All Phenotypes Plg<tm1Jld> MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Plg^tm1Jld
targeted mutation 1, Jay L Degen
MGI:1857291

Summary

16 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Plg^tm1Jld/Plg^tm1Jld	B6.129P2-Plg^tm1Jld	MGI:3690429
hm2	Plg^tm1Jld/Plg^tm1Jld	B6.129P2-Plg^tm1Jld/J	MGI:4418712
hm3	Plg^tm1Jld/Plg^tm1Jld	involves: 129P2/OlaHsd	MGI:3690460
hm4	Plg^tm1Jld/Plg^tm1Jld	involves: 129P2/OlaHsd * Black Swiss	MGI:3690623
hm5	Plg^tm1Jld/Plg^tm1Jld	involves: 129P2/OlaHsd * Black Swiss * C57BL/6J	MGI:3692109
hm6	Plg^tm1Jld/Plg^tm1Jld	involves: 129P2/OlaHsd * C57BL/6 * NIH Black Swiss	MGI:3690363
hm7	Plg^tm1Jld/Plg^tm1Jld	involves: 129P2/OlaHsd * C57BL/6J	MGI:3690642
hm8	Plg^tm1Jld/Plg^tm1Jld	involves: 129P2/OlaHsd * NIH Black Swiss	MGI:3690301
ht9	Plg^tm1Jld/Plg⁺	involves: 129P2/OlaHsd * C57BL/6J	MGI:3690643
cx10	Fga^tm1Jld/Fga^tm1Jld Plg^tm1Jld/Plg^tm1Jld	B6.129P2-Fga^tm1Jld Plg^tm1Jld	MGI:3690628
cx11	Plg^tm1Jld/Plg⁺ Tg(MSR1-Plau)1Ddi/0	B6.Cg-Plg^tm1Jld Tg(MSR1-Plau)1Ddi	MGI:3690232
cx12	Fga^tm1Jld/Fga^tm1Jld Plg^tm1Jld/Plg^tm1Jld	involves: 129P2/OlaHsd	MGI:3690459
cx13	Ngfr^tm1Jae/Ngfr^tm1Jae Plg^tm1Jld/Plg^tm1Jld	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6	MGI:3770689
cx14	Fga^tm1Jld/Fga^tm1Jld Plg^tm1Jld/Plg^tm1Jld	involves: 129P2/OlaHsd * Black Swiss * CF-1	MGI:3690622
cx15	Plg^tm1Jld/Plg^tm1Jld Tg(MMTV-PyVT)634Mul/0	involves: 129P2/OlaHsd * Black Swiss * FVB/N	MGI:3690443
cx16	Apoe^tm1Bres/Apoe^tm1Bres Plg^tm1Jld/Plg^tm1Jld	involves: 129P2/OlaHsd * C57BL/6 * NIH Black Swiss	MGI:3690365

Allelic Composition	Plg^tm1Jld/Plg^tm1Jld
Genetic Background	B6.129P2-Plg^tm1Jld

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

decreased susceptibility to induced morbidity/mortality ( J:44314 )

• show a moderate increase in survival after primary tumor resection at day 10

premature death ( J:120368 )

• median survival is 6 months

reproductive system

reduced female fertility ( J:64966 )

• Background Sensitivity: exhibit more severe infertility than on a mixed 129P2/OlaHsd, Black Swiss, and C57BL/6J background, with fewer than 50% of females becoming pregnant

• second pregnancies are rare

vision/eye

eye hemorrhage ( J:46096 )

• palpebral conjunctival alterations result in hypertrophied, everted eyelids with ulceration and hemorrhage

eye inflammation ( J:46096 )

• formation of papillary or a retrocorneal membrane is seen in several mutants, consistent with chronic intraocular inflammation

conjunctivitis ( J:46096 )

• Background Sensitivity: 100% of older mutants develop conjunctival lesions (palpebral and bulbar conjunctivitis) that are much more severe than on a mixed 129P2/OlaHsd and Black Swiss background

• incidence of lesion development increases with age and lesions develop into extensive, pedunculated plaques over time

• lesions contain acellular material rich in fibrin and are accompanied by a whitish, irregular surface of the palpebral conjunctiva, an increase in vascularization of the lid, and external accumulations of mucus

