Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse   Donating Investigator Chin Howe,   The Wistar Institute

Description
Mice that are homozygous null for Sparc are viable and fertile. They display decreased physical activity when handled but otherwise appear normal. Sparc transcripts and protein products are not detected in these animals. The development of cataracts and osteopenia are the predominant phenotypes. Lenticular opacity starts to develop at 1 to 2 months after birth, progressing to mature cataracts by 5-8 months of age. Intracellular vacuoles are apparent at 1-2 months, leading to a disruption of fiber cell packing. In later stages, the lens capsule ruptures and displacement of lens material into the anterior chamber is evident. At 17 weeks of age, null mice exhibit 50% less trabecular bone than that found in wild type controls. The loss is 70% at 36 weeks. Decreases in both osteoclast and osteoblast numbers are observed, the cumulative effect of which is a negative bone-balance leading to profound osteopenia.

Control Information

	Control
	101045 B6129SF2/J
Considerations for Choosing Controls

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

Sparc^tm1Hwe/Sparc^tm1Hwe

        involves: 129S/SvEv * C57BL/6J

• behavior/neurological phenotype
• hypoactivity
  • mice exhibit passivity and decreased physical activity when handled   (MGI Ref ID J:52120)
• vision/eye phenotype
• abnormal lens morphology
  • at 1.5 months of age, the lenticular nucleus is shifted to a posterior location   (MGI Ref ID J:52120)
  • at 5 months of age, massive lens degredation is seen   (MGI Ref ID J:52120)
  • at 11 months of age, most lens cortical material is absent, and only the nucleus, the remnants of the anterior capsule, and the epithelium remain   (MGI Ref ID J:52120)
  • at 3 months of age, the bow region has an abnormal appearance and is disrupted by large vacuoles and posterior displacement of the lenticular nucleus is seen   (MGI Ref ID J:53514)
• • abnormal lens capsule morphology
    • at 3-4 months of age, a thickening and wrinking of the lens capsule is seen   (MGI Ref ID J:52120)
    • at 3 months of age, the capsule thickness is increased and nuclear debris is present in the posterior subcapsular region   (MGI Ref ID J:53514)
  • • ruptured lens capsule
      • at 5 months of age, rupture of the posterior capsule is observed, with extrusion of lens material into the vitreous cavity   (MGI Ref ID J:52120)
  • abnormal lens epithelium morphology
    • at 3 months of age, the anterior epithelium cells appear plump and cuboidal   (MGI Ref ID J:53514)
  • abnormal lens fiber morphology
    • at 1.5 months of age, nuclei appear in the lens fibers of the anterior cortex, indicating a defect in differentiation   (MGI Ref ID J:52120)
    • at 1.5 months of age, the lens fibers appear swollen and degraded with vacuoles appearing at the equator   (MGI Ref ID J:52120)
    • at 3-4 months of age, swelling and degeneration of lens fibers is more severe and cystic spaces are present at the equator   (MGI Ref ID J:52120)
    • at 3 months of age, incomplete fiber cell elongation results in a posterior displacement of the lenticular nucleus, and the cortical fibers apppear swollen   (MGI Ref ID J:53514)
  • cortical cataracts
    • initiation of cataract formation is seen in all homozygous mice by 1.5 months of age, including diffuse posterior cortical cataracts (66% of mice) and cataracts in the posterior and anterior corticies (34% of mice)   (MGI Ref ID J:52120)
    • at 3.5-4.5 months of age, many cataracts are mature and show clusters of vacuoles in the outer lens cortex   (MGI Ref ID J:52120)
    • at 5-8 months of age, cataract maturation resulted in rupture of the lens capsule, luxation, and adhesion of the iris to the lens   (MGI Ref ID J:52120)
  • posterior subcapsular cataracts
    • posterior subcapsular opacities are observed at 3-4 months of age, with a progressive degree of opacity; by 8 months of age, a full mature cataract is seen   (MGI Ref ID J:53514)
• eye inflammation
  • at 5-8 months of age, macrophages are present in the area of lens capsule rupture   (MGI Ref ID J:52120)
• • vitreous body inflammation
    • at 5-8 months of age, a mild inflammatory infiltrate is present in the vitreous   (MGI Ref ID J:52120)
    • inflammatory cells aer present at 11 months of age   (MGI Ref ID J:52120)
• retinal degeneration
  • observed at 11 months of age   (MGI Ref ID J:52120)
• retinal detachment
  • observed at 11 months of age   (MGI Ref ID J:52120)
• immune system phenotype
• abnormal osteoclast morphology
