JAX Mouse Strain Datasheet - 003827

B6.129S6-Naglu^tm1Efn/J

Stock No:: 003827 |; Naglu-

Cryo Recovery

Overview

Also Known As: Naglu-

These Naglu knock-out mice exhibit massive accumulation of heparan sulfate in liver and kidney and vacuolation in many cells, including macrophages, epithelial cells, and neurons.

Donating Investigator

Elizabeth F. Neufeld, UCLA School of Medicine

Genetic overview

Genetic Background	Generation

Naglu^tm1Efn

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Naglu	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)

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Research Applications

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Base Price

Starting at:

$2,595.00 Domestic price Cryo Recovery

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Details

Detailed Description

At birth, homozygous null mice are viable, normal in size, and do not display any gross physical or behavioral abnormalities. The lysosomal enzyme alpha-N-acetylglucosaminidase (Naglu) is absent in all tissues. Large amounts of heparan sulfate accumulate in liver and kidney, and lesser amounts in other organs. At one month of age, vacuolated macrophages can be found in most tissues. Epithelial cells in kidney and neurons in some parts of the brain are also affected. The vacuolation becomes more prominent with age. At 4-5 months, the mice show abnormal behavior in an open field test. The life span is 8-12 months. Older animals may have urinary retention and difficulty walking and must be euthanized. The null mice were originally described as fertile, but their fertility has decreasd markedly with repeated back-crossing to an inbred strain. These mice are suitable for examining the pathophysiology of the Sanfilippo syndrome type B and for developing therapies for this lysosomal storage disorder.

Development

A targeting vector containing a neomycin resistance gene driven by the mouse phosphoglycerate kinase promoter and a Herpes simplex virus thymidine kinase gene driven by its own promoter was used to disrupt a portion of exon 6. The construct was electroporated into 129S6/SvEv-derived CCE embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric male animals were backcrossed to C57BL/6 females.

Control Suggestions

Wild-type from the colony
000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Genetics

Naglu^tm1Efn

Allele Symbol: Naglu^tm1Efn

Allele Name	targeted mutation 1, Elizabeth F Neufeld
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	MPS IIIB; Naglu-
Gene Symbol and Name	Naglu, alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)
Gene Synonym(s)	CMT2V; MPS-IIIB; MPS3B; NAG; RGD1564228; UFHSD
Strain of Origin	129S/SvEv-Gpi1
Chromosome	11
Molecular Note	Exon 6 of this gene, a region known to harbor several Sanfilippo B mutations, was disrupted by the insertion of a neomycin resistance gene via homologous recombination. Protein from homozygous mutant animals was negative for enzyme activity.
Mutations Made By	Elizabeth Neufeld, UCLA School of Medicine

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Naglu^tm1Efn/Naglu^tm1Efn
either: (involves: 129S/SvEv * C57BL/6) or (involves: C57BL/6)

mortality/aging

premature death
- appear normal, healthy, and fertile up to 6 months of age
- homozygotes survive to 8-12 months

integument phenotype

disheveled coat
- after 6 months of age

spontaneous skin ulceration
- skin ulceration around the genitalia occurs after 6 months of age

behavior/neurological phenotype

abnormal locomotor behavior
- difficulty walking after about 6 months of age

decreased fear-related response
- older mice demonstrate a reduced freezing response to the tone used in fear tests

increased anxiety-related response
- suppressed open field activity in mice over 4.5 months of age

growth/size/body region phenotype

distended abdomen
- after 6 months of age

weight loss
- weight loss starts to occur at some time after 6 months of age

hematopoietic system phenotype

abnormal Kupffer cell morphology
- Kupffer cells are ballooned and contain very few large inclusions

abnormal macrophage morphology
- by 33 days of age, vacuolated macrophages are found in many organs
- vacuolated macrophages become more widely distributed with age to 6 months

immune system phenotype

abnormal Kupffer cell morphology
- Kupffer cells are ballooned and contain very few large inclusions

abnormal macrophage morphology
- by 33 days of age, vacuolated macrophages are found in many organs
- vacuolated macrophages become more widely distributed with age to 6 months

liver/biliary system phenotype

abnormal Kupffer cell morphology
- Kupffer cells are ballooned and contain very few large inclusions

abnormal hepatocyte morphology
- hepatocytes contain many large vacuoles

renal/urinary system phenotype

abnormal podocyte morphology
- extent of vacuolation increases with age to at least 6 months
- vacuolated glomerular epithelial cells seen by 33 days of age

