Search Criteria: Research Area is "Research Tools: Sensorineural Research"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 012942 | B6.129-Gabra2tm1.1Geh/J | Repository- Live |
| These mutant mice carry substitutions of serine to histidine at amino acid position 270 and leucine to alanine at amino acid position 277 of exon 9. The point mutations confer alcohol and anesthesia insensitivity, while retaining near-normal GABA sensitivity. Approximately half of the homozygous mutant mice (from heterozygous crosses) die between birth and weaning. Homozygotes that survive to adulthood are fertile, normal in size and do not display any gross physical abnormalities. Mutant gene product (mRNA) is detected by RT-PCR analysis of whole brain total RNA. The alpha2 subunit protein levels did not differ between mice homozygous for the mutation and wildtype mice in the cortex and hippocampus. Homozygotes exhibit enhanced fear conditioning, reduced sensitivity to anesthesia (isoflurane), increased alcohol consumption without typical conditioned taste aversion, reduced ethanol induced stimulation of motor activity, and recover more slowly from ethanol?induced hypnosis. Den ..... For more information please see the full phenotype on the strain data sheet | ||
| 008198 | B6.129P2-Trpm8tm1Jul/J | Repository- Live |
| Mice homozygous for this TRPM8 targeted mutation are viable and fertile, with no differences in core body temperature compared to wildtype. Functional TRPM8 transcripts are absent in trigeminal ganglia from homozygous mutants however,a truncated, non-functional transcript is generated. Immunostaining of trigeminal ganglia, corneal afferents, and spinal cord dorsal horn reveals loss of TRPM8 expression in homozygous mutants. TRPM8-deficient mice exhibit behavioral deficits in their ability to discriminate between cold and warm surfaces, or to respond to evaporative cooling. Homozygous mice are not completely cold insensitive as they avoid contact with surfaces below 10 C (albeit with reduced efficiency). Cultured sensory neurons and intact sensory nerve fibers from TRPM8-deficient mice exhibit profoundly diminished responses to cold. These TRMP8 (transient receptor potential cation channel, subfamily M, member 8 (also called TRP melastatin 8 or cold and menthol receptor 1 (CMR1))) muta ..... For more information please see the full phenotype on the strain data sheet | ||
| 007558 | B6.129S2-Oprk1tm1Kff/J | Repository- Live |
| Mice homozygous for this kappa-opioid receptor mutant allele (KOR-) are viable and fertile. KOR-selective ligand binding is absent on brain membranes from homozygous mice. In contrast to mutant mice deficient of delta- or mu-opioid receptors (Stock No. 007557 or 007559), KOR- homozygotes have normal mechanical pain thresholds, but greatly increased sensitivity to chemical visceral pain. KOR- homozygotes also exhibit normal spontaneous stress responses (unlike delta-opioid receptor null mice). Homozygous KOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. These KOR mutant mice may be useful in studying biological activity of opioids, analgesics, spinally mediated thermal nociception and chemical visceral pain thresholds. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. These mut ..... | ||
| 007559 | B6.129S2-Oprm1tm1Kff/J | Repository- Live |
| Mice homozygous for this mu-opioid receptor mutant allele (MOR-) are viable and fertile. MOR-selective ligand binding is absent on brain membranes from homozygous mice. Homozygous MOR- mice exhibit a lack of morphine analgesia, reward, and withdrawal. This is accompanied by decreased mechanical, thermal, and chemical pain thresholds. Homozygous MOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. In contrast to mutant mice deficient of delta- or kappa-opioid receptors (Stock No. 007557 or 007558, respectively), MOR- homozygotes exhibit hypolocomotive spontaneous stress responses. Indeed, the reduced anxiety and depressive-like behavior observed in MOR- mutants is in stark contrast to kappa-opioid receptor deficient mice. These MOR mutant mice may be useful in studying the biological activity of opioids, analgesics, and responses to mechanical, chemical and thermal nociception at a supraspinal level. In an attempt to offer alleles ..... | ||
| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and ..... For more information please see the full phenotype on the strain data sheet | ||
| 011104 | B6.Cg-Tg(Atoh1-cre)1Bfri/J | Repository- Live |
| In this strain, mouse Atoh1 (atonal homolog 1 (Drosophila)) regulatory sequences drives cre expression primarily in precursors of granule cell neurons of the cerebellum and dorsal hindbrain/spinal cord in the dp1 domain. When bred with mice containing sequences flanked by similarly oriented loxP sites, flanked sequences will be deleted in the Cre-expressing tissues of the offspring. | ||
| 014545 | B6.Cg-Tg(Chat-COP4*H134R/EYFP)5Gfng/J | Repository- Live |
| Mice hemizygous for the ChAT-mhChR2-YFP BAC transgene (or ChAT-ChR2-YFP BAC transgene) are viable and fertile, with expression of the mhChR2::YFP fusion protein directed to cholinergic neuronal populations by the mouse choline acetyltransferase (Chat or ChAT) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 010536 | B6.Cg-Tg(Pcp2-cre)3555Jdhu/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express Cre recombinase under the control of the mouse Purkinje cell protein (Pcp2). Cre recombinase expression is detected in Purkinje cells of the cerebellar folia and retinal bipolar cells. Expression was not found in spinal cord, heart, liver, kidney or cornea. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in deletion of the targeted gene in the offspring. This mutant mouse strain may be useful in studies of the nervous system, particularly Purkinje cells and retinal bipolar cells. | ||
| 014131 | B6.Cg-Tg(Thy1-CFP)IJrs/GfngJ | Repository- Live |
| These founder line I transgenic mice express Cyan Fluorescent Protein gene under the control of the mouse Thy1, thymus cell antigen 1, theta, promoter. Fluorescence is detected in all motor axons, all retinal ganglion cells, dorsal root ganglion, neurons in cortical layers 2 through 6, and all of the cerebellar mossy fibers. Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 006401 | B6;129P-Trpa1tm1Kykw/J | Repository- Live |
| Homozygous mice are viable and fertile. The donating investigator reports a dramatic loss of fecundity after 5-6 months of age. The targeting vector contains an endoplasmic reticulum (ER) retention signal (KDEL), which is reported to sequester the potential truncated mRNA product in the ER. The vector also contains an IRES-PLAP reporter gene, allowing extracellular antibody staining/chromogenic development tracking of cells normally expressing the endogenous gene. Homozygous mice display behavioral deficits in response to mustard oil, cold, and punctate mechanical stimuli. These mice have a normal startle reflex to loud noise, a normal sense of balance, a normal auditory brainstem response, and normal transduction currents in vestibular hair cells. These mutants may be useful in neurobiological studies involving dorsal root ganglion neurons and cells of the inner ear, as well as for auditory, temperature, or chemical irritant trials. | ||