  • mutant mice have reduced osteoclast cell surface   (MGI Ref ID J:61480)
• • decreased osteoclast cell number
    • mutant mice have 60% less osteoclasts than controls at 17 weeks of age   (MGI Ref ID J:61480)
• eye inflammation
  • at 5-8 months of age, macrophages are present in the area of lens capsule rupture   (MGI Ref ID J:52120)
• • vitreous body inflammation
    • at 5-8 months of age, a mild inflammatory infiltrate is present in the vitreous   (MGI Ref ID J:52120)
    • inflammatory cells aer present at 11 months of age   (MGI Ref ID J:52120)
• skeleton phenotype
• abnormal skeleton morphology   (MGI Ref ID J:61480)
• • abnormal osteoblast morphology   (MGI Ref ID J:61480)
  • • decreased osteoblast cell number
      • mutant mice have 30% less osteoblasts at 17 weeks of age and 60% less at 36 weeks of age, as well as reduced osteoblast cell surface   (MGI Ref ID J:61480)
  • abnormal osteoclast morphology
    • mutant mice have reduced osteoclast cell surface   (MGI Ref ID J:61480)
  • • decreased osteoclast cell number
      • mutant mice have 60% less osteoclasts than controls at 17 weeks of age   (MGI Ref ID J:61480)
  • abnormal trabecular bone morphology
    • mice exhibit 50% reduced trabecular bone volume in the vertebrae, tibia and femur at 11 weeks of age   (MGI Ref ID J:61480)
    • rediographic density is also reduced in the vertebrae, tibia and femur at 11 weeks of age   (MGI Ref ID J:61480)
    • mice have 50% less trabecular bone at 17 weeks of age and 70% less at 36 weeks of age   (MGI Ref ID J:61480)
    • at 17 and 36 weeks of age, mice have 60% less trabeculae and trabecular spacing is increased 2-fold   (MGI Ref ID J:61480)
  • decreased bone mineral density
    • mice exhibit osteopenia, or decreased bone turnover, due to decreased numbers of osteoblasts and osteoclasts   (MGI Ref ID J:61480)
• abnormal skeleton physiology   (MGI Ref ID J:61480)
• • abnormal bone remodeling
    • the bone formation rate of mutant mice is less than that of controls at all ages; by 36 weeks of age, the trabecular bone formation rate is reduced by 85% compared to controls   (MGI Ref ID J:61480)
    • serum osteocalcin level, a marker of osteoblastic function, is undetectable in mutant mice at 36 weeks of age, whereas control mice show low levels; this is likely due to the decreased number of osteoblasts at this age   (MGI Ref ID J:61480)
  • abnormal bone strength
    • at 17 weeks of age, bones of mutant mice do not gain age-related strength, while bones from control mice do   (MGI Ref ID J:61480)
    • at 36 weeks of age, bones of control mice lose strength due to aging, while mutant bones do not lose additional strength   (MGI Ref ID J:61480)
• homeostasis/metabolism phenotype
• delayed wound healing
  • one study shows that mutants exhibit a delay in healing (31 days vs. 24 days in wild-type) of large 25 mm oblong full-thickness excision wounds on the dorsal skin (including the striated muscle layer)   (MGI Ref ID J:102567)
  • this study also shows that initially, granulation tissue formation and extracellular matrix protein production is delayed in small 6 mm full thickness circular lesions, however they are resolved by 6 days   (MGI Ref ID J:102567)
  • in vitro wound-healing assays of dermal fibroblasts show delayed wound closure (with incomplete wound closure at 31 hours compared to complete wound closure by 11 hours in wild-type), due to defective cell migration and not due to cell proliferation defects   (MGI Ref ID J:102567)
• enhanced wound healing
  • the rate of 5-mm excisional wound closure (made by with a punch biopsy tool in the dorsal skin with hair follicles removed) in mutants is significantly increased; the hyperproliferative epithelium at the leading edge of induced wounds is in closer apposition in mutant mice by day 4 compared to controls, and most cutaneous wounds are completely healed by day 11 while wounds in control mice are still closing   (MGI Ref ID J:73724)
  • accelerated wound closure is in part due to increased wound contraction   (MGI Ref ID J:73724)
• tumorigenesis
• increased tumor growth/size
  • implanted tumor cells grow more rapidly in mutant mice than in controls and show alterations in the production and organization of ECM components and a decrease in the infiltration of macrophages   (MGI Ref ID J:81896)
• hematopoietic system phenotype
• abnormal osteoclast morphology
  • mutant mice have reduced osteoclast cell surface   (MGI Ref ID J:61480)
• • decreased osteoclast cell number
    • mutant mice have 60% less osteoclasts than controls at 17 weeks of age   (MGI Ref ID J:61480)

