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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Plattm1Mlg
targeted mutation 1, Richard C Mulligan
MGI:1857288
Summary 7 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Plattm1Mlg/Plattm1Mlg B6.129S2-Plattm1Mlg/J MGI:6433845
hm2
Plattm1Mlg/Plattm1Mlg B6.Cg-Plattm1Mlg MGI:3526398
hm3
Plattm1Mlg/Plattm1Mlg involves: 129S2/SvPas MGI:4943739
hm4
Plattm1Mlg/Plattm1Mlg involves: 129S2/SvPas * C57BL/6 MGI:2662717
hm5
Plattm1Mlg/Plattm1Mlg involves: 129S2/SvPas * C57BL/6J MGI:3690641
cx6
Plattm1Mlg/Plattm1Mlg
Thbdtm2Rdr/Thbdtm2Rdr
involves: 129S2/SvPas MGI:3844988
cx7
Plattm1Mlg/Plattm1Mlg
Plautm1Mlg/Plautm1Mlg
involves: 129S2/SvPas * C57BL/6 MGI:3526176


Genotype
MGI:6433845
hm1
Allelic
Composition
Plattm1Mlg/Plattm1Mlg
Genetic
Background
B6.129S2-Plattm1Mlg/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation (6 available); any Plat mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice infected with a sublethal dose of mouse-adapted SARS-CoV MA15 show a slight, but not significant, acceleration in recovery of weight loss compared to controls
• mice infected with a lethal dose of SARS-CoV MA15 show early mortality compared to wild-type controls, although mice that survive early infection recover
• SARS-CoV MA15 lethally infected mice show a trend toward less hemorrhage in the lungs
• however, SARS-CoV MA15-infected mice show similar viral loads in the lung at 4 and 7 days post infection as wild-type controls
• mice infected with a lethal dose of SARS-CoV MA15 show early mortality compared to wild-type controls, although mice that survive early infection recover

mortality/aging
• mice infected with a lethal dose of SARS-CoV MA15 show early mortality compared to wild-type controls, although mice that survive early infection recover




Genotype
MGI:3526398
hm2
Allelic
Composition
Plattm1Mlg/Plattm1Mlg
Genetic
Background
B6.Cg-Plattm1Mlg
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation (6 available); any Plat mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• homozygotes show normal footshock sensitivity thresholds relative to wild-type mice
• homozygotes show no significant differences in the antinociceptive effect of morphine or development of its tolerance relative to wild-type mice
• notably, homozygotes display a significant reduction in morphine-induced hyperlocomotion relative to wild-type
• the defect of morphine-induced hyperlocomotion is reversed by exogenous administration of tPA or plasmin into the nucleus accumbens (Nacc)
• homozygotes display poor active avoidance behavior relative to wild-type mice
• homozygotes display a significant reduction in morphine-induced conditioned place preference
• homozygotes display poor contextual fear conditioning behavior relative to wild-type mice, indicating impaired hippocampal function
• homozygotes display enhanced cue fear conditioning behavior relative to wild-type mice
• relative to wild-type, mutant mice exhibit a 28% reduction in both the rate and extent of learning a complex motor paradigm of irregular peg running, indicating impaired cerebellar motor learning
• homozygotes display no habitation of object exploration relative to wild-type mice
• homozygotes show no reactivity to spatial change (measured as renewed exploration of displaced objects) relative to wild-type mice
• after up to 3 weeks of daily restraint, homozygotes exhibit absence of stress-induced anxiety in the elevated-plus maze; in wild-type, acute stress resuls in a decrease in open arm entries, with 21 days of daily restraint leading to some habituation (J:81694)
• in response to a low or middle dose of corticotropin-releasing factor (CRF), homozygotes exhibit reduced anxiety (lower number of open arm entries) in the elevated plus-maze, with an increased number of head dips (increased exploration) relative to wild-type (J:94733)
• in response to a high dose of CRF, homozygotes fail to explore the open arms but display a similar number of closed arms entries relative to wild-type mice, indicating normal locomotor activity (J:94733)
• in an empty open field, homozygotes show normal horizontal activity but significantly reduced rearing activity relative to wild-type

