Phenotypes associated with this allele
Allelic Composition |
Mapk1tm1Melo/Mapk1tm1Melo
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Genetic Background |
either: (involves: 129S2/SvPas * C57BL/6) or (involves: 129S2/SvPas * CD-1) |
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk1tm1Melo mutation
(0 available);
any
Mapk1 mutation
(40 available)
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mortality/aging
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• homozygotes die shortly after the implantation stage due to a defect in trophoblast development
• although homozygotes are obtained at normal Mendelian ratios at E6.5-E7.5, severely resorbed embryos are already detected at E8.5, indicating lethality prior to this stage
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embryo
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• at E6.5, homozygotes display an oval shape and lack obvious proximodistal and anteroposterior polarities
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• at E6.5, homozygotes show absence of obvious proximal-distal polarities
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• at E6.5, homozygotes show absence of obvious anterior-posterior polarities
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• at E5.5-E7.5, homozygous mutant embryos are significantly smaller than wild-type or heterozygous embryos
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• homozygotes display loss of the extra-embryonic ectoderm and ectoplacental cone, both direct derivatives of trophoblast stem cells, suggesting a primary defect at the level of polar trophectoderm
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• at E5.5, homozygous mutant embryos are oval in shape, with inner and outer epithelia, and lack identifiable ectoplacental cones
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• at E6.5, homozygous mutant embryos lack an identifiable extra-embryonic ectoderm
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• homozygotes exhibit defective trophoblast development, probably due to abnormal proliferation of trophoblast stem cells in the polar trophectoderm
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• at E6.5, mutant inner layers appear disorganized rather than single layers of pseudostratified epithelia as in wild-type embryos
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• at E5.5 and E6.5, mutant visceral endoderm cells accumulate in the proximal and distal regions of the embryos, respectively
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growth/size/body
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• at E5.5-E7.5, homozygous mutant embryos are significantly smaller than wild-type or heterozygous embryos
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Allelic Composition |
Mapk1tm1Melo/Mapk1+
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Genetic Background |
involves: 129S2/SvPas |
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk1tm1Melo mutation
(0 available);
any
Mapk1 mutation
(40 available)
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cardiovascular system
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• mice show significant cardiac hypertrophy comparable to wild-type following transverse aortic constriction (TAC)
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• mice show significant reductions in fractional shortening at 4 and 8 weeks after TAC
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muscle
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• mice show significant reductions in fractional shortening at 4 and 8 weeks after TAC
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growth/size/body
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• mice show significant cardiac hypertrophy comparable to wild-type following transverse aortic constriction (TAC)
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Allelic Composition |
Mapk1tm1Melo/Mapk1+
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Genetic Background |
involves: 129S2/SvPas * C57BL/6 |
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk1tm1Melo mutation
(0 available);
any
Mapk1 mutation
(40 available)
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mortality/aging
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• Background Sensitivity: fewer heterozygous pups are obtained than expected by a Mendelian ratio from heterozygous intercrosses on a background involving 129S2/SvPas and C57BL/6; in contrast, the number of heterozygous offspring is similar to what is expected on a background involving CD-1
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Allelic Composition |
Mapk1tm1Melo/Mapk1+
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Genetic Background |
involves: C57BL/6 |
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk1tm1Melo mutation
(0 available);
any
Mapk1 mutation
(40 available)
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cardiovascular system
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• after ischemia/reperfusion injury, mice show a decrease in cardiac output compared to wild-type
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• 7 days after ischemia injury, mice have 40% more decrease in ejection fraction compared to wild-type controls and a greater decrease in dP/dtmax
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• 2 fold more cardiomyocytes are undergoing apoptosis 24 hours after ischemia/reperfusion injury as compared to wild-type controls
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• after ischemia/reperfusion injury, mice have 30% increase in left ventricular infarct area
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muscle
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• 7 days after ischemia injury, mice have 40% more decrease in ejection fraction compared to wild-type controls and a greater decrease in dP/dtmax
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• 2 fold more cardiomyocytes are undergoing apoptosis 24 hours after ischemia/reperfusion injury as compared to wild-type controls
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homeostasis/metabolism
cellular
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• 2 fold more cardiomyocytes are undergoing apoptosis 24 hours after ischemia/reperfusion injury as compared to wild-type controls
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk1tm1Melo mutation
(0 available);
any
Mapk1 mutation
(40 available)
Tg(CAG-cat,-Ptpn11*Q97R)1Rbns mutation
(0 available)
Tg(Tek-cre)12Flv mutation
(1 available)
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mortality/aging
cardiovascular system
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• the frequency of double outlet right ventricles is greater than in Tg(CAG-cat,-Ptpn11*Q97R)1Rbns Tg(Tek-cre)12Flv mice
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• the frequency of ventricular septal defects is greater than in Tg(CAG-cat,-Ptpn11*Q97R)1Rbns Tg(Tek-cre)12Flv mice
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• proliferation of endothelial, mesenchymal, and cardiomyocyte cells is increased while apoptosis rates are decreased compared to in wild-type
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liver/biliary system
homeostasis/metabolism
integument
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• mice exhibit nuchal edema
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growth/size/body
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• mice exhibit nuchal edema
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cellular
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk1tm1Melo mutation
(0 available);
any
Mapk1 mutation
(40 available)
Tg(CAG-EGFP)B5Nagy mutation
(3 available)
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cellular
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• in mouse embryonic fibroblasts derived from tetraploid aggregation embryos
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk1tm1Melo mutation
(0 available);
any
Mapk1 mutation
(40 available)
Tg(Myh6-Map2k1*)1Jmol mutation
(1 available)
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cardiovascular system
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• double mutant mice show less hypertrophy at 4 weeks than Tg(Myh6-Map2k1*)1Jmol single transgenic animals
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growth/size/body
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• double mutant mice show less hypertrophy at 4 weeks than Tg(Myh6-Map2k1*)1Jmol single transgenic animals
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapk1tm1Melo mutation
(0 available);
any
Mapk1 mutation
(40 available)
Tg(Myh7-Ptpn11*Q79R)11Rbns mutation
(0 available)
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cardiovascular system
N |
• unlike in Tg(Myh7-Ptpn11*Q79R)11Rbns mice, heart weight, ventricular compaction, cardiac cell proliferation and heart function are normal
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respiratory system
N |
• unlike in Tg(Myh7-Ptpn11*Q79R)11Rbns mice, lung weight is normal
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