• acute inflammatory infiltrates with a predominance of neutrophils frequently accompany conjunctival lesions and occasionally see CD4+ and CD8+ lymphocytes in the infiltrates

abnormal conjunctiva morphology ( J:46096 )

abnormal conjunctival epithelium morphology ( J:46096 )

• exhibit extensive disruption of the conjunctival epithelium in all lesions, associated with hypertrophy, disorganization, and reduplication consistent with chronic, recurrent ulceration and attempted re-epithelialization

abnormal cornea morphology ( J:46096 )

• occasionally observe corneal defects such as stromal haze in mutants with early conjunctival lesions, however lesions always occur in the palperbral conjunctiva prior to corneal defects

• form extensive fibrin rich plaques overlying the cornea, with associated epithelium ulceration, hypertrophy, and disorganization

cornea vascularization ( J:46096 )

• stromal vascularization is frequently associated with corneal lesions

abnormal cornea epithelium morphology ( J:46096 )

• corneal epithelium is frequently absent, necrotic, or hypertrophied

absent cornea epithelium ( J:46096 )

abnormal cornea stroma morphology ( J:46096 )

• ulceration or destruction of the stroma with extensive protruding plaques are seen overlying the cornea

ectropion ( J:46096 )

• palpebral conjunctival alterations result in hypertrophied, everted eyelids with ulceration and hemorrhage

neoplasm

decreased tumor growth/size ( J:44314 )

• homozygotes develop primary tumors with no difference in the rate of appearance or in lung metastasis when inoculated with a metastatic Lewis lung carcinoma expressing high levels of plasminogen activator, however the primary tumors are smaller, less hemorrhagic, display reduced skin ulceration, show delayed dissemination of the tumor to regional lymph nodes, and show a moderate increase in survival after primary tumor resection

digestive/alimentary system

abnormal rectum morphology ( J:46096 )

• 71% developed rectal lesions

cardiovascular system

eye hemorrhage ( J:46096 )

• palpebral conjunctival alterations result in hypertrophied, everted eyelids with ulceration and hemorrhage

cornea vascularization ( J:46096 )

• stromal vascularization is frequently associated with corneal lesions

liver/biliary system

increased hepatocyte proliferation ( J:120368 )

• the number of proliferating hepatocyte is increased (126.6+/-3.9 compare to 95.2+/-3.7 in wild-type mice)

endocrine/exocrine glands

abnormal lactation ( J:64966 )

• Background Sensitivity: more than 75% of females are unable to sustain lactation for 10 days, much higher percentage than on a mixed 129P2/OlaHsd, Black Swiss, and C57BL/6J background

growth/size/body

decreased body weight ( J:46096 )

• weight at 60 days of age is lower

immune system

eye inflammation ( J:46096 )

• formation of papillary or a retrocorneal membrane is seen in several mutants, consistent with chronic intraocular inflammation

conjunctivitis ( J:46096 )

• Background Sensitivity: 100% of older mutants develop conjunctival lesions (palpebral and bulbar conjunctivitis) that are much more severe than on a mixed 129P2/OlaHsd and Black Swiss background

• incidence of lesion development increases with age and lesions develop into extensive, pedunculated plaques over time

• acute inflammatory infiltrates with a predominance of neutrophils frequently accompany conjunctival lesions and occasionally see CD4+ and CD8+ lymphocytes in the infiltrates

integument

abnormal lactation ( J:64966 )

• Background Sensitivity: more than 75% of females are unable to sustain lactation for 10 days, much higher percentage than on a mixed 129P2/OlaHsd, Black Swiss, and C57BL/6J background

cellular

increased hepatocyte proliferation ( J:120368 )

• the number of proliferating hepatocyte is increased (126.6+/-3.9 compare to 95.2+/-3.7 in wild-type mice)

Allelic Composition	Plg^tm1Jld/Plg^tm1Jld
Genetic Background	B6.129P2-Plg^tm1Jld/J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

decreased susceptibility to neuronal excitotoxicity ( J:141739 )

• kainate acid-treated mice exhibit reduced excitotoxicity compared with similarly treated wild-type mice

• however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced excitotoxicity

abnormal microglial cell physiology ( J:141739 )

• kainate acid-induced microglial migration is reduced compared to in similarly treated wild-type mice

• however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced microglial migration

homeostasis/metabolism

decreased susceptibility to neuronal excitotoxicity ( J:141739 )

