at 7 days and 30% at 3 weeks

decreased taurine level
- taurine levels decline between 7 and 10 days; low levels persist

nervous system phenotype

abnormal cerebellar granule cell morphology
- degenerating parallel fibers begin to appear around 7 days and is well advanced by 14 days
- synapses do develop between parallel fibers and stellate and basket cells
- no synapses form between the parallel fibers and the Purkinje cell spines at 14 to 43 days of age

abnormal cerebellum deep nucleus morphology
- area occupied by deep neurons is reduced to 36% of controls but cell numbers are not reduced
- white matter in deep cerebellar nuclei is reduced to 42% of controls
- neurons in the deep nuclei are smaller than seen in controls

abnormal Purkinje cell dendrite morphology
- no synapses form between Purkinje cell spines and the parallel fibers at 14 to 43 days of age
- reduced growth of dendrite arbor

abnormal Purkinje cell morphology
- 60-90% of Purkinje cells are lost
- cells smaller in size with thinner processes
- multiple climbing fiber synaptic connections to each Purkinje cell are maintained
- larger, typical Purkinje cells are absent in intermediate regions of the cerebellum

abnormal synaptic glutamate release
- levels continue to drop over time
- glutamate levels drop between 7 and 10 days

decreased gamma-aminobutyric acid level
- GABA levels in deep cerebellar nuclei are reduced at all ages examined
- GABA levels are 52% of controls at 7 days and 30% at 3 weeks

small cerebellum
- 62% of normal weight at birth
- weight is 36% of normal at 7 days

abnormal cerebellar Purkinje cell layer
- Purkinje cell band thicker at 3 days of age

increased noradrenaline level
- significantly elevated in cerebral cortex
- significantly elevated in cerebellum
- measurably increased in the spinal cord

delaminated Purkinje cell layer
- typical laminar array fails to form

thin cerebellar molecular layer

abnormal Purkinje cell differentiation
- retarded

abnormal cerebellar granule layer morphology

decreased aspartic acid level
- aspartate levels decline between 7 and 10 days; low levels persist

thin cerebellar granule layer

abnormal cerebellar layer morphology

abnormal cerebellum morphology
- cell surface antigen characteristics more embryonic in nature

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

Genotype: Rora^sg/Rora⁺
involves: C57BL/6J

behavior/neurological phenotype

abnormal spatial learning
- mice exhibit impaired spatial learning in a Z-maze filled with water compared with wild-type mice

References

Mamontova A; Seguret-Mace S; Esposito B; Chaniale C; Bouly M; Delhaye-Bouchaud N; Luc G; Staels B; Duverger N; Mariani J; Tedgui A. 1998. Severe atherosclerosis and hypoalphalipoproteinemia in the staggerer mouse, a mutant of the nuclear receptor RORalpha. Circulation 98(24):2738-43PubMed: 9851961 MGI: J:52105
SIDMAN RL; LANE PW; DICKIE MM. 1962. Staggerer, a new mutation in the mouse affecting the cerebellum. Science 137:610-2PubMed: 13912552 MGI: J:13140

Additional References

Hamilton BA; Frankel WN; Kerrebrock AW; Hawkins TL; FitzHugh W; Kusumi K; Russell LB; Mueller KL; van Berkel V; Birren BW; Kruglyak L; Lander ES. 1996. Disruption of the nuclear hormone receptor RORalpha in staggerer mice. Nature 379(6567):736-9PubMed: 8602221 MGI: J:31470
Heuze P; Feron C; Baudoin C. 1997. Early behavioral development of mice is affected by staggerer mutation as soon as postnatal day three. Brain Res Dev Brain Res 101(1-2):81-4PubMed: 9263582 MGI: J:42144
Kopmels B; Wollman EE; Guastavino JM; Delhaye-Bouchaud N; Fradelizi D; Mariani J. 1990. Interleukin-1 hyperproduction by in vitro activated peripheral macrophages from cerebellar mutant mice. J Neurochem 55(6):1980-5PubMed: 2230805 MGI: J:28095
Perandones C; Costanzo RV; Kowaljow V; Pivetta OH; Carminatti H; Radrizzani M. 2004. Correlation between synaptogenesis and the PTEN phosphatase expression in dendrites during postnatal brain development. Brain Res Mol Brain Res 128(1):8-19PubMed: 15337313 MGI: J:92848
Yoon CH. 1972. Developmental mechanism for changes in cerebellum of staggerer mouse, a neurological mutant of genetic origin. Neurology 22(7):743-54PubMed: 4673255 MGI: J:5304
Zanjani HS; Mariani J; Delhaye-Bouchaud N; Herrup K. 1992. Neuronal cell loss in heterozygous staggerer mutant mice: a model for genetic contributions to the aging process. Brain Res Dev Brain Res 67(2):153-60PubMed: 1511513 MGI: J:1431

Additional - Rora^sg related

Technical Support

CONTACT TECHNICAL SUPPORT

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

Rora^sg/Rora^sgmice can be identified by 10-15 days of age by their poor locomotor coordination, lurching movements and frequent falls; homozygotes as young as three days can be distinguished by behavioral testing (Heuze et al.1997). Homozygotes die between two to three weeks of age. Due to their early and high mortality, homozygous mutant mice are not available from our colony. In some cases, the homozygote lifespan can be extended by adding crushed grain to the bottom of the cage and keeping pups with a lactating female. As heterozygotes are indistinguishable phenotypically from wild type mice, they must be identified by a PCR based genotyping assay.
- Additional Breeding and Husbandry Support
Appearance
- black, ataxic, tremors
  Related Genotype: a/a Rora^sg/Rora^sg
  
  black, unaffected
  Related Genotype: a/a +/? or a/a Rora^sg/+
Citation
When using the B6-staggerer mouse strain in a publication, please cite the originating article(s) and include JAX stock #002651 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

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	Heterozygous or Wild-type for Rora<sg>

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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.

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Also Known As:B6-staggerer

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Rorasg

Allele Symbol: Rorasg

Disease Terms

Research Areas By Phenotype

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

Genotype: Rorasg related

Mammalian Phenotype Terms by Genotype

Genotype: Rorasg/Rorasginvolves: obese stock

growth/size/body region phenotype

homeostasis/metabolism phenotype

behavior/neurological phenotype

mortality/aging

nervous system phenotype

Genotype: Rorasg/Rora+involves: C57BL

nervous system phenotype

Genotype: Rorasg/Rorasginvolves: C57BL/6

cardiovascular system phenotype

endocrine/exocrine gland phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

mammalian phenotype

muscle phenotype

nervous system phenotype

behavior/neurological phenotype

reproductive system phenotype

respiratory system phenotype

taste/olfaction phenotype

Genotype: Rorasg/Rorasginvolves: C57BL

cellular phenotype

homeostasis/metabolism phenotype

nervous system phenotype

Genotype: Rorasg/Rora+involves: C57BL/6J

behavior/neurological phenotype

References

Additional References

Additional - Rorasg 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

Licensing Information

Rora^sg

Allele Symbol: Rora^sg

Genotype: Rora^sg related

Genotype: Rora^sg/Rora^sg
involves: obese stock

Genotype: Rora^sg/Rora⁺
involves: C57BL

Genotype: Rora^sg/Rora^sg
involves: C57BL/6

Genotype: Rora^sg/Rora^sg
involves: C57BL

Genotype: Rora^sg/Rora⁺
involves: C57BL/6J

Additional - Rora^sg related