View Research Applications

Research Applications

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

Internal/Organ Research
Wound Healing
      delayed/impaired

Sparc^tm1Hwe related

Endocrine Deficiency Research
Bone/Bone Marrow Defects

Sensorineural Research
Cataracts

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Sparctm1Hwe
Allele Name		targeted mutation 1, Chin Chen Howe
Allele Type		Targeted (knock-out)
Common Name(s)		SP-;
Mutation Made By		Chin Howe,   The Wistar Institute
Strain of Origin		129S/SvEv-Gpi1
ES Cell Line Name		CCE/EK.CCE
ES Cell Line Strain		129S/SvEv-Gpi1
Gene Symbol and Name		Sparc, secreted acidic cysteine rich glycoprotein
Chromosome		11
Gene Common Name(s)		AA517111; BM-40; ON; expressed sequence AA517111; osteonectin;
Molecular Note		Two tandem neomycin resistance cassettes were inserted into exon 4. No mRNA was detected by Northern blot in testis, spleen or thymus of homozygous mice. [MGI Ref ID J:52120]

Genotyping

Genotyping Information

Genotyping Protocols

Sparc^tm1Hwe, Separated PCR
Sparc^tm1Hwe, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Norose K; Clark JI; Syed NA; Basu A; Heber-Katz E; Sage EH; Howe CC. 1998. SPARC deficiency leads to early-onset cataractogenesis. Invest Ophthalmol Vis Sci 39(13):2674-80. [PubMed: 9856777]  [MGI Ref ID J:52120]

Additional References

Sparc^tm1Hwe related

Arnold SA; Rivera LB; Miller AF; Carbon JG; Dineen SP; Xie Y; Castrillon DH; Sage EH; Puolakkainen P; Bradshaw AD; Brekken RA. 2010. Lack of host SPARC enhances vascular function and tumor spread in an orthotopic murine model of pancreatic carcinoma. Dis Model Mech 3(1-2):57-72. [PubMed: 20007485]  [MGI Ref ID J:157672]

Aycock RL; Bradshaw AC; Sage EH; Starcher B. 2004. Development of UV-Induced Squamous Cell Carcinomas Is Suppressed in the Absence of SPARC. J Invest Dermatol 123(3):592-9. [PubMed: 15304102]  [MGI Ref ID J:91793]

Barker TH; Framson P; Puolakkainen PA; Reed M; Funk SE; Sage EH. 2005. Matricellular homologs in the foreign body response: hevin suppresses inflammation, but hevin and SPARC together diminish angiogenesis. Am J Pathol 166(3):923-33. [PubMed: 15743803]  [MGI Ref ID J:96777]

Bassuk JA; Birkebak T; Rothmier JD; Clark JM; Bradshaw A; Muchowski PJ; Howe CC; Clark JI; Sage EH. 1999. Disruption of the Sparc locus in mice alters the differentiation of lenticular epithelial cells and leads to cataract formation. Exp Eye Res 68(3):321-31. [PubMed: 10079140]  [MGI Ref ID J:53514]

Basu A; Kligman LH; Samulewicz SJ; Howe CC. 2001. Impaired wound healing in mice deficient in a matricellular protein SPARC (osteonectin, BM-40). BMC Cell Biol 2:15. [PubMed: 11532190]  [MGI Ref ID J:102567]

Boskey AL; Moore DJ; Amling M; Canalis E; Delany AM. 2003. Infrared analysis of the mineral and matrix in bones of osteonectin-null mice and their wildtype controls. J Bone Miner Res 18(6):1005-11. [PubMed: 12817752]  [MGI Ref ID J:111461]

Bradshaw AD; Graves DC; Motamed K; Sage EH. 2003. SPARC-null mice exhibit increased adiposity without significant differences in overall body weight. Proc Natl Acad Sci U S A 100(10):6045-50. [PubMed: 12721366]  [MGI Ref ID J:99819]

Bradshaw AD; Puolakkainen P; Dasgupta J; Davidson JM; Wight TN; Helene Sage E. 2003. SPARC-null mice display abnormalities in the dermis characterized by decreased collagen fibril diameter and reduced tensile strength. J Invest Dermatol 120(6):949-55. [PubMed: 12787119]  [MGI Ref ID J:83878]

