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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Ptgs2tm1Jed
targeted mutation 1, Joe E Dinchuk
MGI:1857239
Summary 8 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Ptgs2tm1Jed/Ptgs2tm1Jed B6;129S-Ptgs2tm1Jed/J MGI:3604082
hm2
Ptgs2tm1Jed/Ptgs2tm1Jed involves: 129S7/SvEvBrd MGI:2177809
hm3
Ptgs2tm1Jed/Ptgs2tm1Jed involves: 129S7/SvEvBrd * C57BL/6 MGI:3603952
hm4
Ptgs2tm1Jed/Ptgs2tm1Jed involves: 129S7/SvEvBrd * CD-1 MGI:4834871
cx5
Apctm1Mmt/Apc+
Ptgs2tm1Jed/Ptgs2+
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:3603949
cx6
Apctm1Mmt/Apc+
Ptgs2tm1Jed/Ptgs2tm1Jed
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:3603950
cx7
Ptgs2tm1Jed/Ptgs2tm1Jed
Stk11tm1Tpm/Stk11+
involves: 129S7/SvEvBrd * C57BL/6 * CD-1 MGI:3790956
cx8
Ptgs2tm1Jed/Ptgs2+
Stk11tm1Tpm/Stk11+
involves: 129S7/SvEvBrd * C57BL/6 * CD-1 MGI:3790958


Genotype
MGI:3604082
hm1
Allelic
Composition
Ptgs2tm1Jed/Ptgs2tm1Jed
Genetic
Background
B6;129S-Ptgs2tm1Jed/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (73 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• in response to bleomycin-induced lung injury, homozygotes exhibit an aggressive fibroproliferative response, widespread inflammation, loss of alveolar architecture, and increased extracellular matrix protein deposition relative to wild-type mice

digestive/alimentary system
• indomethacin-treated mice exhibit a less prominent disruption in pH gradient in the stomach compared with similarly treated wild-type mice

homeostasis/metabolism
• indomethacin-treated mice exhibit a less prominent disruption in pH gradient in the stomach compared with similarly treated wild-type mice




Genotype
MGI:2177809
hm2
Allelic
Composition
Ptgs2tm1Jed/Ptgs2tm1Jed
Genetic
Background
involves: 129S7/SvEvBrd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (73 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• homozygotes that reach weaning have an average lifespan of ~3.5 months, with a few animals surviving beyond 6 months
• ~65% of homozygous mutant mice die neonatally

renal/urinary system
• all adult homozygotes with renal histopathology are susceptible to development of secondary pyelonephritis
• all adult homozygotes exhibit renal dysplasia
• homozygous newborns show poor collecting duct development
• all adult homozygotes exhibit mild to moderate renal lesions typified by numerous immature small glomeruli found subcapsularly
• homozygous newborns exhibit corticomedullary atrophy
• all adult homozygotes display corticomedullary microcysts
• although fetal metanephri appear normal at E14, kidneys of homozygous newborns appear severely underdeveloped relative to wild-type kidneys
• homozygous newborns show abundant undifferentiated mesenchyme
• all adult homozygotes display mild medullary hypoplasia or atrophy
• all adult homozygotes exhibit mild to moderate renal lesions typified by multiple foci of dysplastic tubules
• adult homozygotes die of chronic renal failure of developmental origin

reproductive system
• mutant ovaries show virtual absence of corpora lutea, despite normal ovarian follicular development
• homozygous females are largely infertile, rarely giving birth to live offspring

endocrine/exocrine glands
• mutant ovaries show virtual absence of corpora lutea, despite normal ovarian follicular development

cardiovascular system
• 50% of adult homozygotes exhibit diffuse myocardial fibrosis of variable severity involving both right and left ventricles

homeostasis/metabolism

immune system
N
• homozygotes exhibit normal immune responses to carrageenan-induced paw edema, TPA-induced edema and arachidonic acid-induced edema
• all adult homozygotes with renal histopathology are susceptible to development of secondary pyelonephritis

hematopoietic system
N
• homozygotes exhibit normal hematologic parameters

growth/size/body
• all adult homozygotes display corticomedullary microcysts




Genotype
MGI:3603952
hm3
Allelic
Composition
Ptgs2tm1Jed/Ptgs2tm1Jed
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (73 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 20% of mice die between 7 and 23 weeks of age