abnormal renal tubule epithelium morphology
- at 3 to 6 months of age, more prominent vacuolation is seen in tubular epithelial cells as well as interstitial cells
- by 33 days of age, epithelial cells are vacuolated in distal but not proximal convoluted tubules, and in Henle's loop
- however, mesangial cells are not vacuolated

ischuria
- urinary retention in the bladder starting at 6 months of age

nervous system phenotype

abnormal Purkinje cell morphology
- rather than vacuoles cells may contain one or more large periodic acid/Schiff positive inclusions

abnormal accessory olfactory bulb morphology
- accessory olfactory bulb with vacuolated neurons

abnormal amygdala morphology
- some vacuolated neurons

abnormal cerebellum deep nucleus morphology
- neurons of cerebellar nuclei containing one or more inclusions similar to those found in Purkinje cells

abnormal cerebral cortex morphology
- some areas of the cortex contain vacuolated neurons

abnormal diencephalon morphology
- neurons in the thalamus and the hypothalamus with vacuoles

abnormal midbrain morphology

abnormal neuron morphology
- by 33 days of age, some neurons in various regions of the brain become vacuolated
- extent of vacuolation increases with age

abnormal olfactory bulb morphology
- olfactory bulb with vacuolated neurons

abnormal pons morphology
- some vacuolated neurons

cardiovascular system phenotype

abnormal Kupffer cell morphology
- Kupffer cells are ballooned and contain very few large inclusions

Genotype: Naglu^tm1Efn/Naglu^tm1Efn
involves: 129S/SvEv * C57BL/6J

mortality/aging

premature death
- average age of death is 315-360 days

skeleton phenotype

abnormal middle ear ossicle morphology
- thickened mucosal layer on stapes and malleus at 30 weeks of age with hyperplasia of mucosal cells

abnormal spiral ligament morphology
- lysosomal storage is seen in the spiral ligament

abnormal stapes morphology
- bone surface of the stapes is pitted, indicating abnormal bone remodeling

cellular phenotype

abnormal lysosome morphology
- mutants exhibit lysosomal distention in multiple tissues, including in the middle and inner ear, in the eye, and in the suprachiasmatic nucleus

behavior/neurological phenotype

abnormal circadian rhythm
- percentage of daily activity which occurs during the light portion of the LD cycle is increased in mutants

delayed circadian phase
- mutants differ from wild-type in their phase angle of entrainment (the time from the light offset to the onset of daily locomotor activity); mutants start their daily activity about 1 hour later than wild-type

impaired coordination
- rotarod testing shows a progressive inability of older, but not younger, mutants to coordinate movement in a rocking paradigm

nervous system phenotype

Purkinje cell degeneration
- age dependent loss of Purkinje cells

abnormal suprachiasmatic nucleus morphology
- the suprachiasmatic nucleus (SCN) shows a large number of pyknotic cells with condensed nuclei and cytoplasms and distended lysosomes

decreased Purkinje cell number
- diffuse decrease in cerebellar Purkinje neuronal counts at the vermis in older, but not younger, mutants

decreased cochlear hair cell number
- complete loss of hair cells in the lower base coincides with degeneration of the organ of Corti

short photoreceptor outer segment
- progressive shortening of the outer segments

hearing/vestibular/ear phenotype

abnormal Reissner membrane morphology
- lysosomal storage is seen in Reissner's membrane

abnormal cochlea morphology
- inflammatory cells are more likely to appear in the perilymphatic scalae of mutants than wild-type and often show lysosomal storage

abnormal crista ampullaris morphology
- abnormal lysosomal storage in the crista ampullaris of the lateral semicircular canal

abnormal inner ear morphology

abnormal inner ear vestibule morphology
- the vestibular maculae and cristae show prominent lysosome storage in both supporting cells and hair cells and the dark cells of the cristae

abnormal middle ear morphology
- lysosomal storage is prominent in the mucosal lining and within osteocytes, chondrocytes, and inflammatory cells
- middle ears at 30 weeks of age show lysosomal storage-related anomalies

abnormal middle ear ossicle morphology
- thickened mucosal layer on stapes and malleus at 30 weeks of age with hyperplasia of mucosal cells

abnormal organ of Corti morphology
- lysosomal storage in the organ of Corti occurs within outer sulcus cells of the lateral organ and pillar cells of the medial organ

abnormal spiral ligament morphology
- lysosomal storage is seen in the spiral ligament

abnormal spiral limbus morphology
- lysosomal storage is seen in the spiral limbus

