Search Criteria: Research Area is "Neurobiology Research: lacZ expression in neural tissue"

New Strains Under Development

JAX^® Mice Strains

Stock Number	Strain Name   Strain Description	Standard Supply
004545	129S-Npytm1Rpa/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. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brain or adrenal gland tissue. Beta-galactosidase activity assays and in situ hybridization demonstrate similar expression patterns for the lacZ gene and the endogenous wildtype gene. Spontaneous seizures are exhibited by some mice at age 6 to 8 weeks. Homozygous mice are susceptible to seizures induced by GABA antagonist treatment. Mutant mice have an increased sensitivity to leptin treatment which results in a greater initial reduction of food intake and weight loss when compared to wildtype mice. This mutant mouse strain may be useful in studies related to the role of neuropeptide Y in obesity.
008233	B6.129-Nrgntm1Kph/J	Repository- Live
	Homozygous neurogranin-deficient (Ng-/-) mice are viable and fertile (although the donating investigator reports that homozygous females do not nurse their pups as well as wildtype or heterozygous mothers). Homozygotes have no mRNA or protein from the targeted gene observed in brain tissues. Expression of lacZ is observed in a manner consistent with the endogenous gene. Ng-/- mice exhibit impaired spatial learning, altered hippocampal short- and long-term plasticity (including long-term potentiation induction), and decreased activated CaMKII. Heterozygotes show similar, yet milder, effects. These neurogranin- (Ng or RC3)-mutant mice may be useful for neurological studies involving memory and learning, neuronal signaling pathways (including calmodulin, alpha-CaMKII, protein kinase A, protein kinase C, MAPK, and CREB), attention deficit-hyperactivity disorder (ADHD), and schizophrenia.
007566	B6.129P2-Clip2tm1.1Gal/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable and fertile. Female homozygotes adults have lower body weights and smaller body length when compared to wildtype. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brain tissue. A splice acceptor site introduced into the lacZ reporter cassette results in a hybrid Clip2-lacZ transcript. Beta galactosidase staining is observed primarily in the hippocampus and in other areas of the brain. Homozygotes exhibit a mild growth retardation. The average copus callosum volume is significantly smaller than wildtype. Homozygotes and heterozygotes exhibit abnormal behavior indicative of hippocampal defects. In contextual fear-conditioning tests, mutant mice have a diminished response, although in cued fear-conditioning tests mutant mice exhibit normal behavior. Synaptic plasticity in the CA1 area of the hippocampus is decreased in mutant mice. Both heterozygotes and homozygotes e ..... For more information please see the full descriiption on the strain data sheet
005317	B6.Cg-Tg(BAT-lacZ)3Picc/J	Repository- Live
	Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These "BAT-GAL" transgenic mice are a reporter strain that express beta-galactosidase in the presence of activated beta-catenin. The transgene expresses the lacZ gene under the control of a regulatory sequence consisting of seven consensus LEF/TCF-binding motifs upstream of the Xenopus siamois gene minimal promoter. Transgenic mice display beta-galactosidase activity beginning at embryonic day 6.0 in the posterior side of the proximal epiblast. Beta-galactosidase expression is detectable in the posterior primitive streak and node at gastrulation, and progresses to the paraxial mesoderm and notochord. Beta-galactosidase activity in developing and adult nervous tissue mimics the pattern of Wnt signaling. When bred to other mutant strains, this reporter strain may be useful for identifying mutations that affect the Wnt-signalling pa ..... For more information please see the full descriiption on the strain data sheet
006465	B6;CBA-Tg(CAG-lacZ-WGA)330Bbm/J	Repository- Live
	These ZW transgenic mice constitutively express lacZ under the control of the CMV enhancer/chicken actin promoter. Expression is widespread, but mosaic, throughout the central and peripheral nervous systems. Purkinje cells display intense beta-galactosidase activity. Approximately 50% of the total neuron population express the transgene, as detected by beta-galactosidase activity. Newborn mice exhibit widespread beta-galactosidase activity. When crossed with a Cre recombinase-expressing strain, lacZ expression is replaced with wheat germ agglutinin (plant lectin) expression in tissues expressing cre. The double reporter system makes it possible to distinguish a lack of reporter (lacZ) expression from a lack of Cre recombinase expression while providing a means to assess Cre excision activity at the individual cell level. This transgenic mouse strain may be useful in tracing transneuronal or trans-synaptic connections and circuits in brain regions or in the s ..... For more information please see the full descriiption on the strain data sheet