| 012355 | B6;SJL-Tg(Pvalb-COP4*H134R/EYFP)15Gfng/J | Repository- Live |
| Mice hemizygous for the Prv-mhChR2-YFP BAC transgene are viable and fertile with expression of the mhChR2::YFP fusion protein directed to neuronal populations by the mouse parvalbumin (Pvalb or Prv) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-expressing neurons with blue light (450-490 nm) leads to rapid ..... For more information please see the full phenotype on the strain data sheet | ||
| 012348 | B6;SJL-Tg(Thy1-COP3/EYFP)8Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-VChR1-YFP transgene are viable and fertile with expression of the VChR1::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The VChR1::YFP fusion protein is composed of a synthetic, mammalian codon-optimized, red-shifted channelrhodopsin-1 derived from Volvox carteri (VChR1) fused in-frame with an enhanced yellow fluorescent protein (EYFP). Compared with ChR2, VChR1 has a markedly (~70 nm) red-shifted action spectrum with a maximum at ~535 nm (green light). The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this VChR1 functions as a green light-driven cation channel that depolarizes the cell and causes action potentials. As such, illumination of VChR1-expressing neurons leads to rapid and reversible photostimulation of action potential firing/neural activity in these cells. The donating investigator spec ..... For more information please see the full phenotype on the strain data sheet | ||
| 012350 | B6;SJL-Tg(Thy1-COP4*H134R/EYFP)20Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-mhChR2-YFP transgene are viable and fertile with expression of the mhChR2::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 (optimized with an N-terminal beta2 nictinic acytlcholine receptor signal peptide and C-terminal ER-export and Golgi-export motifs) that harbors a gain-of-function H134R substitution fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-expressing neurons with blue light ..... For more information please see the full phenotype on the strain data sheet | ||
| 012332 | B6;SJL-Tg(Thy1-HOP/EYFP)2Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-eNpHR-YFP transgene are viable and fertile with expression of the eNpHR::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The donating investigator specifically reports that Thy1-eNpHR-YFP mice derived from founder line 2 exhibit high expression of EYFP in layer 5 pyramidal neurons at cortex, dentate gyrus, thalamus, superior colliculus, inferior culliculus, brainstem, amydagala and cerebellum. These Thy1-eNpHR-YFP line 2 transgenic mice may be useful for rapid control of motor behavior by addition or removal of light, for ex vivo and in vivo studies of neural circuitry/connectivity following illumination, or for fluorescent labeling of neural tissues.
The eNpHR::YFP fusion protein, designed with halorhodopsin from the halophilic bacterium Natronomonas pharaonis (NpHR) fused in-frame with an enhanced yellow fluorescent protein (EYFP), was optimized for expression in mammalian systems ..... | ||
| 012334 | B6;SJL-Tg(Thy1-HOP/EYFP)4Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-eNpHR-YFP transgene are viable and fertile with expression of the eNpHR::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The donating investigator specifically reports that Thy1-eNpHR-YFP mice derived from founder line 4 exhibit high EGFP expression in layer 2/3 and layer 5 pyramidal neurons at cortex, dentate gyrus, thalamus, superior colliculus, inferior culliculus, brainstem, amydagala and cerebellum. These Thy1-eNpHR-YFP line 4 transgenic mice may be useful for rapid control of motor behavior by addition or removal of light, for ex vivo and in vivo studies of neural circuitry/connectivity following illumination, or for fluorescent labeling of neural tissues.
The eNpHR::YFP fusion protein, designed with halorhodopsin from the halophilic bacterium Natronomonas pharaonis (NpHR) fused in-frame with an enhanced yellow fluorescent protein (EYFP), was optimized for expression in mammali ..... | ||
| 014555 | B6;SJL-Tg(Tph2-COP4*H134R/EYFP)5Gfng/J | Repository- Live |
| Mice hemizygous for the TpH2-mhChR2-YFP BAC transgene (or TpH2-ChR2-YFP BAC transgene) are viable and fertile, with expression of the mhChR2::YFP fusion protein directed to serotonergic neuronal populations by the mouse tryptophan hydroxylase 2 (Tph2 or TpH2) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 006912 | C57BL/6-Tg(Tcra2D2,Tcrb2D2)1Kuch/J | Repository- Live |
| Mice hemizygous for this "2D2 TCR" (or MOG 35-55 specific TCR) transgene are viable and fertile. The myelin oligodendrocyte glycoprotein (MOG)-specific transgenic T cells are not deleted nor tolerized and are functionally competent. The majority of thymocytes in 2D2 TCR mice express high and intermediate levels of the transgenic T cell receptor (TCR), indicating efficient positive selection of transgenic T cells. The majority of CD4+ splenocytes express the transgenic TCR (as defined by Valpha3.2 and Vbeta11 expression). Cultured splenocytes are responsive to whole myelin oligodendrocyte glycoprotein (MOG) and to MOG 35-55 peptide, but not to ovalbumin (OVA) control peptides. From between 2.5 to 5 months of age, 4% of 2D2 TCR mice develop spontaneous experimental autoimmune encephalomyelitis (EAE), while within the first year 40% of 2D2 TCR mice develop spontaneous, isolated optic neuritis with neither clinical nor histological evidence of EAE. Standard EAE induction protoco ..... For more information please see the full phenotype on the strain data sheet | ||
| 013701 | STOCK Cep290tm1Jgg/J | Repository- Live |
| These mice possess loxP sites on either side of exon 36 and 37 of the Cep290 (centrosomal protein 290) gene. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. This strain may be useful in studies of retinal degeneration, cilia/flagella development, and fertility. | ||
| 005992 | STOCK Efna2tm1Jgf Efna5tm1Ddmo/J | Repository- Live |
| Mice homozygous for both targeted mutations are viable, fertile, and normal in size. While the donating investigator reports that 10-20% of females homozygous at both loci neglect their litters, no such neglect is reported in the colonies at The Jackson Laboratory (Aug 2009). Double homozygous mice have no endogenous protein expression in inferior colliculus (IC) or superior colliculus (SC), and thus lack the concentration gradient created by the endogenous proteins across the midbrain in wildtype mice. Temporal and nasal retinal axon termination is severely altered: multiple ectopic aborizations in the SC indicate abnormalities in both anteroposterior and dorsoventral topography. Following surgical ablation of portions of the midbrain (including IC and SC), cross-modal innervation by retinal neurons is greater in double homozygous mutants compared to wildtype. Mice heterozygous at both loci are reported to have greater reproductive performance compared to double homozygous mice. Furth ..... For more information please see the full phenotype on the strain data sheet | ||