• kainate acid-treated mice exhibit reduced excitotoxicity compared with similarly treated wild-type mice

• however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced excitotoxicity

immune system

abnormal microglial cell physiology ( J:141739 )

• kainate acid-induced microglial migration is reduced compared to in similarly treated wild-type mice

• however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced microglial migration

cellular

decreased susceptibility to neuronal excitotoxicity ( J:141739 )

• kainate acid-treated mice exhibit reduced excitotoxicity compared with similarly treated wild-type mice

• however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced excitotoxicity

hematopoietic system

abnormal microglial cell physiology ( J:141739 )

• kainate acid-induced microglial migration is reduced compared to in similarly treated wild-type mice

• however, plasmin-mediated cleavage of Ccl2 restores kainate acid-induced microglial migration

Allelic Composition	Plg^tm1Jld/Plg^tm1Jld
Genetic Background	involves: 129P2/OlaHsd

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal nervous system physiology ( J:42819 )

• exhibit resistance to hippocampal neuronal death induced by kainate injection

Allelic Composition	Plg^tm1Jld/Plg^tm1Jld
Genetic Background	involves: 129P2/OlaHsd * Black Swiss

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:36591 )

• mean survival time is 176 days and all died or had to be euthanized by 301 days; 40% die spontaneously

growth/size/body

weight loss ( J:36591 )

• exhibit a progressive weight loss starting around 2 months of age which becomes severe after 4 months of age

cachexia ( J:36591 )

• exhibit severe wasting

digestive/alimentary system

perianal ulcer ( J:36591 )

• exhibit anal-rectal ulceration

esophageal ulcer ( J:36591 )

• 8% (1 of 13) show esophageal ulcer

abnormal rectum morphology ( J:36591 )

• 77% (10 of 13) show rectal ulceration

rectal prolapse ( J:36591 )

• develop spontaneous rectal ulcerations, which over a period of few weeks progress into rectal prolapse

gastrointestinal ulcer ( J:36591 )

• exhibit various ulcers in the gastrointestinal tract, including in the stomach, colon, and duodenum

intestinal ulcer ( J:36591 )

• 24% (3 of 13) exhibit colonic ulcers

duodenal ulcer ( J:36591 )

• 8% (1 of 13) show duodenal ulcers

gastric ulcer ( J:36591 )

• 70% (9 of 13) show glandular stomach ulcers

• 23% (3 of 13) show squamous stomach ulcers

colitis ( J:36591 )

• 8% (1 of 13) show colitis

homeostasis/metabolism

abnormal thrombosis ( J:36591 )

• 8% (1 of 13) show larynx thrombi

• 23% (3 of 13) show tracheal thrombi

abnormal kidney thrombosis ( J:36591 )

• 8% (1 of 13) show kidney thrombi

impaired wound healing ( J:36591 )

• scab is retained longer, and when lost, shows a large, gaping wound field lacking epidermal covering

immune system

colitis ( J:36591 )

• 8% (1 of 13) show colitis

liver/biliary system

abnormal liver morphology ( J:36591 )

• 100% exhibit multiple lesions scattered throughout the liver, characterized by sinusoidal deposits of fibrillar material

reproductive system

abnormal vagina morphology ( J:36591 )

• 57% (4 of 7) virgin females show vaginal lesions

respiratory system

abnormal larynx morphology ( J:36591 )

• 8% (1 of 13) show larynx thrombi

abnormal lung morphology ( J:36591 )

• 39% (5 of 13) show pulmonary lesions

abnormal trachea morphology ( J:36591 )

• 8% (1 of 13) show tracheal necrosis

• 23% (3 of 13) show tracheal thrombi

vision/eye

abnormal conjunctiva morphology ( J:46096 )

• Background Sensitivity: 17% (3 of 18) of older mutants develop conjunctival lesions that are milder than on C57BL/6J background

Allelic Composition	Plg^tm1Jld/Plg^tm1Jld
Genetic Background	involves: 129P2/OlaHsd * Black Swiss * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

reproductive system

reduced female fertility ( J:64966 )

• Background Sensitivity: fertility is reduced less than on a congenic C57BL/6J background, with 26% of females failing to give birth, even though exhibit normal estrus cycles

• second pregnancies are rare

endocrine/exocrine glands

abnormal mammary gland connective tissue morphology ( J:64966 )

