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Strain Name:

B6.FVB(Cg)-Mmp9tm1Tvu/J

Stock Number:

007084

Availability:

Under Development for Distribution Colony

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General Terms and Conditions

Genes & Alleles   Mmp9;   Mmp9tm1Tvu;

Product Information

Strain Details

Type JAX® GEMM® Strain - Congenic
Additional information on JAX® GEMM® Strains.
Type JAX® GEMM® Strain - Targeted Mutation
Type JAX® GEMM® Strain - Transgenic
Specieslaboratory mouse
Donating Investigator IMR Colony,   The Jackson Laboratory

Strain Description
Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of 3-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (6 to 8 times larger vs. wildtype) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by 8 weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses.

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.

Strain Development
A targeting vector containing a neomycin resistance gene driven by the mouse phosphoglycerate kinase promoter was used to disrupt a most of exon 2 and all of intron 2 of the Mmp9 gene. The construct was electroporated into 129S-derived ZW4 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric male animals were mated with Swiss Black females. Progeny animals were mated to Black Swiss mice for an unknown number of generations before being mated with FVB/N animals. Upon arrival at The Jackson Laboratory mice, were mated to C57BL/6J animals for a minimum of N5 generations.

Mammalian Phenotype Terms assigned by genotype

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Mmp9tm1Tvu/Mmp9tm1Tvu

        either: (involves: 129S6/SvEvTac * Black Swiss) or (involves: 129S6/SvEvTac * CD-1)
  • skeleton phenotype
  • abnormal cancellous bone morphology (MGI Ref ID J:47297)
    • area of metaphyseal trabecular bone is shorter
  • abnormal long bone epiphyseal plate morphology (MGI Ref ID J:47297)
    • abnormal growth plate development, however after 3 weeks of age, aberrant apoptosis, vascularization, and ossification compensate to remodel the enlarged growth plate and ultimately produce an axial skeleton of normal appearance except for the shorter long bones
    • abnormal long bone hypertrophic chondrocyte zone (MGI Ref ID J:47297)
      • ectopic areas of ossification begin to appear within the hypertrophic zone at 4 weeks of age
      • apoptosis of hypertrophic chondrocytes is delayed
      • by 3 weeks of age, when the hypertrophic zone is lengthened, aberrant apoptosis begins in the middle of the hypertrophic cartilage and is seen around the areas of ossification throughout the hypertrophic zone at 4 weeks
      • increased width of hypertrophic chondrocyte zone (MGI Ref ID J:47297)
        • exhibit lengthened zone of hypertrophic cartilage with no difference in the reserve or proliferating zones
  • abnormal metatarsal bone morphology (MGI Ref ID J:47297)
    • hypertrophic cartilage zone in the metatarsals is about twice that of wild type at birth and becomes more pronounced with growth so that by 3 weeks, it is 6-8 times as long
  • decreased length of long bones (MGI Ref ID J:47297)
    • long bones are about 10% shorter than in wild type
  • delayed bone ossification (MGI Ref ID J:47297)
    • secondary (epiphyseal) ossification sites are delayed until 2.5 weeks of age, however, by 3 weeks of age, these sites are completely ossified as in wild type
  • osteopetrosis (MGI Ref ID J:47297)
    • ectopic areas of ossification begin to appear within the hypertrophic zone at 4 weeks of age and the ectopic ossification proceeds rapidly so that in some bones the entire zone of hypertrophic cartilage is ossified, leading to a large area of trabecular bone, however this is resolved with subsequent remodeling so that by 8 weeks, bones appear normal
  • limbs/digits/tail phenotype
  • abnormal metatarsal bone morphology (MGI Ref ID J:47297)
    • hypertrophic cartilage zone in the metatarsals is about twice that of wild type at birth and becomes more pronounced with growth so that by 3 weeks, it is 6-8 times as long
  • decreased length of long bones (MGI Ref ID J:47297)
    • long bones are about 10% shorter than in wild type

