All Phenotypes Ddc<tm1.1Rhrs> MGI Mouse

Phenotypes associated with this allele

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

♀	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

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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