• exhibit abnormal stromal extracellular matrix (ECM), with increased collagen deposition and absence of ECM degradation

abnormal mammary gland development ( J:64966 )

• mammary glands are underdeveloped

• mammary glands exhibit delayed epithelial regression accompanied by diminished adipocyte differentiation during involution; glands have less adipose tissue and stroma is instead filled with immature adipocytes and fibrotic tissue

abnormal involution of the mammary gland ( J:64966 )

• glands from lactating females are initially smaller and fail to involute after weaning

• during involution, the alveolar tissue shows only minimal regression, residual alveolar and ductal structures occupy larger volume fractions, collapsed alveoli with epithelial cells shed into the ducts, and uncollapsed necrotic alveoli are seen

• show decreased apoptosis in mammary glands at 5 days of involution, indicating delayed, but not completely blocked, alveolar regression

abnormal mammary gland growth during lactation ( J:64966 )

• in females capable of lactation, mammary glands are lighter and contain less total secretory alveolar tissue after 10 days of lactation, however after 10 days of lactation and 5 days of involution, glands do not show the same degree in gland size reduction as wild-type and are thus heavier

• mammary glands from 7 of 9 dams that were unable to nurse pups (do not lactate) contain almost no secretory alveolar epithelium, instead they have regions of prominent fibrosis, scattered areas of atypical adipose tissue, and sometimes abundant inflammatory cells

• exhibit an accumulation of activated macrophages in the stroma of lactating mammary glands

lactation failure ( J:64966 )

• Background Sensitivity: 28% of females are unable to sustain lactation for 10 days, a much lower percentage than on a congenic C57BL/6J background

• lactation failure is more severe after a second pregnancy, with only 1 of 8 litters surviving

integument

abnormal mammary gland connective tissue morphology ( J:64966 )

• exhibit abnormal stromal extracellular matrix (ECM), with increased collagen deposition and absence of ECM degradation

abnormal mammary gland development ( J:64966 )

• mammary glands are underdeveloped

abnormal involution of the mammary gland ( J:64966 )

• glands from lactating females are initially smaller and fail to involute after weaning

• show decreased apoptosis in mammary glands at 5 days of involution, indicating delayed, but not completely blocked, alveolar regression

abnormal mammary gland growth during lactation ( J:64966 )

• exhibit an accumulation of activated macrophages in the stroma of lactating mammary glands

lactation failure ( J:64966 )

• Background Sensitivity: 28% of females are unable to sustain lactation for 10 days, a much lower percentage than on a congenic C57BL/6J background

• lactation failure is more severe after a second pregnancy, with only 1 of 8 litters surviving

Allelic Composition	Plg^tm1Jld/Plg^tm1Jld
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * NIH Black Swiss

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Gross appearance of aortic arches of Apoe^tm1Bres/Apoe^tm1Bres, Plg^tm1Jld/Plg^tm1Jld and Apoe^tm1Bres/Apoe^tm1Bres Plg^tm1Jld/Plg^tm1Jld mice

mortality/aging

premature death ( J:42927 )

• only about 70% survive beyond 20 weeks of age

growth/size/body

abnormal body weight ( J:42927 )

• average body weight is 25% lower after 2 months of age

cardiovascular system

cardiovascular system phenotype ( J:42927 )

N	• do not develop atherosclerosis

Allelic Composition	Plg^tm1Jld/Plg^tm1Jld
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cardiovascular system

decreased angiogenesis ( J:108675 )

• aortic vessel explants fail to form capillary sprouts in collagen lattices or Matrigel

• explants supplemented with either Plaur or Plat partially regain the ability to form capillary sprouts

Allelic Composition	Plg^tm1Jld/Plg^tm1Jld
Genetic Background	involves: 129P2/OlaHsd * NIH Black Swiss

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cellular

hepatic necrosis ( J:39419 )

• necrosis is apparent within adjacent tissue in a fraction of hepatic lesions

decreased keratinocyte migration ( J:39419 )

• keratinocyte migration is impaired in skin wound healing experiments

homeostasis/metabolism

abnormal thrombosis ( J:39419 )

• young mutants develop multiple spontaneous thrombotic lesions in liver, stomach, colon, rectum, lung, pancreas, and other tissues

impaired wound healing ( J:33897 )

• scab remains in place longer and once lost, the wound field is still gaping and red with a hard and often scaly surface lacking epidermal covering