abnormal stapes morphology
- bone surface of the stapes is pitted, indicating abnormal bone remodeling

conductive hearing loss
- auditory brainstem response (ABR) shows progressive hearing deficits

decreased cochlear hair cell number
- complete loss of hair cells in the lower base coincides with degeneration of the organ of Corti

increased or absent threshold for auditory brainstem response
- increase in high frequency ABR thresholds is significantly greater in mutants up to 16 weeks than in controls

increased susceptibility to otitis media
- middle ears at 30 weeks of age exhibit highly variable otitis media, with and without effusion

organ of Corti degeneration

vision/eye phenotype

abnormal eye electrophysiology
- ERG shows a progressive decrease in the amplitude of the dark-adapted b-wave response

abnormal retina morphology
- aberrant lysosomal storage is seen in the inner retina

abnormal retinal pigment epithelium morphology
- localized disruption and inclusions in the retinal pigment epithelium

abnormal rod electrophysiology
- dark-adapted retinal response is depressed by 5 weeks and becomes progressively less sensitive with increasing age, indicating loss of rod function
- however, cone function appears normal

abnormal sclera morphology
- lysosomal storage in the sclera

short photoreceptor outer segment
- progressive shortening of the outer segments

thin retinal outer nuclear layer
- progressive reduction of the outer nuclear layer

immune system phenotype

increased susceptibility to otitis media
- middle ears at 30 weeks of age exhibit highly variable otitis media, with and without effusion

craniofacial phenotype

abnormal middle ear ossicle morphology
- thickened mucosal layer on stapes and malleus at 30 weeks of age with hyperplasia of mucosal cells

abnormal stapes morphology
- bone surface of the stapes is pitted, indicating abnormal bone remodeling

pigmentation phenotype

abnormal retinal pigment epithelium morphology
- localized disruption and inclusions in the retinal pigment epithelium

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

Genotype: Naglu^tm1Efn/Naglu^tm1Efn
involves: 129S/SvEv * C57BL/6

nervous system phenotype

abnormal cerebral cortex morphology
- vacuolated microglial cells sometimes apposed to neurons

References

Additional References

Gografe SI; Garbuzova-Davis S; Willing AE; Haas K; Chamizo W; Sanberg PR. 2003. Mouse model of Sanfilippo syndrome type B: relation of phenotypic features to background strain. Comp Med 53(6):622-32. PubMed: 14727810 MGI: J:87310