| 013197 | STOCK Sagtm1Jnc/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mutant mice are photosensitive and if not maintained under low light conditions will develop progressive retinal degeneration. No gene product (protein) is detected by Northern blot analysis of retinas from homozygous mice maintained in cyclic (12 hour light: 12 hour dark) conditions. Photoreceptor loss in homozygotes maintained in cyclic light conditions begins at approximately 100 days of age, progressing to loss of more than half of the photoreceptors by 1 year of age. After 1 week of constant light exposure, homozygotes lose 30% of photoreceptors; after 3 weeks of constant light exposure, more than 60% of photoreceptors are lost. Homozygotes maintained under cyclic light conditions exhibit disorganized and 25% shorter retinal rod outer segment layer, as well as reduced levels of retinal rhodopsin. Recovery phase respon ..... For more information please see the full phenotype on the strain data sheet | ||
| 008813 | STOCK Trpa1tm2Kykw Tg(CAG-cre/Esr1*)5Amc/J | Repository- Live |
| These compound mutant mice carry a floxed allele of the Trpa1 (transient receptor potential cation channel, subfamily A, member 1) gene in addition to a tamoxifen inducible cre transgene driven by the chicken beta actin promoter/enhancer coupled with the cytomegalovirus (CMV) immediate-early enhancer (see Stock No. 004682). Restricted to the cytoplasm, the cre/Esr1 protein can only gain access to the nuclear compartment after exposure to tamoxifen. Tamoxifen administration induces cre recombination within the Trpa1 allele, excising the S5/S6 transmembrane domains. Animals not treated with tamoxifen display no observable phenotype. | ||
| 005379 | B6(A)-Rpe65rd12/J | Research Strain |
| 003684 | B6.C3Ga-Mfrprd6/J | Research Strain |
| Male and female mice homozygous for rd6develop a slowly progressive retinal degeneration affecting both rod and cone cells beginning at 3-4 weeks of age, soon after the retina develops. Ophthalmoscopic examination reveals small, evenly distributed white spots throughout the retina from the time the mice are 8 weeks old. The spots remain clearly visible until about 7 months, when clinical signs of retinal degeneration first become evident, and become less easily distinguishable as degeneration progresses. Retinal blood vessels appear pale and attenuated by 7 months and are undetectable by 15 months, when the fundus appears mottled, lightly pigmented and granular. Aberrations of the photoreceptor layer are histologically evident at 3-4 weeks; by one year, only one to three cell layers (of the normal 10-12) remain. The time and distribution of the ophthalmoscopically detectable retinal spots correlate with histologic observation of putative phagocytic cells in the subretinal space ..... For more information please see the full phenotype on the strain data sheet | ||
| 001979 | C3A.BLiA-Pde6b+.O20-Prph2Rd2/J | Research Strain |
| 005987 | 129-Achetm1Loc/J | Cryopreserved - Ready for recovery |
| Homozygous mice have 25% fetal mortality. Those born have retarded growth, fine motor tremors, unusual posture and gait, no righting reflex, malformed pinna, and sealed eyelids. These mice die emaciated and dehydrated by 3 weeks of age. Enriched diets for the nursing female and pups allow homozygous mice to survive to adulthood. Males exhibit no breeding behavior. Homozygous females can become pregnant when bred to heterozygous or wildtype males, but both female and pups do not survive. Acetylcholinesterase (AChE) activity is completely abrogated in serum and tissue from homozygous mice, and approximately half in heterozygotes. Many symptoms of organophosphate poisoning are observed in homozygous mice, including pulsating paws, body tremor, abnormal gait, pinpoint pupils, muscle weakness, and early death following seizure. When restrained, a white mucus forms on the eyes and seizures may occur. Mice also have several developmental delays, low body mass, decreased pain response, sexual ..... For more information please see the full phenotype on the strain data sheet | ||
| 009083 | 129S-Dvl3tm1Awb/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have a perinatal lethal phenotype. Neonates have breathing difficulties and are often cyanotic. Homozygous embryos exhibit cardiac conotruncal abnormalities such as persistent truncus arteriosis (PTA) and double outlet right ventricle (DORV), and cochlear defects (disoriented stereociliary bundles). This mutant mouse strain may be useful in studies of cardiac development, neural tube formation and development of the inner ear. | ||
| 008077 | 129S1/Sv-Bchetm1Loc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock ..... | ||
| 009592 | B6.129(Cg)-Kcnn2tm1.1Jpad/J | Cryopreserved - Ready for recovery |
| Homozygous SK2-delta (SK2-null) mice are viable but subfertile (homozygous males exhibit poor reproductive success and homozygous females are nurturing but produce small, infrequent litters). No RNA or protein expression from the targeted allele is observed in brain tissues, and no EGFP expression is reported. Homozygous mice are smaller than wild-type until approximately 5 weeks of age. SK2-deficient mice exhibit whole body tremor beginning around 10 days of age, with ataxia and impaired righting reflex when placed on their back at young ages. Homozygotes also have inner ear abnormalities (impaired exocytotic response of immature inner hair cells and impaired function/long-term survival of olivocochlear fibers and efferent synapses on cochlear outer hair cells). These SK2-delta mice may be useful in studying the role of small-conductance calcium-activated potassium (SK) channels in after-hyperpolarization and action potentials of neuronal, inner ear (cochlea), and urinary bladder tiss ..... For more information please see the full phenotype on the strain data sheet | ||
| 007766 | B6.129P2(Cg)-Olfr160tm6Mom/MomJ | Cryopreserved - Ready for recovery |
| These mice express enhanced green fluorescent protein (EGFP) under the control of the olfactory receptor 160 (M72) promoter. Glomeruli associated with this marker are located primarily on the dorsal surface of the olfactory bulb. Sporadic fluorescence is observed throughout this zone. This strain may be useful in studies of neuronal connectivity and axonal development. | ||
| 008647 | B6.129P2(Cg)-Trpa1tm1Kykw Tyrc-2J/J | Cryopreserved - Ready for recovery |
| Exons encoding the pore domain of the transient receptor potential cation channel, subfamily A, member 1 gene were deleted in this targeted mutation strain. Animals show reduced sensitivity to pain. RT-PCR of dorsal root ganglia confirmed the absence of mRNA in homozygous mutant mice. Homozygotes are viable and fertile. | ||
| 008646 | B6.129P2(Cg)-Trpa1tm1Kykw/J | Cryopreserved - Ready for recovery |