007225	FVB.129(B6)-Usp18tm1Dzh/J	Repository- Live
	Homozygous Usp18 (or Ubp43) mutant mice on the FVB/N genetic background are viable and fertile, exhibiting none of the severe neurologic disorders that lead to embryonic lethality or early death reported for Ubp43-deficient mice on a C57BL/6 or mixed B6;129 genetic background. In contrast to wildtype mice, thymi from homozygous mice injected with LPS exhibit no protein from the targeted gene. Expression of the lacZ cassette is observed in both heterozygous and homozygous brain tissues. Homozygous mice are hypersensitive to type I interferon (IFN) and undergo apoptosis upon IFN stimulation. Ubp43-deficiency results in enhanced and prolonged STAT1 phosphorylation, DNA binding, and increased induction of hundreds of interferon stimulated genes (ISGs). Homozygous mice exhibit greater resistance to the cytopathic effects caused by a number of viruses (including lymphocytic choriomeningitis virus (LCMV), vesicular stomatitis virus (VSV), and Sindbis virus (SNV)). Ubp43-defici ..... For more information please see the full descriiption on the strain data sheet
005024	FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd/J	Repository- Live
	Mice that are homozygous for the targeted mutant Smn1 allele and carry the SMN2 transgene exhibit symptoms and neuropathology similar to patients afflicted with type I proximal spinal muscular atrophy (SMA). In the initial characterization by the donating investigator, mice were either stillborn or survived 4-6 days. Mice that died at or shortly after birth were slightly smaller (1.33 g. vs. 1.51 g.) than normal littermates. Mice that survive for several days are indistinguishable from normal littermates in the first 48 hours, after which they exhibit decreased suckling and movement, labored breathing and tremoring limbs. Mice succumbing at this later time point are noticeably smaller than normal littermates (1.47 g vs. 4.59). A bell-shaped trunk is also noticeable in affected mice, presumably from intercostal muscle weakness, a characteristic of type I SMA. Histological analysis indicates that affected mice that survive to day 5 exhibit a loss of motor neurons from spina ..... For more information please see the full descriiption on the strain data sheet
003082	129S1/SvImJ-Bcl2tm1Mpin/J	Repository-Cryopreserved
	Heterozygous mice exhibit expression of beta-galactosidase in populations of large sensory neurons. Mice homozygous for the Bcl2tm1Mpin targeted mutation do not produce either the a or b form of the Bcl2 protein. Bcl2 is a major regulator of programmed cell death, a critical process in shaping the developing nervous system. The absence of the Bcl2 does not significantly influence the development of motor neurons before or during the main period of physiological cell death. Rather, Bcl2 exerts its influence beyond this period, subsequent to the phase where the majority of neuronal loss normally takes place. Polycystic kidney disease is less severe in this strain compared to the Bcl2tm1Sjk targeted mutation (Stock No. 002265).
005119	B6.129S6-Npas2tm1Slm/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. Altered gene product (protein), lacking the basic helix-loop-helix (bHLH) domain is detected by Western blot analysis of brain lysates, and is not functional. Northern blot analysis of brain tissue detects a lacZ fusion gene product (mRNA), and does not detect an intact transcript containing the bHLH domain. Beta-galactosidase activity is detected in the cortex, hippocampus, striatum, amygdala, thalamus, and in the barrelfield structures of the cortical somatosensory region. Homozygotes display defective complex emotional long-term memory, as assayed by cued and contextual fear tests. Under conditions of constant darkness, homozygotes exhibit a shortened circadian rhythm period of 23.5 hours and increased nocturnal locomotor activity. Mutant mice do not adapt to restricted feeding conditions, and lose weight due to decreased food consumption. This ..... For more information please see the full descriiption on the strain data sheet