homeostasis/metabolism
• after a 30-min restraint stress, homozygotes exhibit a 30% increase in corticosterone levels relative to wil-type (J:81694)
• unlike wild-type mice, corticosterone levels in mutant mice do not return to pre-stress levels after a 90-min recovery period (J:81694)
• homozygotes show normal up-regulation of corticosterone in response to CRF but sustain elevation of corticosterone level during recovery (J:94733)
• in a model of pulmonary microembolism, wild-type mice are able to clear 125I-microemboli rapidly with complete lysis by 5 hours; in contrast, mutants remain unable to lyse pulmonary microemboli throughout the 5-hr experimental period
• homozygotes exhibit loss of morphine-induced dopamine release in the nucleus accumbens (Nacc)
• the defect of morphine-induced dopamine release is reversed by exogenous administration of tPA or plasmin into the Nacc but not into the ventral tegmental area (VTA)
• in a model of collagen-induced arthritis, 60% of mutant mice have 3 or 4 affected limbs compared with only 18% of wild-type mice
• in arthritic mutants, 45% of affected individual limbs display severe swelling and/or rigidity compared with only 19% from wild-type
• there are no differences in the degree of swelling (i.e. paw thickness) between limbs from mutant and wild-type mice with the same clinical score
• in a model of collagen-induced arthritis, severely affected joints from homozygotes display diffuse fibrin(ogen) deposition relative to wild-type
• within arthritic joints, higher fibrin levels appear to correlate with increased disease severity
• in a model of collagen-induced arthritis, arthritic homozygotes exhibit a significant increase in interleukin-1beta levels in the synovium relative to wild-type
• in a model of collagen-induced arthritis, ankle joint washouts from arthritic homozygotes exhibit a significant increase in TNF levels relative to wild-type

immune system
• in a model of collagen-induced arthritis, severely affected joints from homozygotes display diffuse fibrin(ogen) deposition relative to wild-type
• within arthritic joints, higher fibrin levels appear to correlate with increased disease severity
• in a model of collagen-induced arthritis, arthritic homozygotes exhibit a significant increase in interleukin-1beta levels in the synovium relative to wild-type
• in a model of collagen-induced arthritis, ankle joint washouts from arthritic homozygotes exhibit a significant increase in TNF levels relative to wild-type
• in a model of collagen-induced arthritis, homozygotes develop significant joint inflammation and joint destruction relative to wild-type mice
• severely affected joints from arthritic homozygotes exhibit massive cell infiltration and higher proteoglycan depletion than wild-type mice
• in a model of collagen-induced arthritis, homozygotes develop a significantly more severe arthritis than wild-type mice
• 95% of mutant mice develop arthritis compared with 68% of wild-type mice; no difference in the day of disease onset is observed
• severely affected joints from arthritic homozygotes exhibit higher cartilage damage and bone erosions than wild-type mice

muscle
N
• in response to glycerol-induced injury, homozygotes exhibit normal skeletal muscle regeneration after 5 days; regeneration is complete after 9 days
• at 7 days after injury, most injured fibers regenerate into groups of centrally nucleated myotubes, indicating advanced regeneration; only few necrotic fibers are observed
• at 20 days after injury, virtually no signs of muscle injury are detected, except for centrally located myonuclei inside the regenerated fibers

skeleton
• in a model of collagen-induced arthritis, 60% of mutant mice have 3 or 4 affected limbs compared with only 18% of wild-type mice
• in arthritic mutants, 45% of affected individual limbs display severe swelling and/or rigidity compared with only 19% from wild-type
• there are no differences in the degree of swelling (i.e. paw thickness) between limbs from mutant and wild-type mice with the same clinical score
• in a model of collagen-induced arthritis, homozygotes develop significant joint inflammation and joint destruction relative to wild-type mice
• severely affected joints from arthritic homozygotes exhibit massive cell infiltration and higher proteoglycan depletion than wild-type mice
• in a model of collagen-induced arthritis, homozygotes develop a significantly more severe arthritis than wild-type mice
• 95% of mutant mice develop arthritis compared with 68% of wild-type mice; no difference in the day of disease onset is observed
• severely affected joints from arthritic homozygotes exhibit higher cartilage damage and bone erosions than wild-type mice