| Exons encoding the pore domain of the transient receptor potential cation channel, subfamily A, member 1 gene were deleted in this targeted mutation strain. Animals show reduced sensitivity to pain. RT-PCR of dorsal root ganglia confirmed the absence of mRNA in homozygous mutant mice. Homozygotes are viable and fertile. | ||
| 007767 | B6.129P2-Olfr17tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| 008087 | B6.129S1-Bchetm1Loc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock ..... | ||
| 009379 | B6.129S1-Gpr98tm1Pwh/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. A mutant gene product (protein) is detected by Western blot analysis of embryos. High-intensity sound induces audiogenic seizures that often results in death. Cochlear hair cell stereociliary bundles are do not mature properly, lack ankle links and are disorganized. Hair cells and pillar cells in the basal half of the cochlea degenerate and are lost by 2 months of age. Homozygotes become profoundly deaf by 3 weeks of age. Electroretinographic analysis reveals abnormal light-adapted cone-only responses. Mutant mice exhibit abnormal retinal photoreceptor cells ultrastructure and age-related vision loss. This mutant mouse strain may be useful in studies of Usher syndrome type IIC, cochlear development, deafness and blindness. | ||
| 003462 | B6.129S1-Thrbtm1Df/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Thrbtm1Df targeted mutation are viable and fertile displaying normal growth rates. Homozygous mutant mice exhibit goiter and elevated levels of both thyroid hormone and thyroid stimulating hormone. Defects in liver responses to thyroid hormone and subtle behavioral abnormalities are observed. The mice fail to develop normal hearing, as assessed by impaired auditory-evoked brainstem responses, and are susceptible to audiogenic seizures. This strain provides a recessive model for the human syndrome of generalized thyroid hormone resistance (GTHR). | ||
| 007768 | B6.129S2-Omptm1Mom/MomJ | Cryopreserved - Ready for recovery |
| 007557 | B6.129S2-Oprd1tm1Kff/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this delta-opioid receptor mutant allele (DOR-) are viable and fertile. DOR-selective ligand binding is absent in vitro on brain membranes from homozygous mice. Unlike mutant mice deficient in kappa- or mu-opioid receptors (Stock No. 007558 or 007559, respectively), homozygous DOR- mutants exhibit increased anxiety and depressive-like behavior but no alteration of spontaneous pain perception. Homozygous DOR- mice also have increased ethanol self-administration and increased inflammatory pain. These DOR mutant mice may be useful in studying the biological activity of opioids andanalgesics, mechanical nociception, inflammatory pain, and emotional disorders.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first ch ..... | ||
| 003823 | B6.129S4-Ttpatm1Far/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Ttpa gene are viable, normal in size and do not display any gross physical abnormalities. The Ttpa protein product is required for the maintenance of proper alpha-tocopherol levels, the major form of vitamin E in plasma and tissues. The absence of Ttpa protein product in homozygous-null animals results in a corresponding 95% reduction in alpha-tocopherol. Low levels of alpha-tocopherol render female mice infertile, a condition that can be addressed with vitamin E supplements. Male fertility is unimpaired. These mice provide a viable model for studying vitamin E deficiency. | ||
| 005970 | B6.129S7-Atoh1tm2Hzo/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mutant mice have a perinatal lethal phenotype and die shortly after birth. No gene product (protein) is detected in resting chondrocytes by immunohistochemical analysis of embryonic age 18.5 homozygotes. Beta-galactosidase X-gal staining of neural tissue from embryonic day 14.5 and newborn (postnatal day 0) aged homozygous and heterozygous mice mimicks the endogenous expression pattern. Mice homozygous for this mutation exhibit a phenotype similar to the phenotype observed in mice homozygous for the null (loss of function) targeted mutation. Homozygotes lack cerebellar granule neurons, cochlear and ventricular hair cells, and the pontine nuclei in the brain stem. This mutant mouse strain may be useful in studies of brain and inner ear development. | ||
| 004160 | B6.129X1-Pon1tm1Lus/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No paraoxonase activity is detected in blood plasma. Homozygous animals are extremely sensitive to the toxic effects of the chlorpyrifos and its active form, chlorpyrifos oxon, a potent cholinesterase inhibitor. When fed a high-fat, high-cholesterol diet, homozygous mice are more susceptible to atherosclerosis when compared to wildtype littermates. In vitro studies indicate that high-density lipoproteins derived from homozygous animals are unable to prevent low-density lipoprotein oxidation. This mutant mouse strain represents a model that may be useful in studies related to toxicology (particularly insecticide poisoning) and factors regulating susceptibility to atherosclerosis. | ||
| 010835 | B6.Cg-Tg(Gfap-EGFP)3739Sart/J | Cryopreserved - Ready for recovery |
| Mice harboring the Gfap-EGFP transgene are viable and fertile. The mouse glial fibrillary acidic protein (Gfap) promoter region directs expression of enhanced green fluorescent protein (EGFP) primarily to adult mouse retinal Muller cells. Developmental expression of EGFP mostly parallels GFAP in retinal astrocytes. Expression of EGFP first appears in Muller cells around two weeks of age. However, not all Muller cells express EGFP.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 006576 | B6.FVB-Tg(GNAT2-Dta)98Wwk/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this "Trc-Tox176" transgene (also called "h-GNAT2pro-DTA") are viable and fertile. Expression of diphtheria toxin (DTA) from the transgene is similar to that of endogenous GNAT2, leading to ablation of both rod and cone photoreceptor development in the ventral retina (the abnormality is a result of abnormal cellular development rather than a consequence of retinal degeneration). The dorsal retina has nearly normal development of rods, but the development of cones is limited to about 10%. These transgenic mice exhibit an absence of cone photoreceptors in the retina, as well as the concomitant absence of rod photoreceptors in the ventral retina. The mice may be useful in studies of photoreceptor development, photoreceptor-related retinal diseases, and to profile photoreceptor genes in adult and in developmental stages. | ||
| 011078 | B6;129-Fzd4tm2.1Nat/J | Cryopreserved - Ready for recovery |
| This strain combines a conditional knockout and an alkaline phosphatase (AP) reporter of the frizzled 4 (Fzd4; Fz4) gene. LoxP sites flank the 5' and 3' UTR's. Without recombination, homozygotes of this allele are indistinguishable from wild type mice and the AP reporter is not expressed. Following cre-mediated recombination, the coding region is excised, and the downstream AP reporter is expressed under the control of the Fzd4 promoter in a cell/tissue-specific manner. Loss of Fzd4 signaling causes defective vascular growth which leads to chronic but reversible silencing of retinal neurons. Loss of expression in all endothelial cells disrupts the blood brain barrier in the cerebellum. This strain may be useful in studies of vascular growth, remodeling, maintenance and disease. | ||