005970	B6.129S7-Atoh1tm2Hzo/J	Repository-Cryopreserved
	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.
003139	B6.Cg-Tg(DBHn-lacZ)8Rpk/J	Repository-Cryopreserved
	Transgenic mice carry a beta-galactosidase reporter gene driven by dopamine beta hydroxylase promotor. LacZ expression is seen in neurons of the locus ceruleus and other classic noradrenergic brain stem nuclei, sympathetic ganglion neurons, and adrenal chromaffin cells. LacZ expression is also observed in neurons of the enteric system, the retina, some sensory and all cranial parasympathetic ganglia, and some diencephalic and telencephalic brain nuclei.
002982	B6.Cg-Tg(xstpx-lacZ)32And/J	Repository-Cryopreserved
	This mutant, when crossed with a cre transgenic, will express lacZ in cells where cre is expressed to remove the STOP of translation section which lies between the 2 loxP sites. LacZ expression is restricted to neural and skeletal muscle tissue and heart by the chicken beta-actin promoter that is driving the reporter.
005064	B6;129-Slc30a3tm1Rpa/J	Repository-Cryopreserved
	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 in brain homogenates by Western blot analysis. Beta-galactosidase activity pattern in homozygotes mimics endogenous gene expression. Total zinc levels in the hippocampus and cortex is reduced by approximately 20%. Histochemically reactive and immunoreactive synaptic vesicle zinc is undetectable. There is no N-(6-Methoxy-8-quinolyl)-p-Toluene-Sulfonamide (TSQ) fluorescence in hippocampal tissues, although it is detected in testis and pancreas. This mutant mouse strain may be useful in studies of zinc transport into synaptic vesicles.
006703	B6;129P2-Gucy2dtm1Mom/MomJ	Repository-Cryopreserved
	A subset of necklace glomeruli demarcating main and accessory portions of the olfactory bulb are labeled by lacZ driven by an axonally-expressed guanylate cyclase 2d (GC-D) promoter.
003471	B6;C3H-Tg(CNP-GEO)1Ldh/J	Repository-Cryopreserved
	This transgenic strain is used to trace glial cell lineage from the early stages throughout their development while simultaneously selecting for oligodendrocytes and Schwann cells. The transgenic mice contain a bacterial b-galactosidase and neomycin phosphotransferase fusion protein (bgeo) under the control of murine 2'3'-cyclic nucleotide 3'-phosphodiesterase (muCNP) promoters I and II. No overt phenotype is observed.
004141	B6;CBA-Tg(UAS-lacZ)65Rth/J	Repository-Cryopreserved
	Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Expression of the transgenic lacZ gene is directed by upstream activating sequence (UAS) elements. This strain serves as a reporter for mice employing GAL4/UAS bigenic system for controlled gene expression in the developing CNS. In this system, a transgenic strain expressing the yeast transcriptional activator GAL4 (see Stock No. 003829) is bred to a second transgenic, target strain bearing an UAS-regulated gene. In the double transgenic offspring, an UAS-regulated gene would be selectively expressed in tissues expressing GAL4.
002865	B6CBA-Tg(Wnt1-lacZ)206Amc/J	Repository-Cryopreserved
	These transgenic mice show no phenotypic defects. LacZ is expressed in the dorsal CNS. This strain is useful as a marker for CNS development, specifically for the migrating cranial and trunk neural crest.
004127	FVB-Tg(Nes-rtTA)306Rvs/J	Repository-Cryopreserved
	Mice that are hemizygous for this transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat nestin intron II enhancer/promoter. According to the donating investigator, expression occurs in the neuroepithelium of the developing nervous system (embryonic days 10-17), in some neuron subsets of the adult mouse (e.g. cerebellum, hippocampal dentate gyrus, subventricular zone, spinal cord) and in adult testes. The rtTA gene is cotranscribed with the lacZ reporter gene Bgeo, which allows verification of the site of rtTA expression. When Tg(Nes-rtTA) hemizygous mice are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene may be regulated by the tetracycline analog, doxycycli ..... For more information please see the full descriiption on the strain data sheet
003487	FVB/NJ-Tg(XGFAP-lacZ)3Mes/J	Repository-Cryopreserved
	Mice carrying this transgene express beta galactosidase in the nuclei of astrocytes. The donating investigator reports that more recent studies on this particular line indicate low level expression of the lacZ reporter gene in many neuronal populations as well. The transgene integrated on the X chromosome and therefore undergoes X-inactivation. This strain may be useful for cell culture and transplantation studies.