Mmp9tm1Tvu/Mmp9tm1Tvu

        either: FVB.129S6-Mmp9tm1Tvu or (involves: 129S6/SvEvTac)
  • cardiovascular system phenotype
  • altered response to myocardial infarction (MGI Ref ID J:68211)
    • exhibit less left ventricular dilation after experimental myocardial infarction and show less collagen accumulation in the infracted area than seen in wild type
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction (MGI Ref ID J:68211)
    • exhibit less left ventricular dilation after experimental myocardial infarction and show less collagen accumulation in the infracted area than seen in wild type

Mmp9tm1Tvu/Mmp9tm1Tvu

        either: (involves: 129S6/SvEvTac) or (involves: 129S6/SvEvTac * C57BL/6J)
  • cardiovascular system phenotype
  • abnormal angiogenesis (MGI Ref ID J:95880)
    • exhibit reduced angiogenic response to peripheral leg ischemia; do not observe an increase in capillary density and see reduced capillary perfusion capacity and fewer points of capillary intersections (decreased branching) after ischemia

Mmp9tm1Tvu/Mmp9tm1Tvu

        involves: 129S6/SvEvTac
  • cardiovascular system phenotype
  • abnormal blood vessel healing (MGI Ref ID J:109006)
    • exhibit attenuated arterial remodeling in response to vascular injury (ligation of carotid artery) compared to wild type, with decreases in late lumen loss, neointimal thickening, and migration of smooth muscle cells into the neointima and an accumulation of interstitial collagen
  • muscle phenotype
  • abnormal vascular smooth muscle physiology (MGI Ref ID J:109006)
    • isolated aortic smooth muscle cells show decreased migration and capacity to contract collagen in vitro
  • nervous system phenotype
  • abnormal myelination (MGI Ref ID J:105765)
    • exhibit decreased myelination in the corpus callosum at P7 and P10, but not at P14, as evidenced by decreased MBP expression
  • abnormal oligodendrocyte morphology (MGI Ref ID J:105765)
    • exhibit a decrease in the number of mature oligondendrocytes at P10, however no differences in oligodendrocyte precursor cell numbers
  • homeostasis/metabolism phenotype
  • abnormal blood vessel healing (MGI Ref ID J:109006)
    • exhibit attenuated arterial remodeling in response to vascular injury (ligation of carotid artery) compared to wild type, with decreases in late lumen loss, neointimal thickening, and migration of smooth muscle cells into the neointima and an accumulation of interstitial collagen

Mmp9tm1Tvu/Mmp9tm1Tvu

        involves: 129S6/SvEvTac * C57BL/6J
  • cardiovascular system phenotype
  • abnormal angiogenesis (MGI Ref ID J:101783)
    • exhibit significantly reduced carotid artery intimal hyperplasia in response to vascular injury and fewer intimal smooth muscle cells
  • muscle phenotype
  • abnormal vascular smooth muscle physiology (MGI Ref ID J:101783)
    • exhibit impairment of smooth muscle cell migration through a gelatin-coated membrane towards a chemoattractant and in a wound assay4
    • isolated smooth muscle cells exhibit impaired ability to compact collagen gels, to assemble fibrillar collagen from exogenous monomers, and to attach to gelatin

Mmp9tm1Tvu/Mmp9tm1Tvu

        FVB.129S6-Mmp9tm1Tvu
  • cardiovascular system phenotype
  • abnormal physiological neovascularization (MGI Ref ID J:104786)
    • exhibit increased neovascularization post myocardial infarction, as shown by increased total vessel density and normalized vessel distribution between subendo- and epicardial regions relative to wild type after coronary artery ligation
  • altered response to myocardial infarction (MGI Ref ID J:104786)
    • exhibit an increased infarct-to-septal wall thickness ratio, attenuated wall thinning, improved left ventricular function, and reduced peak macrophage infiltration into the infarct zone relative to wild type after myocardial infarction
  • increased angiogenesis (MGI Ref ID J:104786)
    • exhibit an increased angiogenic potential after myocardial infarction, as shown by the presence of newly formed vessels in the infarct region
  • increased ventricle muscle contractility (MGI Ref ID J:104786)
    • exhibit higher end-systolic pressure and dP/dtmax than wild type after myocardial infarction, despite similar infarct sizes
  • muscle phenotype
  • increased ventricle muscle contractility (MGI Ref ID J:104786)
    • exhibit higher end-systolic pressure and dP/dtmax than wild type after myocardial infarction, despite similar infarct sizes
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction (MGI Ref ID J:104786)
    • exhibit an increased infarct-to-septal wall thickness ratio, attenuated wall thinning, improved left ventricular function, and reduced peak macrophage infiltration into the infarct zone relative to wild type after myocardial infarction

Mmp9tm1Tvu/Mmp9tm1Tvu

        129S6/SvEvTac-Mmp9tm1Tvu
  • immune system phenotype
  • *normal* immune system phenotype (MGI Ref ID J:113463)
    • mice exhibit a normal local Shwartman response namely thrombohemorrhagic vasculitis

Gene & Allele Details

Allele Symbol Mmp9tm1Tvu
Allele Name targeted mutation 1, Thiennu H Vu
Common Name(s) GelB-; Gelatinase B-Null; MMP-9 KO; MMP-9-; MMP-9KO; Mmp9-;
Mutation Made By Zena Werb,   University of California, San Francisco
Strain of Origin129S6/SvEvTac
ES Cell Line NameOther (see notes)
ES Cell Line Strain129
Gene Symbol and Name Mmp9, matrix metallopeptidase 9
Chromosome 2
Gene Common Name(s) AW743869; B/MMP9; CLG4B; Clg4b; GELB; Gel B; Gelatinase B; MMP-9; collagenase IVB, basement membrane, 92 kDa; expressed sequence AW743869;
General Note ES cell line = ZW4 (129S6/SvEvTac)
Molecular Note Part of exon 2 and all of intron 2 were replaced with a cassette containing the neomycin resistance gene driven by a PGK promoter. [MGI Ref ID J:47297]

Genotyping Protocols

Mmp9 tm1Tvu

Colony Maintenance

Breeding & HusbandryThis strain originated on a B6;129 background, was mated to Black Swiss mice for an unknown number of generations and crossed to FVB/N mice for five generations. It then was crossed to C57BL/6J mice for at least five generations. Coat color expected from breeding:nonagouti
Diet Information LabDiet® 5K52/5K67

Related Strains

Strains carrying   Mmp9tm1Tvu allele
004104   FVB.Cg-Mmp9tm1Tvu/J
View Strains carrying   Mmp9tm1Tvu     (1 strain)

Additional Web Information

Congenic Nomenclature

Research Applications

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

Cardiovascular Research
Ischemia studies

Developmental Biology Research
Defects in Extracellular Matrix Molecules
Skeletal Defects

Endocrine Deficiency Research
Bone/Bone Marrow Defects

Immunology and Inflammation Research
Inflammation

Mmp9tm1Tvu related

Cancer Research
Increased Tumor Incidence (Skin Cancers: Resistant)

Developmental Biology Research
Defects in Extracellular Matrix Molecules

Endocrine Deficiency Research
Bone/Bone Marrow Defects

Immunology and Inflammation Research
Inflammation

References

Selected Reference(s)

Coussens LM; Tinkle CL; Hanahan D; Werb Z. 2000. MMP-9 supplied by bone marrow-derived cells contributes to skin carcinogenesis Cell 103(3):481-90. [PubMed: 11081634]  [MGI Ref ID J:65699]

Additional References

Price and Supply Information

Strain Name: B6.FVB(Cg)-Mmp9tm1Tvu/J
Stock Number: 007084
 

This strain is currently Under Development for Distribution Colony.
To register your interest in this strain go to the Strain Interest Form.

Estimated Available for Sale Date: 06-OCT-08

Please note: Estimated available for sale dates are provided to keep customers better informed on strains under development. Please note that our Colony Managers routinely monitor the target date and edit it based on breeding performance and other factors. The length of time it takes to make a new strain available for sale depends on genotype, age, number of animals sent by the Donating Investigator, breeding performance, additional strain development (backcrossing, making homozygous), and anticipated demand for the strain/interest registered.

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Supply Details

Standard SupplyUnder Development for Distribution Colony
Supply Notes This strain is included in the Induced Mutant Resource Colony collection.
LicensingSee General Terms and Conditions below  

General Terms and Conditions

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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