Bradshaw AD; Reed MJ; Sage EH. 2002. SPARC-null mice exhibit accelerated cutaneous wound closure. J Histochem Cytochem 50(1):1-10. [PubMed: 11748289]  [MGI Ref ID J:73724]

Brekken RA; Puolakkainen P; Graves DC; Workman G; Lubkin SR; Sage EH. 2003. Enhanced growth of tumors in SPARC null mice is associated with changes in the ECM. J Clin Invest 111(4):487-95. [PubMed: 12588887]  [MGI Ref ID J:81896]

Card L; Henderson N; Zhang Y; Bornstein P; Bradshaw AD. 2010. Expression in SPARC-null mice of collagen type I lacking the globular domain of the alpha1(I) N-propeptide results in abdominal hernias and loss of dermal collagen. Matrix Biol 29(7):559-64. [PubMed: 20708079]  [MGI Ref ID J:166793]

Delany AM; Amling M; Priemel M; Howe C; Baron R; Canalis E. 2000. Osteopenia and decreased bone formation in osteonectin-deficient mice [published erratum appears in J Clin Invest 2000 May;105(9):1325] J Clin Invest 105(7):915-23. [PubMed: 10749571]  [MGI Ref ID J:61480]

Delany AM; Kalajzic I; Bradshaw AD; Sage EH; Canalis E. 2003. Osteonectin-null mutation compromises osteoblast formation, maturation, and survival. Endocrinology 144(6):2588-96. [PubMed: 12746322]  [MGI Ref ID J:83749]

Francki A; Bradshaw AD; Bassuk JA; Howe CC; Couser WG; Sage EH. 1999. SPARC regulates the expression of collagen type I and transforming growth factor-beta1 in mesangial cells. J Biol Chem 274(45):32145-52. [PubMed: 10542250]  [MGI Ref ID J:115124]

Greiling TM; Stone B; Clark JI. 2009. Absence of SPARC leads to impaired lens circulation. Exp Eye Res 89(3):416-25. [PubMed: 19401199]  [MGI Ref ID J:151198]

Gruber HE; Sage EH; Norton HJ; Funk S; Ingram J; Hanley EN Jr. 2005. Targeted deletion of the SPARC gene accelerates disc degeneration in the aging mouse. J Histochem Cytochem 53(9):1131-8. [PubMed: 15879573]  [MGI Ref ID J:101698]

Haddadin RI; Oh DJ; Kang MH; Filippopoulos T; Gupta M; Hart L; Sage EH; Rhee DJ. 2009. SPARC-null mice exhibit lower intraocular pressures. Invest Ophthalmol Vis Sci 50(8):3771-7. [PubMed: 19168904]  [MGI Ref ID J:154575]

Harris BS; Zhang Y; Card L; Rivera LB; Brekken RA; Bradshaw AD. 2011. SPARC regulates collagen interaction with cardiac fibroblast cell surfaces. Am J Physiol Heart Circ Physiol 301(3):H841-7. [PubMed: 21666116]  [MGI Ref ID J:176928]

Jones EV; Bernardinelli Y; Tse YC; Chierzi S; Wong TP; Murai KK. 2011. Astrocytes Control Glutamate Receptor Levels at Developing Synapses through SPARC-{beta}-Integrin Interactions. J Neurosci 31(11):4154-65. [PubMed: 21411656]  [MGI Ref ID J:170454]

Kelly KA; Allport JR; Yu AM; Sinh S; Sage EH; Gerszten RE; Weissleder R. 2007. SPARC is a VCAM-1 counter-ligand that mediates leukocyte transmigration. J Leukoc Biol 81(3):748-56. [PubMed: 17178915]  [MGI Ref ID J:118613]

Lehmann S; O'kelly J; Raynaud S; Funk SE; Sage EH; Koeffler HP. 2007. Common deleted genes in the 5q- syndrome: thrombocytopenia and reduced erythroid colony formation in SPARC null mice. Leukemia 21(9):1931-6. [PubMed: 17625608]  [MGI Ref ID J:124417]

Machado do Reis L; Kessler CB; Adams DJ; Lorenzo J; Jorgetti V; Delany AM. 2008. Accentuated osteoclastic response to parathyroid hormone undermines bone mass acquisition in osteonectin-null mice. Bone 43(2):264-73. [PubMed: 18499553]  [MGI Ref ID J:137943]

