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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Ptger4tm1Bhk
targeted mutation 1, Beverly H Koller
MGI:2137850
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Ptger4tm1Bhk/Ptger4tm1Bhk involves: 129P2/OlaHsd * 129S/SvEv MGI:2175007
hm2
Ptger4tm1Bhk/Ptger4tm1Bhk involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:3590045


Genotype
MGI:2175007
hm1
Allelic
Composition
Ptger4tm1Bhk/Ptger4tm1Bhk
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptger4tm1Bhk mutation (0 available); any Ptger4 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• homozygotes obtained from crosses with 129S/SvEv mice are alive at 12 hours after birth; however, most of them die within 48 hours after birth
• no homozygotes survive to weaning
• Background Sensitivity: selective breeding of the 5% of homozygotes that survive on a mixed genetic (129P2/OlaHsd x C57BL/6 x DBA/2) background results in a 21% survival rate

growth/size/body
• homozygotes exhibit a higher lung-to-body-weight ratio relative to wild-type mice

cardiovascular system
• mutant lungs display congestion of pulmonary septal capillaries
• in a number of homozygotes that die at >24 h after birth, mutant livers display changes compatible with passive congestion
• such changes are suggestive of acute ischemia secondary to heart failure
• mutant lungs exhibit congestion of pulmonary septal capillaries
• although the DA appears constricted relative to the fetal DA at 3 hrs after birth, homozygous newborns exhibit obvious patency of the DA at both 7 and 12 hrs after birth
• at 12 hrs, swelling of the intima absent and the endothelium remains a single layer of cells contiguous with that of the aorta
• homozygotes exhibit hemorrhaging into the alveolar spaces and major respiratory ducts
• homozygotes show a postnatal drop in pulmonary vascular resistance
• mutant lungs display a left-to-right shunt of blood

respiratory system
• homozygotes exhibit hemorrhaging into the alveolar spaces and major respiratory ducts
• mutant lungs exhibit congestion of pulmonary septal capillaries
• homozygotes exhibit a higher lung-to-body-weight ratio relative to wild-type mice

immune system
• homozygotes display dilated perivascular lymphatics

liver/biliary system
• in a number of homozygotes that die at >24 h after birth, mutant livers display changes compatible with passive congestion
• such changes are suggestive of acute ischemia secondary to heart failure
• in a number of homozygotes dying at >24 h after birth, mutant livers contain macrovesicular lipid deposits
• in a number of homozygotes dying at >24 h after birth, mutant livers contain microvesicular lipid deposits

homeostasis/metabolism

cellular
• although the DA appears constricted relative to the fetal DA at 3 hrs after birth, homozygous newborns exhibit obvious patency of the DA at both 7 and 12 hrs after birth
• at 12 hrs, swelling of the intima absent and the endothelium remains a single layer of cells contiguous with that of the aorta




Genotype
MGI:3590045
hm2
Allelic
Composition
Ptger4tm1Bhk/Ptger4tm1Bhk
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptger4tm1Bhk mutation (0 available); any Ptger4 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• only 5% of homozygotes survive on a mixed genetic background; selective breeding of these mice results in a 21% survival rate

cardiovascular system
• at 9 weeks, all surviving homozygotes exhibit closure of the ductus arteriosus and appear healthy; however, closure is restricted to the region of the DA immediately adjacent to the pulmonary trunk, resulting in a funnel-shaped diverticulum that remains open at the aortic end
• notably, indomethacin fails to induce DA closure in homozgous mutant fetuses

immune system
N
• at 8-10 weeks, surviving homozygotes show no significant changes in lymphocyte, monocyte, neutrophil, basophil, or eosinophil counts relative to wild-type mice
• after CAIA induction, peritoneal macrophages from diseased homozygotes release less IL-6 than wild-type mice under baseline conditions; however, no difference in IL-6 levels is noted after stimulation with LPS
• after CAIA induction, diseased homozygotes display serum amyloid A levels comparable to those observed in non-diseased homozygotes
• after CAIA induction, diseased mutant livers exhibit significantly reduced IL-1beta levels relative to wild-type livers
• after CAIA induction, diseased homozygotes display an attenuated increase in serum and peritoneal exudate IL-6 levels relative to wild-type mice
• homozygotes exhibit a significant reduction in both severity and incidence of collagen antibody-induced rheumatoid arthritis (CAIA) relative to wild-type controls, based on paw swelling/redness and joint ankylosis
• in the CAIA model, 8 of 24 homozygotes develop arthritis with significantly fewer severely arthritic joints than wild-type mice
• stifle joints exhibit reduced bone damage, proteoglycan loss, and type II collagen breakdown, consistent with attenuated clinical signs

skeleton
• homozygotes exhibit a significant reduction in both severity and incidence of collagen antibody-induced rheumatoid arthritis (CAIA) relative to wild-type controls, based on paw swelling/redness and joint ankylosis
• in the CAIA model, 8 of 24 homozygotes develop arthritis with significantly fewer severely arthritic joints than wild-type mice
• stifle joints exhibit reduced bone damage, proteoglycan loss, and type II collagen breakdown, consistent with attenuated clinical signs

homeostasis/metabolism
• after CAIA induction, diseased homozygotes display serum amyloid A levels comparable to those observed in non-diseased homozygotes
• after CAIA induction, diseased homozygotes display an attenuated increase in peritoneal exudate PGE2 levels relative to wild-type mice
• after CAIA induction, diseased mutant livers exhibit significantly reduced IL-1beta levels relative to wild-type livers
• after CAIA induction, diseased homozygotes display an attenuated increase in serum and peritoneal exudate IL-6 levels relative to wild-type mice

hematopoietic system
• after CAIA induction, peritoneal macrophages from diseased homozygotes release less IL-6 than wild-type mice under baseline conditions; however, no difference in IL-6 levels is noted after stimulation with LPS

cellular
• at 9 weeks, all surviving homozygotes exhibit closure of the ductus arteriosus and appear healthy; however, closure is restricted to the region of the DA immediately adjacent to the pulmonary trunk, resulting in a funnel-shaped diverticulum that remains open at the aortic end
• notably, indomethacin fails to induce DA closure in homozgous mutant fetuses





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last database update
12/10/2024
MGI 6.24
The Jackson Laboratory