All Phenotypes Tg(Ggt1-cre)M3Egn MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Tg(Ggt1-cre)M3Egn
transgene insertion M3, Eric G Neilson
MGI:3811269

Summary

5 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Ddc^tm1.1Rhrs/Ddc^tm1.1Rhrs Tg(Ggt1-cre)M3Egn/0	129.Cg-Ddc^tm1.1Rhrs Tg(Ggt1-cre)M3Egn	MGI:5296380
cn2	Ddc^tm1.1Rhrs/Ddc^tm1.1Rhrs Tg(Ggt1-cre)M3Egn/0	involves: 129 * C57BL/6 * SJL	MGI:5296379
cn3	Pkd1^tm3Jzh/Pkd1^tm3Jzh Tg(Ggt1-cre)M3Egn/0	involves: 129P2/OlaHsd * C57BL/6 * SJL	MGI:3811282
cn4	Gsk3b^tm2Jrw/Gsk3b^tm2Jrw Tg(Ggt1-cre)M3Egn/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J * SJL	MGI:5429170
cn5	Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ Tg(Ggt1-cre)M3Egn/?	involves: 129S4/SvJaeSor * C57BL/6 * SJL	MGI:3811271

Allelic Composition	Ddc^tm1.1Rhrs/Ddc^tm1.1Rhrs Tg(Ggt1-cre)M3Egn/0
Genetic Background	129.Cg-Ddc^tm1.1Rhrs Tg(Ggt1-cre)M3Egn

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ddc^tm1.1Rhrs mutation (1 available); any Ddc mutation (127 available)
Tg(Ggt1-cre)M3Egn mutation (1 available)

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

mortality/aging

premature death ( J:175630 )

• 10 of 19 mice die by 20 months of age

homeostasis/metabolism

increased circulating creatinine level ( J:175630 )

• at 20 months of age

decreased circulating aldosterone level ( J:175630 )

• on a normal salt diet

decreased dopamine level ( J:175630 )

• in the kidney and urine but not brain or plasma

albuminuria ( J:175630 )

• in angiotensin II-treated mice

decreased renin activity ( J:175630 )

• on a normal salt diet

increased renin activity ( J:175630 )

• 15-fold in hydralazine-treated mice compared with 3-fold in similarly treated wild-type mice

abnormal response/metabolism to endogenous compounds ( J:175630 )

• natriuresis and diuresis response to L-DOPA treatment is attenuated compared to in similarly treated wild-type mice

• angiotensin II-treated mice exhibit increased albuminuria and tubulointerstitial injury compared with similarly treated wild-type mice

renal/urinary system

increased kidney weight ( J:175630 )

• at 20 months of age

albuminuria ( J:175630 )

• in angiotensin II-treated mice

abnormal kidney physiology ( J:175630 )

• at 20 months of age, mice exhibit increased renal injury index with increased macrophage, neutrophil, and lymphocyte infiltration compared with wild-type mice

tubulointerstitial nephritis ( J:175630 )

• in angiotensin II-treated mice

cardiovascular system

increased heart weight ( J:175630 )

• at 20 months of age

salt-sensitive hypertension ( J:175630 )

increased mean systemic arterial blood pressure ( J:175630 )

• at 20 months of age

increased systemic arterial systolic blood pressure ( J:175630 )

• by 3 months of age on a normal salt diet

• on a high salt diet for 4 weeks

• following angiotensin II exposure until day 5

• however, mice exhibit normal blood pressure on a low salt diet

immune system

tubulointerstitial nephritis ( J:175630 )

• in angiotensin II-treated mice

cellular

oxidative stress ( J:175630 )

• in response to a high salt diet as measured by urinary excretion of F2-isoprostane

• in angiotensin II-treated mice

growth/size/body

increased heart weight ( J:175630 )

• at 20 months of age

increased kidney weight ( J:175630 )

• at 20 months of age

Allelic Composition	Ddc^tm1.1Rhrs/Ddc^tm1.1Rhrs Tg(Ggt1-cre)M3Egn/0
Genetic Background	involves: 129 * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ddc^tm1.1Rhrs mutation (1 available); any Ddc mutation (127 available)
Tg(Ggt1-cre)M3Egn mutation (1 available)

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

mortality/aging

premature death ( J:175630 )

• 10 of 19 mice die by 20 months of age

homeostasis/metabolism

increased circulating creatinine level ( J:175630 )

• at 20 months of age

decreased circulating aldosterone level ( J:175630 )

• on a normal salt diet

decreased dopamine level ( J:175630 )

• in the kidney and urine but not brain or plasma

albuminuria ( J:175630 )

• in angiotensin II-treated mice

decreased renin activity ( J:175630 )

• on a normal salt diet

increased renin activity ( J:175630 )

• 15-fold in hydralazine-treated mice compared with 3-fold in similarly treated wild-type mice

abnormal response/metabolism to endogenous compounds ( J:175630 )

• natriuresis and diuresis response to L-DOPA treatment is attenuated compared to in similarly treated wild-type mice

• angiotensin II-treated mice exhibit increased albuminuria and tubulointerstitial injury compared with similarly treated wild-type mice

renal/urinary system

increased kidney weight ( J:175630 )

• at 20 months of age

albuminuria ( J:175630 )

• in angiotensin II-treated mice

abnormal kidney physiology ( J:175630 )

• at 20 months of age, mice exhibit increased renal injury index with increased macrophage, neutrophil, and lymphocyte infiltration compared with wild-type mice

tubulointerstitial nephritis ( J:175630 )

• in angiotensin II-treated mice

cardiovascular system

increased heart weight ( J:175630 )

• at 20 months of age

salt-sensitive hypertension ( J:175630 )

increased mean systemic arterial blood pressure ( J:175630 )

• at 20 months of age

increased systemic arterial systolic blood pressure ( J:175630 )

• by 3 months of age on a normal salt diet

• on a high salt diet for 4 weeks

• following angiotensin II exposure until day 5

• however, mice exhibit normal blood pressure on a low salt diet

immune system

tubulointerstitial nephritis ( J:175630 )

• in angiotensin II-treated mice

cellular

oxidative stress ( J:175630 )

• in response to a high salt diet as measured by urinary excretion of F2-isoprostane

• in angiotensin II-treated mice

growth/size/body

increased heart weight ( J:175630 )

• at 20 months of age

increased kidney weight ( J:175630 )

• at 20 months of age

Allelic Composition	Pkd1^tm3Jzh/Pkd1^tm3Jzh Tg(Ggt1-cre)M3Egn/0
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pkd1^tm3Jzh mutation (0 available); any Pkd1 mutation (154 available)
Tg(Ggt1-cre)M3Egn mutation (1 available)

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

mortality/aging

premature death ( J:140012 )

• most mice die by one month of age from renal failure

renal/urinary system

increased renal tubule apoptosis ( J:140012 )

• increased apoptosis is observed in both cysts and normal looking epithelial tubules of 2 day old mice

polycystic kidney ( J:140012 )

• cystic kidneys are first detectable at 10 days of age

• the disease is progressive with cysts dominating the kidney architecture by 26 days of age

• however, glomerular cysts are not observed

• cysts of proximal and distal origin develop at different rates with distal cysts progressively increasing in size until death

• proximal cysts stop growing at 15 days of age and start to regress or completely disappear before death

cellular

increased renal tubule apoptosis ( J:140012 )

• increased apoptosis is observed in both cysts and normal looking epithelial tubules of 2 day old mice

growth/size/body

polycystic kidney ( J:140012 )

• cystic kidneys are first detectable at 10 days of age

• the disease is progressive with cysts dominating the kidney architecture by 26 days of age

• however, glomerular cysts are not observed

• cysts of proximal and distal origin develop at different rates with distal cysts progressively increasing in size until death

• proximal cysts stop growing at 15 days of age and start to regress or completely disappear before death

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
polycystic kidney disease 1		DOID:0110858	OMIM:173900	J:140012

Allelic Composition	Gsk3b^tm2Jrw/Gsk3b^tm2Jrw Tg(Ggt1-cre)M3Egn/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gsk3b^tm2Jrw mutation (2 available); any Gsk3b mutation (113 available)
Tg(Ggt1-cre)M3Egn mutation (1 available)

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

renal/urinary system

renal/urinary system phenotype ( J:167190 )

N	• mutant kidneys are normal in terms of gross appearance, size, color, and glomerular and tubulointerstitial histology • kidney function, urine albumin excretion, and urine-concentrating ability remain normal

abnormal renal tubule morphology ( J:167190 )

• mice exhibit increased glycogen content in the renal cortical tubules, as shown by PAS staining and biochemical analysis

• EM revealed increased deposition of glycogen particles closely associated with tubules of smooth endoplasmic reticulum

abnormal proximal convoluted tubule morphology ( J:167190 )

• intense glycogen staining is primarily detected in the brush border of the renal tubules

homeostasis/metabolism

increased glycogen level ( J:167190 )

• mice exhibit increased glycogen accumulation in the renal cortical tubules

Allelic Composition	Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ Tg(Ggt1-cre)M3Egn/?
Genetic Background	involves: 129S4/SvJaeSor * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^tm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Ggt1-cre)M3Egn mutation (1 available)

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

normal phenotype

no abnormal phenotype detected ( J:111660 )

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