• wounds appear to shrink and heal over several weeks, but about a third of the wounds are not healed 6 weeks after the original incision

• keratinocyte migration is impaired in skin wound healing experiments

integument

decreased keratinocyte migration ( J:39419 )

• keratinocyte migration is impaired in skin wound healing experiments

digestive/alimentary system

perianal ulcer ( J:39419 )

• exhibit anal-rectal tissue ulceration with surface exudates and surrounding fibrin deposition

abnormal colon morphology ( J:39419 )

• 3 of 17 develop colonic ulcers, proximal to the rectum, at 7 and 10 weeks of age, showing a necrotic surface epithelium covered by exudates

rectal prolapse ( J:39419 )

• oldest of the mice that show inflammatory rectal lesions exhibit rectal prolapse

abnormal stomach morphology ( J:39419 )

gastric ulcer ( J:39419 )

• 10 of 17 show gastric ulcers at 5 to 21 weeks of age, including 7 with ulcerated lesions in the glandular portion of the stomach, 2 with an ulcer in the squamous portion of the stomach, and 1 with an ulcer at the junction of the two portions

proctitis ( J:39419 )

• 7 of 43 develop inflammatory rectal lesions between 5 and 21 weeks of age

immune system

proctitis ( J:39419 )

• 7 of 43 develop inflammatory rectal lesions between 5 and 21 weeks of age

liver/biliary system

abnormal liver morphology ( J:39419 )

• exhibit multiple hepatic fibrin deposits identified as fibrinogen that show varying degrees of organization with infiltration of spindle cells

hepatic necrosis ( J:39419 )

• necrosis is apparent within adjacent tissue in a fraction of hepatic lesions

respiratory system

abnormal lung morphology ( J:39419 )

• 7 of 17 show pulmonary lesions, with capillary fibrin thrombi in 4 mutants and organizing patches of alveolar fibrin in 4 mutants

cardiovascular system

venoocclusion ( J:39419 )

• young mutants exhibit vascular occlusions

Allelic Composition	Plg^tm1Jld/Plg⁺
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cardiovascular system

decreased angiogenesis ( J:108675 )

• aortic vessel explants show almost complete lack of capillary sprouting in collagen lattices

Allelic Composition	Fga^tm1Jld/Fga^tm1Jld Plg^tm1Jld/Plg^tm1Jld
Genetic Background	B6.129P2-Fga^tm1Jld Plg^tm1Jld

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fga^tm1Jld mutation (0 available); any Fga mutation (43 available)
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

vision/eye

vision/eye phenotype ( J:46096 )

N	• do not develop conjunctivitis as is seen in single Plg homozygotes

Allelic Composition	Plg^tm1Jld/Plg⁺ Tg(MSR1-Plau)1Ddi/0
Genetic Background	B6.Cg-Plg^tm1Jld Tg(MSR1-Plau)1Ddi

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)
Tg(MSR1-Plau)1Ddi mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cardiovascular system

abnormal heart morphology ( J:113474 )

• exhibit significantly less cardiac fibrosis than seen in single Tg(MSR1-Plau)1Ddi mutants and no increase in cardiac macrophage accumulation

Allelic Composition	Fga^tm1Jld/Fga^tm1Jld Plg^tm1Jld/Plg^tm1Jld
Genetic Background	involves: 129P2/OlaHsd

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal nervous system physiology ( J:42819 )

• exhibit resistance to hippocampal neuronal death induced by kainate injection to a similar extent as seen in single Plg homozygotes, suggesting a non-fibrin substrate for plasmin

Allelic Composition	Ngfr^tm1Jae/Ngfr^tm1Jae Plg^tm1Jld/Plg^tm1Jld
Genetic Background	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ngfr^tm1Jae mutation (2 available); any Ngfr mutation (30 available)
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:120368 )

• median survival is 2.5 months

liver/biliary system

increased hepatocyte apoptosis ( J:120368 )

• mice exhibit apoptosis in the liver that is restricted to hepatocytes

hepatic necrosis ( J:120368 )

• mice exhibit prominent liver lesions at 10 weeks with large necrotic lesions

increased hepatocyte proliferation ( J:120368 )

• the number of proliferating hepatocyte is decreased (74.2+/-9.1 compare to 95.2+/-3.7 in wild-type mice)

growth/size/body

decreased body size ( J:120368 )