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New Strains Under Development

(See informational text following listing of strains)

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Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.

View a Data sheet for New Strains Under Development
Select the strain name to link to the strain data sheet.

	Stock Number	Strain Name   Strain Description	Standard Supply
	008602	129-Cdontm2Rsk/J	Under Development for Production
	Homozygous CdonlacZ-2 (or CdolacZ-2) mice on a "129/Sv" genetic background are viable and fertile, harboring a beta-galactosidase (lacZ) "knock-in" mutation that also abolishes targeted gene expression. LacZ expression mimics the pattern observed for the endogenous gene. On a 129/Sv background, Cdo-deficient mice exhibit craniofacial midline defects identified as microforms of holoprosencephaly (HPE; a common defect of human forebrain development) with partial penetrance, grossly normal limb development and no perinatal lethality. These CdonlacZ-2 (or CdolacZ-2) mice are a genetic model of HPE and may be useful in studying craniofacial/brain development and the regulation of Sonic Hedgehog (Shh) signaling pathways, as well as for lacZ expression in Cdo-expressing tissues. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background dif ..... For more information please see the full description on the strain data sheet
	008344	B6;DBA-Tg(Fos-tTA,Fos-EGFP*)1Mmay Tg(tetO-lacZ,tTA*)1Mmay/J	Under Development for Production
	The TetTag mouse is a bi-transgenic mutant that has tetracycline (or tetracycline analog) inducible expression of beta-galactosidase in activated neurons. Two independently generated transgenic strains were crossed to produce this bi-transgenic TetTag strain. In the first transgenic construct, the tetracycline-controlled transactivator (rTA) protein and a two hour half-life Green Fluorescent Protein (shEGFP) are expressed under the direction of the fos, FBJ osteosarcoma oncogene, minimal promoter. The second transgenic construct expresses a nuclear-localizing beta-galactosidase gene and the doxycycline insensitive tetracycline regulated transactivator (containing point mutation, H100Y), under the control of the tetO, tetracycline-responsive regulatory element. In the absence of tetracycline or a tetracycline analog (such as doxycycline), selective expression of beta-galactosidase is observed in activated neurons. Doxycycline administration prevents expression beta-galactosidase ..... For more information please see the full description on the strain data sheet
	008203	FVB.Cg-Smn1tm1Msd Tg(ACTA1-SMN)63Ahmb Tg(SMN2)89Ahmb/J	Under Development for Production
	As described for SMA mice (see Stock No. 005024), mice homozygous for Smn1tm1Msd targeted mutation (Smn null allele) and human SMN2 low copy line 89 transgene exhibit symptoms, neuropathology, and early lethality similar to human type I proximal spinal muscular atrophy (SMA) patients. As an addition to that SMA model, this strain also carries the HSA-SMN transgene; with the human alpha-skeletal actin (HSA or ACTA1) promoter directing full-length human SMN expression at high levels in skeletal muscle. When the HSA-SMN transgene is derived from HSA69-SMN founder mice, skeletal muscle-specific SMN expression is preserved, and homozygous SMN2; Smn; HSA69-SMN mutant animals (Stock No. 008209) have the same phenotype as homozygous SMA mice. In contrast, expression of the HSA-SMN transgene derived from HSA63-SMN founder mice is leaky; with hi ..... For more information please see the full description on the strain data sheet
	008209	FVB.Cg-Smn1tm1Msd Tg(ACTA1-SMN)69Ahmb Tg(SMN2)89Ahmb/J	Under Development for Production
	As described for SMA mice (see Stock No. 005024), mice homozygous for Smn1tm1Msd targeted mutation (Smn null allele) and human SMN2 low copy line 89 transgene exhibit symptoms, neuropathology, and early lethality similar to human type I proximal spinal muscular atrophy (SMA) patients. As an addition to that SMA model, this strain also carries the HSA-SMN transgene; with the human alpha-skeletal actin (HSA or ACTA1) promoter directing full-length human SMN expression at high levels in skeletal muscle. When the HSA-SMN transgene is derived from HSA69-SMN founder mice, skeletal muscle-specific SMN expression is preserved, and homozygous SMN2; Smn; HSA69-SMN mutant animals (Stock No. 008209) have the same phenotype as homozygous SMA mice. In contrast, expression of the HSA-SMN transgene derived from HSA63-SMN founder mice is leaky; with hi ..... For more information please see the full description on the strain data sheet
	008206	FVB.Cg-Smn1tm1Msd Tg(SMN2)566Ahmb/J	Under Development for Production