| 006717 | B6;129P2-Olfr124tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| Mice carrying the Olfr124tm1Mom allele have tau-linked green fluorescent protein co-expressed with the OLFR124 protein. OLFR124 expressing olfactory sensory neurons are found densely packed in the septal organ and at a much lower density in the main olfactory epithelium, and have been found to respond to a notably wide array of compounds. | ||
| 006720 | B6;129P2-Olfr124tm4Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons with the Olfr124 locus actively transcribed can be identified as expressing red fluorescent protein, even though no OLFR124 protein is expressed. The density of these cells in the septal organ is 14 times lower than OLFR124 expressing cells in mice with an intact Olfr124 locus tagged with an IRES-tauGFP. Of the OLFR124 deficient neurons, only 18% in the septal organ and only 14% in the main olfactory epithelium responded to all 5 odorants that stimulate 100% of OLFR124 expressing olfactory sensory neurons. This indicates that OLFR124 is responsible for the unusually broad response profile of the olfactory sensory neurons that express it. | ||
| 006689 | B6;129P2-Olfr151tm19Mom/MomJ | Cryopreserved - Ready for recovery |
| 006675 | B6;129P2-Olfr151tm25Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr151 also co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 006676 | B6;129P2-Olfr151tm26Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr151 also co-express the tauGFP fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. | ||
| 006596 | B6;129P2-Olfr160tm4Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr160 also co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 006595 | B6;129P2-Olfr17tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr17 also co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 004946 | B6;129P2-Omptm2(spH)Mom/J | Cryopreserved - Ready for recovery |
| These mutant mice express synapto-pHluorin (spH) from the endogenous locus encoding the olfactory marker protein (OMP) as a result of a targeted knockin mutation that replaces the OMP coding region with that of spH. The OMP locus directs expression of spH at high levels and exclusively in mature sensory neurons of the main olfactory epithelium (OSNs) and the vomeronasal epithelium. SpH is a pH-sensitive variant of the green fluorescent protein (ecliptic pHluorin) fused to the mouse synaptic vesicle-associated protein (VAMP2). The protein is localized preferentially in synaptic vesicles, but is also present on the plasma membrane of OSN axons and nerve terminals. The fluorescent domain of spH is exposed to the acidic lumen of synaptic vesicles where it is ~ 20 fold less fluorescent than at neutral pH. Upon synaptic release, the lumen of the synaptic vesicles becomes continuous with the extracellular space resulting in an increase in pH that causes a rapid increase in fluorescence. In mu ..... For more information please see the full phenotype on the strain data sheet | ||
| 006667 | B6;129P2-Omptm3Mom/MomJ | Cryopreserved - Ready for recovery |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by GFP. The targeted mutation results in a knockout. Mature olfactory sensory neurons express GFP at high levels. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. Homozygous mice are subfertile. | ||
| 006668 | B6;129P2-Omptm4(cre)Mom/MomJ | Cryopreserved - Ready for recovery |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by Cre. The targeted mutation results in a knockout. Mature olfactory sensory neurons express the Cre recombinase at high levels. Homozygous mice are subfertile. As an example, when crossed to a strain with widespread expression of GFP and a loxP-flanked Bgeo reporter (see Stock No. 004178), this mutant mouse strain may be useful in lineage tracing. | ||
| 006726 | B6;129P2-Vmn2r81tm2Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the vomeronasal receptor Vmn2r81 also co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 008686 | B6;129P2-Vmn2r81tm4Mom/MomJ | Cryopreserved - Ready for recovery |
| This mutant is valuable in characterizing the development of vomeronasal sensory neurons and the vomeronasal organ. While the axons of vomeronasal sensory neurons bearing the wild-type Vmn2r81 coalesce into glomeruli at several sites in the posterior accessory olfactory bulb, those of Vmn2r81tm4Mom homozygotes instead spread out diffusely over the posterior accessory olfactory bulb and a few extend into the anterior olfactory bulb. Distinct from normal vomeronasal sensory neurons at 3 weeks of age, 25% of those expressing lacZ, indicative of active transcription at the Vmn2r81 locus, also co-express transcript for another family ABD V2R gene. 68% of wild-type Vmn2r81-expressing neurons co-express Vmn2r2 but rarely co-express Vmn2r1. However, 9.5% of lacZ-bearing neurons also co-express Vmn2r1 and only 8.1% co-express Vmn2r2. 93% of wild-type Vmn2r81-expressing neurons co-express Omp, a marker of matu ..... For more information please see the full phenotype on the strain data sheet | ||
| 006594 | B6;129S2-Omptm1Mom/MomJ | Cryopreserved - Ready for recovery |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by taulacZ, a fusion protein of the microtubule-binding protein tau (from bovine origin) and beta-galactosidase. The targeted mutation results in a knockout. Mature olfactory sensory neurons express beta-galactosidase at high levels. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. Homozygous mice are subfertile. | ||
| 004953 | B6;129S6-Gucy2etm1Gar/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of eye tissue. Progressive loss of electroretinograms (ERGs) of cone cells from homozygotes begins at age 3 to 5 weeks. ERGs are completely lost in mice older than 8 weeks of age. Histological analysis of mutants between 4 and 5 weeks of age reveals retinal cone cell atrophy and a reduction in the number of cone cells. Isolated retinal rod cells exhibit reduced a-wave and b-wave ERGs, and impaired photoresponse. This mutant mouse strain may be useful in studies of incomplete achromatopsia, progressive cone-rod dystrophy, retinitis pigmentosa and Leber congenital amaurosis. | ||
| 006160 | B6;129X1-Avpr1btm1Wsy/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable, fertile, normal in size, exhibit apparently normal sexual behavior, and do not display any gross physical abnormalities. Homozygous mice exhibit less social agression, altered chemoinvestigatory behavior, and impaired social recognition. These mice may be useful in studies of agressive behavior, social motivation, and appropriate behavioral responses, and may be potential models of autism and agression accompanying dementia and traumatic brain injury. | ||