nervous system
• after restraint, homozygotes show reduced neuronal remodeling in the medial amygdala, with absence of stress-induced ERK1/2 phosphorylation at all time points tested (J:81694)
• in response to CRF, homozygotes exhibit attenuated expression of Fos (an indicator of neuronal activation) in the central and medial amygdala but show normal Fos responses in paraventricular nuclei (J:94733)
• in response to tetanic stimulation, hippocampal CA1 slices from mutant mice show a significant reduction in the late phase of LTP relative to wild-type
• notably, a slight but significant reduction of the early phase of hippocampal LTP is also observed
• in response to tetanic stimulation of corticostriatal fibers, homozygotes display absence of LTD in a significant portion of striatal neurons




Genotype
MGI:4943739
hm3
Allelic
Composition
Plattm1Mlg/Plattm1Mlg
Genetic
Background
involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation (6 available); any Plat mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion
• significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion

homeostasis/metabolism
• significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion

immune system
• significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion

hematopoietic system
• significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion




Genotype
MGI:2662717
hm4
Allelic
Composition
Plattm1Mlg/Plattm1Mlg
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation (6 available); any Plat mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• homozygotes display a normal lifespan relative to wild-type mice

cardiovascular system
• in response to laser-induced injury of the Bruch's membrane, homozygotes display almost complete absence of choroidal neovascularization (CNV) at the site of trauma; in contrast, wild-type mice show a robust neovascular reaction
• resistance to CNV is associated with excessive fibrinogen-fibrin deposition at the site of choroidal trauma and in retinal vessels
• at 2 weeks after transverse aortic banding (TAB) i.e. acute pressure overload, homozygotes and wild-type mice exhibit a significant LV hypertrophy which persists for up to 7 weeks
• similar to wild-type mice, homozygotes display a ~35% increase in LV/body weight ratio and a ~40% increase in the LV cardiomyocyte size
• in response to pressure overload, wild-type and mutant mice display similar signs of maladaptation (i.e. myolysis, myocardial fibrosis and increased intercapillary distance)
• 11 days after bleomycin treatment, mutant lungs show areas of fibrosis surrounded by areas of extensive intra-alveolar hemorrhage
• hemorrhagic areas contain numerous hemosiderin-laden macrophages, indicating chronic pulmonary hemorrhage
• in a photothrombotic model of middle cerebral artery occlusion (MCAO), delayed heparin administration increases cerebral hemorrhage associated with ischemia in wild-type but NOT in mutant mice
• in this MCAO model, heparin administration induces tPA activity and mRNA expression in microglial cells, and enhances MMP9 expression and proteolytic activation in the ischemic brains of wild-type but NOT of mutant mice
• at 7 weeks after TAB, wild-type and mutant mice exhibit a similar degree of LV dilatation, obvious signs of LV systolic dysfunction, and pump failure
• at 7 weeks after TAB, impaired fractional shortening and abnormal cardiac pump result in respiratory distress due to pulmonary congestion

growth/size/body
N
• at 5 weeks of age, homozygotes exhibit a normal body weight relative to wild-type mice
• no macroscopic or histologic abnormalities are observed up to 14 months of age
• at 2 weeks after transverse aortic banding (TAB) i.e. acute pressure overload, homozygotes and wild-type mice exhibit a significant LV hypertrophy which persists for up to 7 weeks
• similar to wild-type mice, homozygotes display a ~35% increase in LV/body weight ratio and a ~40% increase in the LV cardiomyocyte size

hematopoietic system
• bleomycin-treated homozygotes display a delayed, but significant, increase in macrophage levels reaching wild-type levels at 9 days post-drug treatment