McCurdy SM; Dai Q; Zhang J; Zamilpa R; Ramirez TA; Dayah T; Nguyen N; Jin YF; Bradshaw AD; Lindsey ML. 2011. SPARC Mediates Early Extracellular Matrix Remodeling Following Myocardial Infarction. Am J Physiol Heart Circ Physiol :. [PubMed: 21602472]  [MGI Ref ID J:173342]

Nie J; Sage EH. 2009. SPARC inhibits adipogenesis by its enhancement of beta-catenin signaling. J Biol Chem 284(2):1279-90. [PubMed: 18990699]  [MGI Ref ID J:145572]

Norose K; Lo WK; Clark JI; Sage EH; Howe CC. 2000. Lenses of SPARC-null mice exhibit an abnormal cell surface-basement membrane interface. Exp Eye Res 71(3):295-307. [PubMed: 10973738]  [MGI Ref ID J:64877]

Nozaki M; Sakurai E; Raisler BJ; Baffi JZ; Witta J; Ogura Y; Brekken RA; Sage EH; Ambati BK; Ambati J. 2006. Loss of SPARC-mediated VEGFR-1 suppression after injury reveals a novel antiangiogenic activity of VEGF-A. J Clin Invest 116(2):422-9. [PubMed: 16453023]  [MGI Ref ID J:105442]

Perdue N; Yan Q. 2006. Caveolin-1 is up-regulated in transdifferentiated lens epithelial cells but minimal in normal human and murine lenses. Exp Eye Res 83(5):1154-61. [PubMed: 16914142]  [MGI Ref ID J:116358]

Puolakkainen P; Bradshaw AD; Kyriakides TR; Reed M; Brekken R; Wight T; Bornstein P; Ratner B; Sage EH. 2003. Compromised Production of Extracellular Matrix in Mice Lacking Secreted Protein, Acidic and Rich in Cysteine (SPARC) Leads to a Reduced Foreign Body Reaction to Implanted Biomaterials. Am J Pathol 162(2):627-35. [PubMed: 12547720]  [MGI Ref ID J:81614]

Puolakkainen PA; Bradshaw AD; Brekken RA; Reed MJ; Kyriakides T; Funk SE; Gooden MD; Vernon RB; Wight TN; Bornstein P; Sage EH. 2005. SPARC-thrombospondin-2-double-null mice exhibit enhanced cutaneous wound healing and increased fibrovascular invasion of subcutaneous polyvinyl alcohol sponges. J Histochem Cytochem 53(5):571-81. [PubMed: 15872050]  [MGI Ref ID J:105538]

Rempel SA; Hawley RC; Gutierrez JA; Mouzon E; Bobbitt KR; Lemke N; Schultz CR; Schultz LR; Golembieski W; Koblinski J; VanOsdol S; Miller CG. 2007. Splenic and immune alterations of the Sparc-null mouse accompany a lack of immune response. Genes Immun 8(3):262-74. [PubMed: 17344888]  [MGI Ref ID J:147548]

Rentz TJ; Poobalarahi F; Bornstein P; Sage EH; Bradshaw AD. 2007. SPARC regulates processing of procollagen I and collagen fibrillogenesis in dermal fibroblasts. J Biol Chem 282(30):22062-71. [PubMed: 17522057]  [MGI Ref ID J:124607]

Rotta G; Matteoli G; Mazzini E; Nuciforo P; Colombo MP; Rescigno M. 2008. Contrasting roles of SPARC-related granuloma in bacterial containment and in the induction of anti-Salmonella typhimurium immunity. J Exp Med 205(3):657-67. [PubMed: 18316416]  [MGI Ref ID J:133133]

Said N; Frierson HF Jr; Chernauskas D; Conaway M; Motamed K; Theodorescu D. 2009. The role of SPARC in the TRAMP model of prostate carcinogenesis and progression. Oncogene 28(39):3487-98. [PubMed: 19597474]  [MGI Ref ID J:153913]

Said N; Motamed K. 2005. Absence of Host-Secreted Protein Acidic and Rich in Cysteine (SPARC) Augments Peritoneal Ovarian Carcinomatosis. Am J Pathol 167(6):1739-52. [PubMed: 16314484]  [MGI Ref ID J:103643]

Sangaletti S; Gioiosa L; Guiducci C; Rotta G; Rescigno M; Stoppacciaro A; Chiodoni C; Colombo MP. 2005. Accelerated dendritic-cell migration and T-cell priming in SPARC-deficient mice. J Cell Sci 118(Pt 16):3685-94. [PubMed: 16046482]  [MGI Ref ID J:101449]