	As described for SMA mice (see Stock No. 005024), mice homozygous for Smn1tm1Msd targeted mutation (Smn null allele) and single copy human SMN2 low copy line 89 exhibit symptoms, neuropathology, and early lethality similar to human type I proximal spinal muscular atrophy (SMA) patients. In contrast to that SMA model, this strain carries the high copy SMN2 (founder line 566) transgene instead of the single copy SMN2 (line 89) transgene. As a result of the high SMN2 copy number, mice homozygous for the Smn1tm1Msd targeted mutation and high copy SMN2 line 566 (16 copies when homozygous) are rescued from all overt features of the severe SMA phenotype. Homozygous Smn; SMN2 high copy line 566 mice have a shorter and thicker tail. These Smn; SMN2 high copy line 566 mutant mice may be useful in neuromuscular studies including spinal muscular atrophy (SMA).
	007912	STOCK En1tm2Alj/J	Under Development for Production
	En-1lki (or En1lacZ) mutant mice harbor a β-galactosidase "knock-in" allele that also abolishes endogenous gene function. While heterozygotes are viable and fertile, homozygous mice die at birth (unless when maintained on a C57BL/6 genetic background). Under control of the upstream promoter/enhancer elements, lacZ expression is observed in a pattern almost identical to the wildtype gene. These En-1lacZ mice may be useful for reporter protein expression in En1-expressing tissues in studying engrailed protein function in limb patterning along the dorso-ventral axis, spinal cord V1 interneuron development, embryonic mesencephalon and rhombomere 1 (cerebellum) development, as well as developing somites, and skin. Of note, these mice may also be useful in conjunction with other engrailed mutants (such as Stock No. 007916, Stock No. For more information please see the full description on the strain data sheet
	008211	STOCK Gli1tm2Alj/J	Under Development for Production
	Mice homozygous for the Gli1lz (or Gli1lacZ) allele are viable and semi-fertile, with a "knock-in" of β-galactosidase (lacZ) inserted into the first coding exon (exon 2) and replacing the genomic fragment encoding the entire N-terminal and zinc-finger domains of the targeted locus (exons 2-7); abolishing endogenous gene function even if alternative splicing occurs. Under control of the upstream promoter/enhancer elements, lacZ expression is observed in a pattern indistinguishable from wildtype gene mRNA expression. As Gli1 transcription is a readout of high level Hedgehog signaling, these Gli1lz (or Gli1lacZ) mice may be useful for studying Hedgehog/Sonic Hedgehog signaling in axis patterning, proliferation, and cell fate specification of Hedgehog responding cells at different stages of embryogenesis.
	007922	STOCK Gli2tm2.1Alj/J	Under Development for Production
	Mice homozygous for this Gli2lzki allele harbor a <β-galactosidase "knock-in" (lzki) allele that also abolishes endogenous gene function. As such, homozygous mice die at birth with many defects including absence of Sonic Hedgehog-expressing floor plate cells, reduction of Nkx2.2-expressing V3 interneurons in the spinal cord, and defects in midbrain, cerebellum and lung development. Under control of the upstream promoter/enhancer elements, lacZ expression is observed in a pattern identical to the wild-type gene. Heterozygotes are viable and fertile. These Gli2lzki mice may be useful for studying Hedgehog/Sonic Hedgehog signaling in the development of many organs (such as central nervous system and axis patterning), as well as the role of Gli2 in adult organs.
	008212	STOCK Smn1tm1Msd Tg(Prnp-SMN)92Ahmb Tg(SMN2)89Ahmb/J	Under Development for Production
	As described for SMA mice (see Stock No. 005024), mice homozygous for Smn1tm1Msd targeted mutation (Smn null allele) and human SMN2 transgene (SMN2 low copy line 89) exhibit symptoms, neuropathology, and early lethality similar to human type I proximal spinal muscular atrophy (SMA) patients. As an addition to that SMA model, this strain also carries the PrP-SMN transgene; with the mouse prion protein (PrP or Prnp) promoter directing full-length human SMN expression at high levels in neurons (with low expression in skeletal muscle and liver). When the PrP-SMN transgene is derived from PrP92-SMN founder mice, high SMN expression in spinal cord and brain is observed. Homozygous SMN2; Smn; Prp92-SMN mice are rescued from the severe SMA phenotype, have significantly increased lifespan (average of 210 days) and have normal lumbar motor neuron root counts. Homozygous SMN2; Smn; PrP92-SMN mal ..... For more information please see the full description on the strain data sheet

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New Strains Under Development

• Receive periodic updates on the status of the colony UNDER DEVELOPMENT
• Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
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The 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. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.

1. Strains that will be made available from a live distribution colony at The Jackson Laboratory.
   These strains are designated as: "Under Development for Distribution Colony"
2. Strains that will be made available through the Cryopreservation Repository.
   These strains are designated as: "Under Development for Cryopreservation Repository"

It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.

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