reproductive system
N
• in vitro, oocyte-cumulus cell complexes retrieved from eCG-primed ovaries of adult homozygotes display normal follicular growth and oocyte maturation
• in vitro-matured oocytes obtained from adult female homozygotes show no significant differences in fertilization or preimplantation development
• extrusion of the first polar body is rarely noted
• pseudopregnant female homozygotes fail to exhibit an increase in uterine weight in response to intraluminal infusion of oil (a deciduogenic stimulus)
• intraluminal infusion of PGI2 (but not PGE2) or cholera toxin as the deciduogenic stimulus partially restores decidualization in ovaroectomized steroid hormonally prepared mutant mice
• females homozygotes exhibit significantly reduced superovulation, despite normal ovarian response to gonadotropins (J:43609)
• any recovered eggs appear developmentally abnormal, with virtually no extrusion of the first polar body (J:43609)
• adult (2- to 8-month-old) female homozygotes exhibit a poor ovulation rate upon induction with eCG and hCG (J:69034)
• immature (3-week-old) female homozygotes exhibit a superior ovulation rate relative to adult homozygotes, suggesting that the ovulatory process becomes defective with aging (J:69034)
• in blastocyst transfer experiments, wild-type blastocysts fail to exhibit the initial attachment reaction and do not implant into uteri of pseudopregnant female homozygous mutant mice
• failure of implantation and subsequent decidualization occur despite normal uterine responsiveness to steroid hormones
• number of term pregnancies reduced (J:109548)
• only 20% of homozygous females can sustain term pregnancy (J:118171)
• homozygous females produce small litters compared to wild-type
• female homozygotes display complete failure of fertilization, despite the presence of numerous sperm at the fertilization site

embryo
• pseudopregnant female homozygotes fail to exhibit an increase in uterine weight in response to intraluminal infusion of oil (a deciduogenic stimulus)
• intraluminal infusion of PGI2 (but not PGE2) or cholera toxin as the deciduogenic stimulus partially restores decidualization in ovaroectomized steroid hormonally prepared mutant mice

renal/urinary system
N
• adult mice exhibit normal urinalysis and 24-hr urine output under non-stressed conditions
• no significant differences in urine osmolarity or in daily urinary excretion of sodium, potassium and chloride are observed
• early cystic changes affecting different tubule sections and glomeruli at P10, with slightly variable pathologic progression
• severe cyst formation by P28
• massive tubular cysts in severely affected kidneys at P14
• by P14, all mice exhibit cystic subcapsular glomeruli
• by P14, all mice exhibit outer cortical dysplasia
• inner cortical nephron hypertrophy by P42
• small, crowded glomeruli in subcapsular region at P10 (J:104002)
• outer cortical glomerular hypoplasia at P42 (J:104002)
• hypoplastic (J:109548)
• average glomerular diameter is reduced to 29.4 um from 39.2 um in wild-type (J:118171)
• at >6 weeks of age, renal cortex is abnormal with small immature glomeruli and deteriorating tubules; these changes are not seen in 2-month old COX-1 knockin mice
• focally variable glomerular sclerosis by P42 (J:104002)
• however, no inflammatory infiltrate or vascular pathology is observed at any age (J:104002)
• moderate (J:109548)
• peri-glomerular fibrosis by P42
• hypertrophy of juxtamedullary glomeruli at P28
• inner cortical glomerular hypertrophy by P42
• mice exhibit progressive cystic dysplasia during the later stages of kidney development
• however, prenatal and early postnatal kidney development appears normal
• diffuse interstitial fibrosis by P42
• starting at P10, total kidney mass is significantly reduced relative to that in wild-type controls
• kidney-specific growth suppression persists to P42 with no significant change
• by P14, all mice exhibit loss of proximal tubular mass
• variable loss of normal proximal tubule mantle at P10
• by P14, all mice exhibit loss of brush border definition
• variable tubular dilation at P10
• severe diffuse tubular dilation by P42
• hypertrophy of juxtamedullary tubules by P28
• at 8 weeks of age, some mice exhibit more severe cystic degeneration than others
• adult mice exhibit a ~50% reduction in GFR relative to wild-type controls, as measured by inulin clearance
• mice exhibit progressive renal insufficiency