Savani RC; Zhou Z; Arguiri E; Wang S; Vu D; Howe CC; DeLisser HM. 2000. Bleomycin-induced pulmonary injury in mice deficient in SPARC Am J Physiol Lung Cell Mol Physiol 279(4):L743-50. [PubMed: 11000135]  [MGI Ref ID J:65230]

Schellings MW; Vanhoutte D; Swinnen M; Cleutjens JP; Debets J; van Leeuwen RE; d'Hooge J; Van de Werf F; Carmeliet P; Pinto YM; Sage EH; Heymans S. 2009. Absence of SPARC results in increased cardiac rupture and dysfunction after acute myocardial infarction. J Exp Med 206(1):113-23. [PubMed: 19103879]  [MGI Ref ID J:144036]

Seet LF; Su R; Barathi VA; Lee WS; Poh R; Heng YM; Manser E; Vithana EN; Aung T; Weaver M; Sage EH; Wong TT. 2010. SPARC deficiency results in improved surgical survival in a novel mouse model of glaucoma filtration surgery. PLoS One 5(2):e9415. [PubMed: 20195533]  [MGI Ref ID J:157899]

Socha MJ; Manhiani M; Said N; Imig JD; Motamed K. 2007. Secreted protein acidic and rich in cysteine deficiency ameliorates renal inflammation and fibrosis in angiotensin hypertension. Am J Pathol 171(4):1104-12. [PubMed: 17717147]  [MGI Ref ID J:125520]

Strandjord TP; Madtes DK; Weiss DJ; Sage EH. 1999. Collagen accumulation is decreased in SPARC-null mice with bleomycin-induced pulmonary fibrosis. Am J Physiol 277(3 Pt 1):L628-35. [PubMed: 10484471]  [MGI Ref ID J:146430]

Sullivan MM; Barker TH; Funk SE; Karchin A; Seo NS; Hook M; Sanders J; Starcher B; Wight TN; Puolakkainen P; Sage EH. 2006. Matricellular hevin regulates decorin production and collagen assembly. J Biol Chem 281(37):27621-32. [PubMed: 16844696]  [MGI Ref ID J:116917]

Sussman AN; Sun T; Krofft RM; Durvasula RV. 2009. SPARC accelerates disease progression in experimental crescentic glomerulonephritis. Am J Pathol 174(5):1827-36. [PubMed: 19342370]  [MGI Ref ID J:147976]

Trombetta JM; Bradshaw AD. 2010. SPARC/osteonectin functions to maintain homeostasis of the collagenous extracellular matrix in the periodontal ligament. J Histochem Cytochem 58(10):871-9. [PubMed: 20566756]  [MGI Ref ID J:170030]

Wong SY; Crowley D; Bronson RT; Hynes RO. 2008. Analyses of the role of endogenous SPARC in mouse models of prostate and breast cancer. Clin Exp Metastasis 25(2):109-18. [PubMed: 18058030]  [MGI Ref ID J:133592]

Yan Q; Blake D; Clark JI; Sage EH. 2003. Expression of the matricellular protein SPARC in murine lens: SPARC is necessary for the structural integrity of the capsular basement membrane. J Histochem Cytochem 51(4):503-11. [PubMed: 12642629]  [MGI Ref ID J:124742]

Yan Q; Clark JI; Wight TN; Sage EH. 2002. Alterations in the lens capsule contribute to cataractogenesis in SPARC-null mice. J Cell Sci 115(Pt 13):2747-56. [PubMed: 12077365]  [MGI Ref ID J:77916]

Yan Q; Perdue N; Blake D; Sage EH. 2005. Absence of SPARC in murine lens epithelium leads to increased deposition of laminin-1 in lens capsule. Invest Ophthalmol Vis Sci 46(12):4652-60. [PubMed: 16303962]  [MGI Ref ID J:103786]

Yuen J; Li Y; Shapiro LG; Clark JI; Arnett E; Sage EH; Brinkley JF. 2008. Automated, computerized, feature-based phenotype analysis of slit lamp images of the mouse lens. Exp Eye Res 86(4):562-75. [PubMed: 18304532]  [MGI Ref ID J:135641]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, RG10/RG30.

Colony Maintenance

Breeding & Husbandry	This strain arose on a B6;129S background. It is maintained by the donating investigator as a homozygote on a B6;129S background.

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	101045 B6129SF2/J
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In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.