| 007977 | B6;CBA-Tg(Hf/Olfr16-GFP)7Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes the full coding sequence of Olfr16 with an IRES-tauGFP just after the stop codon resulting in bicistronic expression. This coding sequence is under the control 405 base pairs of regulatory sequence just upstream of the transcription start site with an additional 2.1 kb H element in the forward orientation upstream of this promoter to assess the ability of this element to enhance expression. This line for this transgenic construct expresses a mildly enhanced but normal pattern of expression for this olfactory receptor. | ||
| 007975 | B6;CBA-Tg(OR8A1-taulacZ)1Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes tau-linked-LacZ under the control of a minimal promoter comprised of 154 base pairs upstream of the human OR8a1 transcription start site and 146 base pairs of the 5' nontranslated exon 1. It does not drive expression of any olfactory receptor sequence. It is useful in mapping promoter elements important for human olfactory receptor expression. Histology shows mosaic expression of LacZ in the main olfactory epithelium. | ||
| 007972 | B6;CBA-Tg(Olfr151-taulacZ)4Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes tau-linked-LacZ under the control of a minimal promoter comprised of 161 base pairs upstream of the Olfr151 transcription start site and 176 base pairs of the 5' nontranslated exon 1. It does not drive expression of any olfactory receptor sequence. It is useful in mapping promoter elements important for olfactory receptor expression and the related olfactory sensory neuron development. Histology shows LacZ activity spread over a large domain of the dorsal aspect of the medial half-bulb, not coalescing into glomeruli. | ||
| 007973 | B6;CBA-Tg(Olfr16-taulacZ)1Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes tau-linked-LacZ under the control of a minimal promoter comprised of 148 base pairs upstream of the Olfr116 transcription start site and 154 base pairs of the 5' nontranslated exon 1. It does not drive expression of any olfactory receptor sequence. It is useful in mapping promoter elements important for olfactory receptor expression and the related olfactory sensory neuron development. Histology shows LacZ expressing olfactory neurons projecting diffusely to a large domain centrally in the medial half-bulb, not coalescing into glomeruli. | ||
| 007976 | B6;CBA-Tg(Olfr713-taulacZ)4Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes tau-linked-LacZ under the control of a minimal promoter comprised of 143 base pairs upstream of the Olfr713 transcription start site and 163 base pairs of the 5' nontranslated exon 1. It does not drive expression of any olfactory receptor sequence. It is useful in mapping promoter elements important for olfactory receptor expression and the related olfactory sensory neuron development. Histology shows mosaic expression of LacZ in the ventral main olfactory epithelium. | ||
| 006743 | B6;CBA-Tg(P-taulacZ)11Mom/MomJ | Cryopreserved - Ready for recovery |
| The Tg(P-taulacZ)11Mom transgene is expressed in approximately 10% of olfactory sensory neurons, which are also expected to co-express an endogenous olfactory receptor. This transgene is preferentially expressed in olfactory sensory neurons that co-express class II olfactory receptors, with a 100-fold lower expression found in class I expressing neurons. Immunohistochemistry shows expression in NCAM2 staining glomeruli, which are generally dorsally projecting, and a ventral subset of NQO1 staining glomeruli, which are generally ventrally projecting. Expression is absent in glomeruli in the dorsal-medial and anterior-dorsal olfacotry bulb giving an unlabeled butterfly-shaped pattern in a dorsal view. | ||
| 006793 | B6;CBA-Tg(P-taulacZ)13Mom/MomJ | Cryopreserved - Ready for recovery |
| The Tg(P-taulacZ)13Mom transgene is expressed in approximately 10% of olfactory sensory neurons, which are also expected to co-express an endogenous olfactory receptor. This transgene is preferentially expressed in olfactory sensory neurons that co-express class II olfactory receptors, with a 100-fold lower expression found in class I expressing neurons. Immunohistochemistry shows expression in NCAM2 staining glomeruli, which are generally dorsally projecting, and a ventral subset of NQO1 staining glomeruli, which are generally ventrally projecting. Expression is absent in glomeruli in the dorsal-medial and anterior-dorsal olfacotry bulb giving an unlabeled butterfly-shaped pattern in a dorsal view. | ||
| 006742 | B6;CBA-Tg(P-taulacZ)8Mom/MomJ | Cryopreserved - Ready for recovery |
| The Tg(P-taulacZ)8Mom transgene is expressed in approximately 10% of olfactory sensory neurons, which are also expected to co-express an endogenous olfactory receptor. This transgene is preferentially expressed in olfactory sensory neurons that co-express class II olfactory receptors, with a 100-fold lower expression found in class I expressing neurons. Immunohistochemistry shows expression in NCAM2 staining glomeruli, which are generally dorsally projecting, and a ventral subset of NQO1 staining glomeruli, which are generally ventrally projecting. Expression is absent in glomeruli in the dorsal-medial and anterior-dorsal olfacotry bulb giving an unlabeled butterfly-shaped pattern in a dorsal view. When mice co-express both this transgene and a YFP labelled null allele of Olfr545, a class I olfactory receptor, they label distinct regions; when mice co-express both this transgene and a GFP labelled null allele of Olfr160, a class II olfactory receptor, they label the same reg ..... For more information please see the full phenotype on the strain data sheet | ||
| 012341 | B6;SJL-Tg(Thy1-COP3/EYFP)1Gfng/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the Thy1-VChR1-YFP transgene are viable and fertile with expression of the VChR1::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The VChR1::YFP fusion protein is composed of a synthetic, mammalian codon-optimized, red-shifted channelrhodopsin-1 derived from Volvox carteri (VChR1) fused in-frame with an enhanced yellow fluorescent protein (EYFP). Compared with ChR2, VChR1 has a markedly (~70 nm) red-shifted action spectrum with a maximum at ~535 nm (green light). The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this VChR1 functions as a green light-driven cation channel that depolarizes the cell and causes action potentials. As such, illumination of VChR1-expressing neurons leads to rapid and reversible photostimulation of action potential firing/neural activity in these cells. The donating investigator spec ..... For more information please see the full phenotype on the strain data sheet | ||