• at 5 weeks of age

cellular

increased hepatocyte apoptosis ( J:120368 )

• mice exhibit apoptosis in the liver that is restricted to hepatocytes

hepatic necrosis ( J:120368 )

• mice exhibit prominent liver lesions at 10 weeks with large necrotic lesions

increased hepatocyte proliferation ( J:120368 )

• the number of proliferating hepatocyte is decreased (74.2+/-9.1 compare to 95.2+/-3.7 in wild-type mice)

Allelic Composition	Fga^tm1Jld/Fga^tm1Jld Plg^tm1Jld/Plg^tm1Jld
Genetic Background	involves: 129P2/OlaHsd * Black Swiss * CF-1

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

mortality/aging ( J:36591 )

N	• show rescue from the early morbidity and premature death seen in single Plg homozygotes and show no signs of weight loss or wasting

homeostasis/metabolism

abnormal blood coagulation ( J:36591 )

• shortly after birth, a small fraction of neonates show peritoneal bleeding from which they generally recover, indicating lack of clotting function

• exhibit distinctly larger deposits of dried blood at wound margins and scabs of wounds appear initially less stable than in controls and resumed bleeding is occasionally apparent

abnormal wound healing ( J:36591 )

• exhibit distinctly larger deposits of dried blood at wound margins, however do not exhibit any of the wound healing defects seen in single Plg homozygotes

• scabs of wounds appear initially less stable than in controls and resume bleeding is occasionally apparent

liver/biliary system

abnormal liver morphology ( J:36591 )

• 6% (1 of 17) show hemorrhagic organized liver lesion

• 6% (1 of 17) show dystrophic calcification in liver

focal hepatic necrosis ( J:36591 )

• 41% (7 of 17) show sporadic necrotic liver foci

immune system

immune system phenotype ( J:36591 )

N	• exhibit rescue of the various ulcerations and lesions seen in single Plg homozygotes

digestive/alimentary system

abnormal duodenum morphology ( J:36591 )

• 6% (1 of 17) show dystrophic calcification in duodenum

cellular

focal hepatic necrosis ( J:36591 )

• 41% (7 of 17) show sporadic necrotic liver foci

Allelic Composition	Plg^tm1Jld/Plg^tm1Jld Tg(MMTV-PyVT)634Mul/0
Genetic Background	involves: 129P2/OlaHsd * Black Swiss * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)
Tg(MMTV-PyVT)634Mul mutation (2 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

increased mammary adenocarcinoma incidence ( J:48285 )

• develop mammary tumors within 99 days after birth similar to those seen in Tg(MMTV-PyVT)634Mul mutants

decreased metastatic potential ( J:48285 )

• exhibit significantly reduced lung metastasis with respect to frequency of occurrence, total number of metastases, and total metastatic tumor burden, compared with Tg(MMTV-PyVT)634Mul mutants

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:48285 )

• develop mammary tumors within 99 days after birth similar to those seen in Tg(MMTV-PyVT)634Mul mutants

integument

increased mammary adenocarcinoma incidence ( J:48285 )

• develop mammary tumors within 99 days after birth similar to those seen in Tg(MMTV-PyVT)634Mul mutants

Allelic Composition	Apoe^tm1Bres/Apoe^tm1Bres Plg^tm1Jld/Plg^tm1Jld
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * NIH Black Swiss

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoe^tm1Bres mutation (11 available); any Apoe mutation (145 available)
Plg^tm1Jld mutation (3 available); any Plg mutation (4 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Gross appearance of aortic arches of Apoe^tm1Bres/Apoe^tm1Bres, Plg^tm1Jld/Plg^tm1Jld and Apoe^tm1Bres/Apoe^tm1Bres Plg^tm1Jld/Plg^tm1Jld mice

mortality/aging

premature death ( J:42927 )

• only about 50% survive beyond 20 weeks of age

growth/size/body

abnormal body weight ( J:42927 )

• exhibit a larger decrease in body weight after 2 months of age than single Plg homozygotes

cardiovascular system

atherosclerotic lesions ( J:42927 )

• exhibit accelerated formation of and more extensive intimal lesions compared to single homozygous Apoe mutants

• lesions contain fibrinogen deposits

homeostasis/metabolism

decreased circulating HDL cholesterol level ( J:42927 )

• small reduction in HDL cholesterol

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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