immune system
N
• homozygotes exhibit normal matrix degradation and invasion into the peritoneal cavity by thioglycollate-stimulated macrophages
• bleomycin-treated homozygotes display a delayed, but significant, increase in macrophage levels reaching wild-type levels at 9 days post-drug treatment
• after bleomycin treatment, homozygotes exhibit areas of fibrin(ogen) deposits, especially in the vasculature of the lung, where fibrin thrombi are observed (J:63134)
• after laser-induced injury of the Bruch's membrane, homozygotes show massive accumulation of fibrinogen-fibrin both in the retinal vessels, and in the bottom of the laser-induced trauma (J:82604)

muscle
• at 2 weeks after transverse aortic banding (TAB) i.e. acute pressure overload, homozygotes and wild-type mice exhibit a significant LV hypertrophy which persists for up to 7 weeks
• similar to wild-type mice, homozygotes display a ~35% increase in LV/body weight ratio and a ~40% increase in the LV cardiomyocyte size
• at 7 weeks after TAB, wild-type and mutant mice exhibit a similar degree of LV dilatation, obvious signs of LV systolic dysfunction, and pump failure
• at 7 weeks after TAB, impaired fractional shortening and abnormal cardiac pump result in respiratory distress due to pulmonary congestion

reproductive system
N
• homozygotes display normal litter size and frequency of litters relative to wild-type mice

respiratory system
• 11 days after bleomycin treatment, mutant lungs show areas of fibrosis surrounded by areas of extensive intra-alveolar hemorrhage
• hemorrhagic areas contain numerous hemosiderin-laden macrophages, indicating chronic pulmonary hemorrhage
• bleomycin-treated homozygotes exhibit an enhanced increase in lung hydroxyproline (collagen) content relative to bleomycin-treated wild-type mice
• histological analysis after lung injury indicates extensive interstitial fibrosis in mutant mice relative to wild-type
• notably, homozygotes survive only 11 days post-drug treatment
• 75% of bleomycin-treated homozygotes die as early as 7 days after treatment, as a result of hemorrhage and extensive fibrotic lesions

vision/eye
• in response to laser-induced injury of the Bruch's membrane, homozygotes display almost complete absence of choroidal neovascularization (CNV) at the site of trauma; in contrast, wild-type mice show a robust neovascular reaction
• resistance to CNV is associated with excessive fibrinogen-fibrin deposition at the site of choroidal trauma and in retinal vessels
• at 12 and 24 h after intravitreal injection of low-dose (30 nmol/mouse) NMDA, homozygotes contain significantly less retinal apoptotic neurons in the ganglion cell layer (GCL) and inner nuclear layer (INL) relative to wild-type; no differences are noted at 72 h after low-dose NMDA injection
• at higher doses of NMDA, homozygotes show no differences in retinal damage relative to wild-type mice
• homozygotes are partially resistant to NMDA-induced retinal damage relative to wild-type mice
• in contrast, neither intravitreal kainic acid nor transient ischemia results in significant differences in retinal damage in mutant vs. wild-type mice

nervous system
• in a photothrombotic model of middle cerebral artery occlusion (MCAO), delayed heparin administration increases cerebral hemorrhage associated with ischemia in wild-type but NOT in mutant mice
• in this MCAO model, heparin administration induces tPA activity and mRNA expression in microglial cells, and enhances MMP9 expression and proteolytic activation in the ischemic brains of wild-type but NOT of mutant mice
• homozygotes subjected to focal cerebral ischemia induced by persistent occlusion of the left middle cerebral artery produce an infarct with a size that is significantly smaller than that produced in wild-type mice

homeostasis/metabolism
• homozygotes exhibit a significant reduction in the rate of lysis of 125I-fibrin-labeled pulmonary plasma clots relative to wild-type mice
• in response to injection of pro-inflammatory endotoxin in the footpad, homozygotes exhibit overt venous thrombosis at a significantly higher incidence (76% versus 54%) and to a much larger extent than wild-type mice (55% of mutants show >4 thrombosed veins per tissue section versus only 15% in wild-type)
• after bleomycin treatment, homozygotes exhibit areas of fibrin(ogen) deposits, especially in the vasculature of the lung, where fibrin thrombi are observed (J:63134)
• after laser-induced injury of the Bruch's membrane, homozygotes show massive accumulation of fibrinogen-fibrin both in the retinal vessels, and in the bottom of the laser-induced trauma (J:82604)
• homozygotes subjected to focal cerebral ischemia induced by persistent occlusion of the left middle cerebral artery produce an infarct with a size that is significantly smaller than that produced in wild-type mice

cellular
• at 12 and 24 h after intravitreal injection of low-dose (30 nmol/mouse) NMDA, homozygotes contain significantly less retinal apoptotic neurons in the ganglion cell layer (GCL) and inner nuclear layer (INL) relative to wild-type; no differences are noted at 72 h after low-dose NMDA injection
• at higher doses of NMDA, homozygotes show no differences in retinal damage relative to wild-type mice




Genotype
MGI:3690641
hm5
Allelic
Composition
Plattm1Mlg/Plattm1Mlg
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation (6 available); any Plat mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• aortic vessel explants show almost complete inhibition of capillary sprouting in both collagen lattices and Matrigel




Genotype
MGI:3844988
cx6
Allelic
Composition
Plattm1Mlg/Plattm1Mlg
Thbdtm2Rdr/Thbdtm2Rdr
Genetic
Background
involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation (6 available); any Plat mutation (26 available)
Thbdtm2Rdr mutation (0 available); any Thbd mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging




Genotype
MGI:3526176
cx7
Allelic
Composition
Plattm1Mlg/Plattm1Mlg
Plautm1Mlg/Plautm1Mlg
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation (6 available); any Plat mutation (26 available)
Plautm1Mlg mutation (3 available); any Plau mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• double homozygotes exhibit a reduced lifespan with 17% dying at ~17 weeks of age
• 9 out of 22 double homozygotes survive until the end of an observation period of 30-40 weeks; only 3 out of 10 double mutants survive until 40-50 weeks

integument
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the face
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the ears around the eartag

cellular
• pre-terminal double mutants display intestinal adhesions and occasionally ischemic tissue necrosis (uterus and intestines), possibly due to thrombosis

digestive/alimentary system
• at 8-12 weeks of age, 37% of double homozygotes display rectal prolapse of a non-infectious origin
• in double mutants, rectal prolapse develops with variable penetrance and onset but appears significantly earlier and at a much higher incidence than in single mutant mice

growth/size/body
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the face
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the ears around the eartag
• at ~17 weeks, 17% of double homozygotes appear runted prior to death
• at 23 weeks, the body weight of double homozygotes is approximately 2/3 that of wild-type mice
• at ~17 weeks, 17% of double homozygotes exhibit cachexia prior to death
• after 3 weeks of age, double homozygotes appear growth retarded relative to wild-type mice

hearing/vestibular/ear
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the ears around the eartag

reproductive system
• double homozygous breeding pairs produce slightly fewer offspring per litter than wild-type breeding pairs
• double homozygotes display a significant reduction in fertility possibly because of poor health or large fibrin deposition in the gonads

respiratory system
• at ~17 weeks, 17% of double homozygotes exhibit dyspnea prior to death

vision/eye
• at 8-12 weeks of age, 5% of double homozygotes exhibit extensive non-healing ulcerations at the eyelids

homeostasis/metabolism
• double homozygotes exhibit a severe reduction in the rate of spontaneous plasma clot lysis relative to wild-type or Plattm1Mlg mutant mice
• in double mutants, lysis of 125I-fibrin-labeled pulmonary plasma clots remains significantly lower for up to 48 hrs but is not significantly different after 72 hrs
• pre-terminal double mutants exhibit spontaneous fibrin deposits in the liver, intestines, gonads, lungs, in non-healing ulcerations of the skin, ears and prolapsed rectum, and occasionally in the kidneys

craniofacial
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the face
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the ears around the eartag





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB), Gene Ontology (GO)
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last database update
11/16/2021
MGI 6.17
The Jackson Laboratory