cardiovascular system
N
• normal systolic blood pressure in awake or anesthetized mice relative to wild-type controls
• fails to close in 40% of mice
• at birth, mice exhibit a significantly higher heart weight:body weight ratio relative to control mice
• however, a normal ratio is observed during postnatal growth and early adulthood
• dye extravasation in the ear vasculature is decreased by 50-60% with bradykinin challenge compared to wild-type

digestive/alimentary system
• at 5 months of age, mice show chronic peritonitis

homeostasis/metabolism
N
• adult mice exhibit normal plasma sodium, potassium, bicarbonate and chloride levels relative to wild-type controls
• adult mice exhibit a 1.5-fold increase in plasma creatinine levels relative to controls
• adult mice exhibit a 2.5-fold increase in plasma BUN levels relative to controls (J:104002)
• BUN levels are increased ~2-fold vs wild-type at 6 months of age (J:118171)
• near absence of LPS induced synthesis

immune system
• at 5 months of age, mice show chronic peritonitis

behavior/neurological
N
• mice exhibit normal daily water intake under non-stressed conditions

growth/size/body
N
• mice display normal somatic growth from birth to 42 days of age
• at birth, mice exhibit a significantly higher heart weight:body weight ratio relative to control mice
• however, a normal ratio is observed during postnatal growth and early adulthood
• early cystic changes affecting different tubule sections and glomeruli at P10, with slightly variable pathologic progression
• severe cyst formation by P28
• massive tubular cysts in severely affected kidneys at P14
• by P14, all mice exhibit cystic subcapsular glomeruli

cellular
• fails to close in 40% of mice
• extrusion of the first polar body is rarely noted




Genotype
MGI:4834871
hm4
Allelic
Composition
Ptgs2tm1Jed/Ptgs2tm1Jed
Genetic
Background
involves: 129S7/SvEvBrd * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (73 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• following infection with Pseudomonas aeruginosa (PA103) bacterila counts in the right lung are lower compared to wild-type controls
• improved clearance is not the result of increased macrophage or neutrophil recruitment or cytokine production as these measures are similar to wild-type controls




Genotype
MGI:3603949
cx5
Allelic
Composition
Apctm1Mmt/Apc+
Ptgs2tm1Jed/Ptgs2+
Genetic
Background
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (158 available)
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (73 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• at 10 weeks, double heterozygotes develop only ~34% of the polyp number detected in the intestinal tracts of mice heterozygous for Apctm1Mmt alone
• at 10 weeks, double heterozygotes exhibit only 1.5 1.9 colonic polyps versus 6.8 7.2 detected in mice heterozygous for Apctm1Mmt alone




Genotype
MGI:3603950
cx6
Allelic
Composition
Apctm1Mmt/Apc+
Ptgs2tm1Jed/Ptgs2tm1Jed
Genetic
Background
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (158 available)
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (73 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• at 10 weeks, these mutants develop only ~14% of the polyp number detected in the intestinal tracts of mice heterozygous for Apctm1Mmt alone
• the size of intestinal polyps is significantly smaller (<1.0 mm) than that observed in mice heterozygous for Apctm1Mmt alone, with no polyps larger than 2.0 mm in diameter
• histologically, well-developed polyps are not covered with the normal intestinal epithelium and appear flatter than polyps found in Apctm1Mmt heterozygous controls
• notably, no colonic polyps are observed




Genotype
MGI:3790956
cx7
Allelic
Composition
Ptgs2tm1Jed/Ptgs2tm1Jed
Stk11tm1Tpm/Stk11+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (73 available)
Stk11tm1Tpm mutation (0 available); any Stk11 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• large polyps (>2 mm) are reduced in number compared to Stk11 heterozygotes at 8.5 months
• large polyps (>2 mm) are reduced in number compared to Stk11 heterozygotes at 8.5 months

neoplasm
• 53-54% decrease in tumor burden is seen at 10 months in mice treated with celecoxib between 3.5 and 10 months compared to untreated controls




Genotype
MGI:3790958
cx8
Allelic
Composition
Ptgs2tm1Jed/Ptgs2+
Stk11tm1Tpm/Stk11+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (73 available)
Stk11tm1Tpm mutation (0 available); any Stk11 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• large polyps (>2 mm) are reduced in number compared to Stk11 heterozygotes at 8.5 months
• large polyps (>2 mm) are reduced in number compared to Stk11 heterozygotes at 8.5 months





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory