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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Lpcat3tm1c(EUCOMM)Wtsi
targeted mutation 1c, Wellcome Trust Sanger Institute
MGI:5822780
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Lpcat3tm1c(EUCOMM)Wtsi/Lpcat3tm1c(EUCOMM)Wtsi involves: C57BL/6 * C57BL/6N * SJL MGI:5822851
cn2
Lpcat3tm1c(EUCOMM)Wtsi/Lpcat3tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6N * SJL MGI:5822858
cn3
Lpcat3tm1c(EUCOMM)Wtsi/Lpcat3tm1c(EUCOMM)Wtsi
Tg(Vil1-cre)997Gum/0
involves: C57BL/6 * C57BL/6N * SJL MGI:5822876


Genotype
MGI:5822851
hm1
Allelic
Composition
Lpcat3tm1c(EUCOMM)Wtsi/Lpcat3tm1c(EUCOMM)Wtsi
Genetic
Background
involves: C57BL/6 * C57BL/6N * SJL
Cell Lines EPD0455_5_A07
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lpcat3tm1c(EUCOMM)Wtsi mutation (0 available); any Lpcat3 mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• at 3 weeks after injection with a Cre-expressing adenoviral vector, adult mice show a more pronounced decrease in fasting plasma TG levels relative to mice homozygous for Lpcat3tm1c(EUCOMM)Wtsi and hemizygous for Tg(Alb-cre)21Mgn
• after adenovirus injection, adult mice also exhibit a decrease in ad-lib (fed) plasma TG levels, not observed in mice homozygous for Lpcat3tm1c(EUCOMM)Wtsi and hemizygous for Tg(Alb-cre)21Mgn

liver/biliary system
• after adenovirus injection, fasted mice show a markedly reduced rate of hepatic TG secretion in response to treatment with the lipase inhibitor tyloxapol




Genotype
MGI:5822858
cn2
Allelic
Composition
Lpcat3tm1c(EUCOMM)Wtsi/Lpcat3tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: C57BL/6 * C57BL/6N * SJL
Cell Lines EPD0455_5_A07
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lpcat3tm1c(EUCOMM)Wtsi mutation (0 available); any Lpcat3 mutation (26 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• fractionation of plasma lipoproteins revealed lower levels of apolipoprotein B (apoB) in the VLDL fraction of chow-fed mice following an overnight fast
• however, total plasma apoB levels and protein levels of apoB in liver are similar to those in control mice
• increased levels of plasma apoB-100 following a western diet for 9 weeks
• absence of arachidonoyl phospholipids profoundly affects lipid movement within membranes and lipidation of apoB-containing lipoproteins
• mice secrete lipid-poor very low-density lipoprotein (VLDL) lacking arachidonoyl phospholipids
• plasma VLDL particles are markedly smaller and poorly lipidated
• EM analysis of liver samples showed reduced nascent lipoprotein particle size in the lumen of Golgi and secretory vesicles
• decreased plasma triglyceride (TG) levels following an overnight fast on a chow diet
• lower total plasma TG levels following a western diet (40% high fat and 0.2% cholesterol) for 9 weeks
• TG levels in the VLDL plasma fraction are markedly reduced following an overnight fast
• striking loss of TG in the VLDL plasma lipoprotein fraction following a western diet for 9 weeks
• prominent accumulation of hepatic cholesterol following a western diet for 9 weeks
• increase in total cholesterol ester and a number of cholesterol ester species on a chow diet, with generally similar results on a western diet
• ~70% reduction in the abundance of 16:0, 20:4 phosphatidylcholine (PC) and 18:0, 20:4 PC (two of the most abundant arachidonoyl PC species in liver membranes) on a chow diet with compensatory increases in the abundance of other PC species, esp. those containing monounsaturated chains such as 16:0, 18:1 PC and 18:0, 18:1 PC
• increased abundance of certain PC species, such as 16:0, 18:1 PC, on a western diet with similar deficits in 16:0, 20:4 PC and 18:0, 20:4 PC as observed on a chow diet
• additional reductions in 16:1, 18:2 PC and 18:1, 20:4 PC in western diet-fed livers
• severe reductions of phosphatidlyethanolamine (PE) species containing arachidonate chains on both chow and western diets
• highly selective reductions in 16:0, 20:4 PC and 18:0, 20:4 PC in plasma VLDL fractions on a chow diet, suggesting that phospholipid deficits of liver membranes are passed on to the VLDL particles that they generate
• severe loss of arachidonate in liver on a chow diet is observed in phospholipids (PLs), but not in TGs or in cholesterol esters
• total level of PC is not significantly altered in liver under either diet
• highly selective reductions in 16:0, 20:4 PC and 18:0, 20:4 PC in plasma VLDL fractions on a chow diet, suggesting that phospholipid deficits of liver membranes are passed on to the VLDL particles that they generate
• prominent accumulation of hepatic TGs following a western diet for 9 weeks
• trend towards increased TG stores in the liver following an overnight fast
• accumulation of hepatic TGs following a high-sucrose diet for 3 weeks

liver/biliary system
• prominent accumulation of hepatic cholesterol following a western diet for 9 weeks
• increase in total cholesterol ester and a number of cholesterol ester species on a chow diet, with generally similar results on a western diet
• trend towards increased TG stores in the liver following an overnight fast
• prominent accumulation of hepatic TGs following a western diet for 9 weeks
• accumulation of hepatic TGs following a high-sucrose diet for 3 weeks
• histological evidence of increased lipid accumulation in the liver on a chow diet




Genotype
MGI:5822876
cn3
Allelic
Composition
Lpcat3tm1c(EUCOMM)Wtsi/Lpcat3tm1c(EUCOMM)Wtsi
Tg(Vil1-cre)997Gum/0
Genetic
Background
involves: C57BL/6 * C57BL/6N * SJL
Cell Lines EPD0455_5_A07
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lpcat3tm1c(EUCOMM)Wtsi mutation (0 available); any Lpcat3 mutation (26 available)
Tg(Vil1-cre)997Gum mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• decreased body weight at 1 week of age
• however, body weight is normal at birth
• pups fail to thrive and exhibit severe growth retardation
• however, suckling is normal

homeostasis/metabolism
• blood glucose levels are very low at 1 week of age
• plasma insulin levels are significantly lower at 1 week of age
• massive accumulation of cytosolic lipid droplets in intestinal enterocytes at 1 week of age
• plasma triglyceride (TG) levels are significantly lower at 1 week of age

digestive/alimentary system
• massive accumulation of cytosolic lipid droplets in intestinal enterocytes at 1 week of age





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
11/12/2024
MGI 6.24
The Jackson Laboratory