| 012344 | B6;SJL-Tg(Thy1-COP3/EYFP)4Gfng/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the Thy1-VChR1-YFP transgene are viable and fertile with expression of the VChR1::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The VChR1::YFP fusion protein is composed of a synthetic, mammalian codon-optimized, red-shifted channelrhodopsin-1 derived from Volvox carteri (VChR1) fused in-frame with an enhanced yellow fluorescent protein (EYFP). Compared with ChR2, VChR1 has a markedly (~70 nm) red-shifted action spectrum with a maximum at ~535 nm (green light). The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this VChR1 functions as a green light-driven cation channel that depolarizes the cell and causes action potentials. As such, illumination of VChR1-expressing neurons leads to rapid and reversible photostimulation of action potential firing/neural activity in these cells. The donating investigator spec ..... For more information please see the full phenotype on the strain data sheet | ||
| 001957 | C3A Pde6brd1.O20/A-Prph2Rd2/J | Cryopreserved - Ready for recovery |
| 006579 | C57BL/6-Tg(Camk2a-Bdnf)A9Stl/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable and fertile, although the donating investigator reports that hemizygous mice have breeding problems likely resulting from a social anxiety-related phenotype. These "BDNF (line A9)" mice express the rat brain-derived neurotrophic factor (BDNF) primarily in forebrain regions, including the neocortex and hippocampus. Weak transgenic BDNF expression is detected also in cerebellum. Within the primary visual cortex, transgene expression is highest in the superficial layers. Hemizygous mice exhibit accelerated maturation of GABAergic innervation and inhibition, earlier termination of the critical period for ocular dominance plasticity, and accelerated development of visual acuity. These transgenic mice may be useful for studies involving BDNF overexpression and synaptic maturation and plasticity in the visual cortex. | ||
| 005095 | C57BL/6J-Clcn2nmf240/J | Cryopreserved - Ready for recovery |
| Homozygotes exhibit grainy retinas by 3 weeks of age which progresses into large white patches distributed across the entire retina by 12 weeks of age. At 10 days of age the apical processes of the retinal pigment epithelium are abnormally elongated, by 14 days of age the retinal outer nuclear layer is reduced in thickness and contains pyknotic nuclei and the photoreceptor outer segments are disorganized and shortened. By 3 weeks of age the photoreceptor layer is reduced to one to two layers of cells and the outer segments are not visible. Both dark and light adapted flash electroretinograms show reduced amplitude responses as early as 14 days of age and this worsens progressively to near zero by 26 days of age. Male infertility is associated with decreased weight of the testes and epididymides and azoospermia as early as 6 weeks of age with severe degradation of spermatogenesis. Progressive leukoencephalopathy is also found, with vacuoles in the white matter tracts and cerebellum ..... For more information please see the full phenotype on the strain data sheet | ||
| 008648 | CBA.129P2(Cg)-Trpa1tm1Kykw/J | Cryopreserved - Ready for recovery |
| Exons encoding the pore domain of the transient receptor potential cation channel, subfamily A, member 1 gene were deleted in this targeted mutation strain. Animals show reduced sensitivity to pain. RT-PCR of dorsal root ganglia confirmed the absence of mRNA in homozygous mutant mice. Homozygotes are viable and fertile. | ||
| 001981 | O20/A-Prph2Rd2/J | Cryopreserved - Ready for recovery |
| 013167 | STOCK Ahi1tm2.1Jgg/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exons 6 and 7 of the Ahi1 (Abelson helper integration site 1) targeted gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific conditional expression of the gene. This strain may be useful in studies of retinopathy, nephronophthisis and Joubert syndrome. | ||
| 007674 | STOCK Esrrbtm1.1Nat/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Nr3b2CKO allele possess loxP sites flanking exon 2 of the targeted gene and are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have the exon containing the initiator methionine codon and encoding the N-terminal 132 amino acids (including part of the DNA-binding domain) deleted in the cre-expressing tissue(s). Of note, if the conditional Nr3b2CKO is deleted by Cre recombinase in the placenta and embryo, embryonic lethality will result (placental defect). If the conditional Nr3b2CKO is deleted by Cre recombinase only in the embryo, the resulting mice exhibit an inner ear defect (decreased endolymph production) resulting in deafness and defective balance. These Nr3b2CKO mutant mice may be useful in generating conditional mutations to study disorders of hearing and balance, inner ear development (such as endolymph-producing epithelia withi ..... For more information please see the full phenotype on the strain data sheet | ||
| 006702 | STOCK Ntstm1Mom/MomJ | Cryopreserved - Ready for recovery |
| Through bicistronic expression of enhanced green fluorescing protein and neurotensin, this strain permits the visualization of the mitral and tufted cells of the main olfactory bulb thereby permitting developmental analysis in the lateral olfactory tract. | ||
| 006645 | STOCK Olfr151tm12(Olfr16)Mom/MomJ | Cryopreserved - Ready for recovery |
| The coding region of the olfactory receptor Olf151 was replaced by that of the mouse olfactory receptor Olfr16. Olfactory sensory neurons that express the mutated locus co-express taulacZ by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 006691 | STOCK Olfr151tm14(Adrb2)Mom/MomJ | Cryopreserved - Ready for recovery |
| 006635 | STOCK Olfr151tm15(V1rb2)Mom/MomJ | Cryopreserved - Ready for recovery |
| The coding region of the olfactory receptor Olfr151 (formerly M71) was replaced by that of the V1rb2 vomeronasal receptor (termed VRi2 in Rodriguez et al.,1999, Cell 97, 199-208). Olfactory sensory neurons that express the mutated locus co-express taulacZ by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of b-galactosidase enzymatic activity, or by immunofluorescence with anti-b-galactosidase antibodies. | ||
| 006692 | STOCK Olfr151tm16(Olfr160/Olfr161)Mom/MomJ | Cryopreserved - Ready for recovery |
| 006693 | STOCK Olfr151tm17Mom/MomJ | Cryopreserved - Ready for recovery |
| 006688 | STOCK Olfr151tm18(GFP)Mom/MomJ | Cryopreserved - Ready for recovery |
| 006694 | STOCK Olfr151tm20Mom/MomJ | Cryopreserved - Ready for recovery |
| 006695 | STOCK Olfr151tm21Mom/MomJ | Cryopreserved - Ready for recovery |
| 006690 | STOCK Olfr151tm23Mom/MomJ | Cryopreserved - Ready for recovery |
| 006677 | STOCK Olfr151tm28(cre)Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr151 also co-express the Cre recombinase by virtue of IRES-mediated co-translation. | ||
| 006652 | STOCK Olfr160tm2(GFP)Mom/MomJ | Cryopreserved - Ready for recovery |
| 006696 | STOCK Olfr160tm3Mom/MomJ | Cryopreserved - Ready for recovery |
| 006678 | STOCK Olfr160tm6Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr160 also co-express the tauGFP fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. | ||
| 006669 | STOCK Olfr17tm7Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the olfactory receptor Olfr17 also co-express the tauGFP fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. | ||