Additional - Naglu^tm1Efn related

Ausseil J; Desmaris N; Bigou S; Attali R; Corbineau S; Vitry S; Parent M; Cheillan D; Fuller M; Maire I; Vanier MT; Heard JM. 2008. Early neurodegeneration progresses independently of microglial activation by heparan sulfate in the brain of mucopolysaccharidosis IIIB mice. PLoS One 3(5):e2296. PubMed: 18509511 MGI: J:136381
Cheillan D; Malleval C; Ausseil J; Vitry S; Heard JM; Maire I; Honnorat J; Belin MF; Touret M. 2008. Abnormal expression of truncated CRMP-1 protein in the brain cortex of MPSIIIB mice. Mol Genet Metab 94(1):135-8. PubMed: 18325808 MGI: J:134471
Cho SK; Gao N; Pearce DA; Lehrman MA; Hofmann SL. 2005. Characterization of lipid-linked oligosaccharide accumulation in mouse models of Batten disease. Glycobiology 15(6):637-48. PubMed: 15647513 MGI: J:112499
Cressant A; Desmaris N; Verot L; Brejot T; Froissart R; Vanier MT; Maire I; Heard JM. 2004. Improved behavior and neuropathology in the mouse model of Sanfilippo type IIIB disease after adeno-associated virus-mediated gene transfer in the striatum. J Neurosci 24(45):10229-39. PubMed: 15537895 MGI: J:96575
Di Natale P; Di Domenico C; Gargiulo N; Castaldo S; Gonzalez Y Reyero E; Mithbaokar P; De Felice M; Follenzi A; Naldini L; Villani GR. 2005. Treatment of the mouse model of mucopolysaccharidosis type IIIB with lentiviral-NAGLU vector. Biochem J 388(Pt 2):639-46. PubMed: 15649123 MGI: J:117532
Fu H; Bartz JD; Stephens RL Jr; McCarty DM. 2012. Peripheral nervous system neuropathology and progressive sensory impairments in a mouse model of Mucopolysaccharidosis IIIB. PLoS One 7(9):e45992. PubMed: 23049915 MGI: J:191944
Garbuzova-Davis S; Louis MK; Haller EM; Derasari HM; Rawls AE; Sanberg PR. 2011. Blood-brain barrier impairment in an animal model of MPS III B. PLoS One 6(3):e16601. PubMed: 21408219 MGI: J:171706
Gografe SI; Garbuzova-Davis S; Willing AE; Haas K; Chamizo W; Sanberg PR. 2003. Mouse model of Sanfilippo syndrome type B: relation of phenotypic features to background strain. Comp Med 53(6):622-32. PubMed: 14727810 MGI: J:87310
Heldermon CD; Hennig AK; Ohlemiller KK; Ogilvie JM; Herzog ED; Breidenbach A; Vogler C; Wozniak DF; Sands MS. 2007. Development of sensory, motor and behavioral deficits in the murine model of Sanfilippo syndrome type B. PLoS One 2(1):e772. PubMed: 17712420 MGI: J:129390
Kan SH; Aoyagi-Scharber M; Le SQ; Vincelette J; Ohmi K; Bullens S; Wendt DJ; Christianson TM; Tiger PM; Brown JR; Lawrence R; Yip BK; Holtzinger J; Bagri A; Crippen-Harmon D; Vondrak KN; Chen Z; Hague CM; Woloszynek JC; Cheung DS; Webster KA; Adintori EG; Lo MJ; Wong W; Fitzpatrick PA; LeBowitz JH; Crawford BE; Bunting S; Dickson PI; Neufeld EF. 2014. Delivery of an enzyme-IGFII fusion protein to the mouse brain is therapeutic for mucopolysaccharidosis type IIIB. Proc Natl Acad Sci U S A 111(41):14870-5. PubMed: 25267636 MGI: J:216443
Langford-Smith A; Malinowska M; Langford-Smith KJ; Wegrzyn G; Jones S; Wynn R; Wraith JE; Wilkinson FL; Bigger BW. 2011. Hyperactive behaviour in the mouse model of mucopolysaccharidosis IIIB in the open field and home cage environments. Genes Brain Behav 10(6):673-82. PubMed: 21635693 MGI: J:186608
Langford-Smith K; Arasaradnam M; Wraith JE; Wynn R; Bigger BW. 2010. Evaluation of heparin cofactor II-thrombin complex as a biomarker on blood spots from mucopolysaccharidosis I, IIIA and IIIB mice. Mol Genet Metab 99(3):269-74. PubMed: 19926322 MGI: J:158031
Li HH; Yu WH; Rozengurt N; Zhao HZ; Lyons KM; Anagnostaras S; Fanselow MS; Suzuki K; Vanier MT; Neufeld EF. 1999. Mouse model of Sanfilippo syndrome type B produced by targeted disruption of the gene encoding alpha-N-acetylglucosaminidase. Proc Natl Acad Sci U S A 96(25):14505-10. PubMed: 10588735 MGI: J:58950
Li HH; Zhao HZ; Neufeld EF; Cai Y; Gomez-Pinilla F. 2002. Attenuated plasticity in neurons and astrocytes in the mouse model of Sanfilippo syndrome type B. J Neurosci Res 69(1):30-8. PubMed: 12111813 MGI: J:113178
Malinowska M; Wilkinson FL; Bennett W; Langford-Smith KJ; O'Leary HA; Jakobkiewicz-Banecka J; Wynn R; Wraith JE; Wegrzyn G; Bigger BW. 2009. Genistein reduces lysosomal storage in peripheral tissues of mucopolysaccharide IIIB mice. Mol Genet Metab 98(3):235-42. PubMed: 19632871 MGI: J:155027
Mohammed EE; Snella EM; Rutz-Mendicino MM; Echevarria FD; Awedikian R; Whitley EM; Ellinwood NM. 2012. Accelerated clinical disease and pathology in mucopolysaccharidosis type IIIB and GalNAc transferase double knockout mice. Mol Genet Metab 107(1-2):129-35. PubMed: 22867887 MGI: J:188147
Ohmi K; Greenberg DS; Rajavel KS; Ryazantsev S; Li HH; Neufeld EF. 2003. Activated microglia in cortex of mouse models of mucopolysaccharidoses I and IIIB. Proc Natl Acad Sci U S A 100(4):1902-7. PubMed: 12576554 MGI: J:81974
Ohmi K; Kudo LC; Ryazantsev S; Zhao HZ; Karsten SL; Neufeld EF. 2009. Sanfilippo syndrome type B, a lysosomal storage disease, is also a tauopathy. Proc Natl Acad Sci U S A 106(20):8332-7. PubMed: 19416848 MGI: J:148534
Ohmi K; Zhao HZ; Neufeld EF. 2011. Defects in the medial entorhinal cortex and dentate gyrus in the mouse model of Sanfilippo syndrome type B. PLoS One 6(11):e27461. PubMed: 22096577 MGI: J:180969
Ribera A; Haurigot V; Garcia M; Marco S; Motas S; Villacampa P; Maggioni L; Leon X; Molas M; Sanchez V; Munoz S; Leborgne C; Moll X; Pumarola M; Mingozzi F; Ruberte J; Anor S; Bosch F. 2015. Biochemical, histological and functional correction of mucopolysaccharidosis Type IIIB by intra-cerebrospinal fluid gene therapy. Hum Mol Genet 24(7):2078-95. PubMed: 25524704 MGI: J:219595
Ryazantsev S; Yu WH; Zhao HZ; Neufeld EF; Ohmi K. 2007. Lysosomal accumulation of SCMAS (subunit c of mitochondrial ATP synthase) in neurons of the mouse model of mucopolysaccharidosis III B. Mol Genet Metab 90(4):393-401. PubMed: 17185018 MGI: J:121457
Schiattarella GG; Cerulo G; De Pasquale V; Cocchiaro P; Paciello O; Avallone L; Belfiore MP; Iacobellis F; Di Napoli D; Magliulo F; Perrino C; Trimarco B; Esposito G; Di Natale P; Pavone LM. 2015. The Murine Model of Mucopolysaccharidosis IIIB Develops Cardiopathies over Time Leading to Heart Failure. PLoS One 10(7):e0131662. PubMed: 26147524 MGI: J:238392
Villani GR; Di Domenico C; Musella A; Cecere F; Di Napoli D; Di Natale P. 2009. Mucopolysaccharidosis IIIB: oxidative damage and cytotoxic cell involvement in the neuronal pathogenesis. Brain Res 1279:99-108. PubMed: 19409882 MGI: J:157220
Vitry S; Bruyere J; Hocquemiller M; Bigou S; Ausseil J; Colle MA; Prevost MC; Heard JM. 2010. Storage vesicles in neurons are related to Golgi complex alterations in mucopolysaccharidosis IIIB. Am J Pathol 177(6):2984-99. PubMed: 21037080 MGI: J:167634
Woloszynek JC; Coleman T; Semenkovich CF; Sands MS. 2007. Lysosomal dysfunction results in altered energy balance. J Biol Chem 282(49):35765-71. PubMed: 17911106 MGI: J:129210