| 004510 | STOCK Rom1tm1Mci/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and normal in size. When heterozygous mice are bred together, homozygous animals occur at a greatly reduced frequency (~6%). No gene product (protein) is detected in retinal tissue from homozygotes by Western blot analysis. Onset of progressive retinal degeneration occurs at 2 months of age beginning with a thinning of the outer nuclear layer of retinal cells. Rod outer segments in 2 month old mice display disorganized arrangement, irregular gaps and amorphous aggregates. At 4 months of age organization of rod outer segments improves. TUNEL assay of mutant retinal tissue show photoreceptor degeneration is due to apoptotic cell death. Ultra structural organization of rod outer segment disks is disorganized, often with patches of enlarged disks. Electroretinogram a-wave analysis of photoreceptor function reveals a diminished maximal photoreceptor response (50% lower than wildtype). This mutant mouse strain may be useful in stu ..... For more information please see the full phenotype on the strain data sheet | ||
| 006631 | STOCK Vmn1r49tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| Vomeronasal sensory neurons that express the vomeronasal receptor V1rb2 also co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. | ||
| 006632 | STOCK Vmn1r49tm2Mom/MomJ | Cryopreserved - Ready for recovery |
| This targeted mutant is valuable in mapping the patterns of axonal projections of vemeronasal sensory neurons. Vomeronasal sensory neurons that express the vomeronasal receptor V1rb2 also co-express the tauGFP fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. The V1rb2 gene is expressed monoallelically, and homozygotes have fluorescence in approximately twice as many vomeronasal sensory neurons as do heterozygotes. | ||
| 006633 | STOCK Vmn1r49tm3Mom/MomJ | Cryopreserved - Ready for recovery |
| This mutation causes a deletion of the coding region of the vomeronasal receptor V1rb2 and encodes two detectable tags. Vomeronasal sensory neurons that express the mutated locus co-express GFP and the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, by immunofluorescence with anti-GFP antibodies, by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. There is a three fold diminution in neurons expressing this disrupted allele relative to those that express a tagged endogenous sequence, and the pattern of innervation of the accessory olfactory bulb differs, with axons failing to converge onto distinct glomeruli. | ||
| 006657 | STOCK Vmn2r26tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| 005105 | STOCK Tg(Chx10-EGFP/cre,-ALPP)2Clc/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The transgene insert contains a fusion product involving Cre recombinase and an Enhanced Green Fluorescent Protein (EGFP) and a fusion product involving an internal ribosome entry site/human placental alkaline phosphatase under the control of the mouse Chx10, C. elegans ceh-10 homeo domain containing homolog promoter. This strain serves as a multifunctional reporter strain. Expression of the Chx10 BAC, as detected by in situ hybridization, mimics the endogenous Chx10 gene expression pattern. Alkaline phosphatase expression is mosaic, but specific to the retina and Muller glial cells. EGFP expression is detected in the outer neuroblastic layer of the retina at embryonic days 14.5, 17.5 and neonates. When crossed to a cre reporter strain, the resulting mice exhibit mosaicism in reporter gene expression. This mutant mouse str ..... For more information please see the full phenotype on the strain data sheet | ||
| 007577 | STOCK Tg(Gt(ROSA)26Sor-BCHE*G117H)837Loc/J | Cryopreserved - Ready for recovery |
| Transgenic "G117H BChE" mice are viable and fertile. These mice express a mutant form of human butyrylcholinesterase (BCHE or BChE), harboring a single amino acid change at codon 117 (His for Gly), under the control of the ROSA26 promoter. This mutation has the unusual ability to hydrolyze organophosphorus toxicants (OP), as well as acetylcholine and is resistant to inhibition by OP. All tested tissues show G117H BChE enzymatic activity. In the founder mice and immediate offspring, plasma concentrations of the mutant protein are approximately 25% of endogenous wildtype mouse BChe. No reported abnormalities result from BChE overexpression in homozygous mutant mice. Transgenic mice injected with the OP echothiophate are protected from the severe toxicity and lethality observed in wildtype controls. This is the first transgenic mouse strain that expresses human BChE as well as the first mammal with hereditary OP resistance. These G117H BChE transgenic mice may be useful for biodefe ..... For more information please see the full phenotype on the strain data sheet | ||
| 014546 | B6.Cg-Tg(Chat-COP4*H134R/EYFP)6Gfng/J | Under Development - Now Accepting Orders |
| Mice hemizygous for the ChAT-mhChR2-YFP BAC transgene (or ChAT-ChR2-YFP BAC transgene) are viable and fertile (see note below), with expression of the mhChR2::YFP fusion protein directed to cholinergic neuronal populations by the mouse choline acetyltransferase (Chat or ChAT) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illum ..... For more information please see the full phenotype on the strain data sheet | ||
| 014548 | B6.Cg-Tg(Slc32a1-COP4*H134R/EYFP)8Gfng/J | Under Development - Now Accepting Orders |
| Mice hemizygous for the VGAT-mhChR2-YFP BAC transgene (or VGAT-ChR2-YFP BAC transgene) are viable and fertile, with expression of the mhChR2::YFP fusion protein directed to GABAergic interneuronal populations by the mouse vesicular GABA transporter (VGAT or Slc32a1) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mh ..... For more information please see the full phenotype on the strain data sheet | ||
| 014173 | STOCK Tyrc-2J Omptm1.1(COP4*/EYFP)Tboz/J | Under Development - Now Accepting Orders |
| These OMP-ChR2-YFP (OCY-58) mice express a ChR2(H134R)-EYFP fusion gene from the olfactory marker protein locus (Omp). Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. ChR2(H134R)-EYFP is expressed in all mature olfactory sensory neurons, rendering them light sensitive. Light directed at the olfactory epithelium or the glomeruli can elicit activity in mitral/tufted (M/T) cells of the olfactory bulb and can drive odor guided behavior. These mutant mice thus allow precise, timed delivery of stimuli input to the olfactory system. The Donating Investigator reports that this this targeted mutation creates a null allele. Due to possible olfactory deficits, analysis should be performed in heterozygous mice. The Donating Investigator recommends keeping the strain on the albino B6 background to avoid possible interference by pigmented melanocytes.
The ChR2(H134R)-EYFP fusio ..... | ||
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New Strains Awaiting TransferThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion.
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