Service	Genotype	Price
	Heterozygous or wildtype for Naglu<tm1Efn>

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Also Known As: Naglu-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Naglutm1Efn

Allele Symbol: Naglutm1Efn

Disease Terms

Research Areas By Genotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Naglutm1Efn/Naglutm1Efneither: (involves: 129S/SvEv * C57BL/6) or (involves: C57BL/6)

mortality/aging

integument phenotype

behavior/neurological phenotype

growth/size/body region phenotype

hematopoietic system phenotype

immune system phenotype

liver/biliary system phenotype

renal/urinary system phenotype

nervous system phenotype

cardiovascular system phenotype

Genotype: Naglutm1Efn/Naglutm1Efninvolves: 129S/SvEv * C57BL/6J

mortality/aging

skeleton phenotype

cellular phenotype

behavior/neurological phenotype

nervous system phenotype

hearing/vestibular/ear phenotype

vision/eye phenotype

immune system phenotype

craniofacial phenotype

pigmentation phenotype

Genotype: Naglutm1Efn/Naglutm1Efninvolves: 129S/SvEv * C57BL/6

nervous system phenotype

References

Additional References

Additional - Naglutm1Efn related

Genotyping Protocols

Breeding Considerations

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Progeny testing is not required

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Naglu^tm1Efn

Allele Symbol: Naglu^tm1Efn

Genotype: Naglu^tm1Efn/Naglu^tm1Efn
either: (involves: 129S/SvEv * C57BL/6) or (involves: C57BL/6)

Genotype: Naglu^tm1Efn/Naglu^tm1Efn
involves: 129S/SvEv * C57BL/6J

Genotype: Naglu^tm1Efn/Naglu^tm1Efn
involves: 129S/SvEv * C57BL/6

Additional - Naglu^tm1Efn related