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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Aqp2-cre)1Dek
transgene insertion 1, Donald E Kohan
MGI:3712435
Summary 7 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Cldn4tm1.1Jhou/Cldn4tm1.1Jhou
Tg(Aqp2-cre)1Dek/0
B6.Cg-Cldn4tm1.1Jhou Tg(Aqp2-cre)1Dek MGI:5609166
cn2
Cldn8tm1.1Jhou/Cldn8tm1.1Jhou
Tg(Aqp2-cre)1Dek/0
B6.Cg-Cldn8tm1.1Jhou Tg(Aqp2-cre)1Dek MGI:5803713
cn3
Edn1tm1Ywa/Edn1tm1Ywa
Tg(Aqp2-cre)1Dek/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:3714388
cn4
Ednratm2Ywa/Ednratm2Ywa
Tg(Aqp2-cre)1Dek/0
involves: 129S7/SvEvBrd * C57BL/6 * SJL MGI:3714397
cn5
Adcy6tm1.1Dek/Adcy6tm1.1Dek
Tg(Aqp2-cre)1Dek/0
involves: 129X1/SvJ * C57BL/6 * SJL MGI:5490605
cn6
Ppargtm1.1Gonz/Ppargtm1.1Gonz
Tg(Aqp2-cre)1Dek/0
involves: 129X1/SvJ * C57BL/6 * SJL MGI:5437733
tg7
Tg(Aqp2-cre)1Dek/0 involves: C57BL/6 * SJL MGI:3714393


Genotype
MGI:5609166
cn1
Allelic
Composition
Cldn4tm1.1Jhou/Cldn4tm1.1Jhou
Tg(Aqp2-cre)1Dek/0
Genetic
Background
B6.Cg-Cldn4tm1.1Jhou Tg(Aqp2-cre)1Dek
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cldn4tm1.1Jhou mutation (0 available); any Cldn4 mutation (10 available)
Tg(Aqp2-cre)1Dek mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mean blood pressure of anesthetized mice is lower than in controls
• mean blood pressure of unanesthetized and unrestrained males is lower than in control throughout the 24 hour observation period, with a significant difference during the dark cycle
• hypotension is exacerbated by a low-salt diet

homeostasis/metabolism
• arterial bicarbonate levels are higher
• mice fed a low-salt diet exhibit higher plasma aldosterone levels than those on a regular diet
• plasma potassium shows a trend toward hyperkalemia however, renal handling of potassium is normal
• plasma chloride levels are lower in 10-12 week old mice
• mice fed a low-salt diet maintain the hypochloremia that is seen on a regular diet
• renal loss of chloride, with fractional excretion of chloride increased by 1.79-fold and absolute excretion of chloride increased by 1.96-fold
• mice fed a low-salt diet maintain the chloriuresis that is seen on a regular diet
• the reduction of urinary sodium excretion is slower in mutants from regular to low-salt diet, indicating defects in low-salt-induced renal reabsorption
• renal loss of sodium, with fractional excretion increased by 1.52-fold and absolute excretion increased by 1.66-fold
• mice fed a low-salt diet maintain the natriuresis that is seen on a regular diet
• arterial bicarbonate levels are higher, however arterial pH is maintained at similar levels to controls, indicating compensated metabolic alkalosis

renal/urinary system
• renal loss of chloride, with fractional excretion of chloride increased by 1.79-fold and absolute excretion of chloride increased by 1.96-fold
• mice fed a low-salt diet maintain the chloriuresis that is seen on a regular diet
• renal loss of sodium, with fractional excretion increased by 1.52-fold and absolute excretion increased by 1.66-fold
• mice fed a low-salt diet maintain the natriuresis that is seen on a regular diet
• the reduction of urinary salt excretion (chloride and sodium) is slower in mutants from regular to low-salt diet, indicating defects in low-salt-induced renal reabsorption
• the reduction of urinary sodium excretion is slower in mutants from regular to low-salt diet, indicating defects in low-salt-induced renal reabsorption
• urinary volume is higher in 10-12 week old mice
• however, glomerular filtration rates are similar to wild-type mice and urinary osmotic pressure is normal
• mice fed a low-salt diet for 5 days exhibit a more severe urinary volume loss than on a regular diet (53% vs. 31% loss)

growth/size/body
• mice fed a low-salt diet for 5 days show a decrease in body weight

hematopoietic system
• mice fed a low-salt diet exhibit higher hematocrit levels than on a regular diet




Genotype
MGI:5803713
cn2
Allelic
Composition
Cldn8tm1.1Jhou/Cldn8tm1.1Jhou
Tg(Aqp2-cre)1Dek/0
Genetic
Background
B6.Cg-Cldn8tm1.1Jhou Tg(Aqp2-cre)1Dek
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cldn8tm1.1Jhou mutation (0 available); any Cldn8 mutation (30 available)
Tg(Aqp2-cre)1Dek mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Delocalization of claudin-4 in the tight junction of Cldn8tm1.1Jhou/Cldn8tm1.1Jhou Tg(Aqp2-cre)1Dek/0 kidney collecting duct

homeostasis/metabolism
• significantly increased arterial HCO3- level (PHCO3) at 10-12 weeks of age
• however, arterial pH is normal
• plasma aldosterone level is significantly increased by 1.48-fold relative to controls
• significantly reduced plasma K+ level (PK) at 10-12 weeks of age, indicating hypokalemia
• significantly reduced plasma Cl- level (PCl) at 10-12 weeks of age
• however, plasma Na+ level (PNa) is normal
• significantly increased urinary Cl- excretion rates, with fractional excretion increased by 1.72-fold and absolute excretion increased by 1.67-fold relative to controls
• significant renal wasting of K+, with fractional excretion increased by 1.75-fold and absolute excretion increased by 1.67-fold relative to controls
• significantly increased urinary Na+ excretion rates, with fractional excretion increased by 1.49-fold and absolute excretion increased by 1.51-fold relative to controls
• metabolic alkalosis due renal loss of Cl- at 10-12 weeks of age

renal/urinary system
• significantly increased urinary Cl- excretion rates, with fractional excretion increased by 1.72-fold and absolute excretion increased by 1.67-fold relative to controls
• significant renal wasting of K+, with fractional excretion increased by 1.75-fold and absolute excretion increased by 1.67-fold relative to controls
• significantly increased urinary Na+ excretion rates, with fractional excretion increased by 1.49-fold and absolute excretion increased by 1.51-fold relative to controls
• mice show delocalization of claudin-4 from the tight junction (TJ) in the collecting duct relative to control mice
• however, collecting duct histology, barrier function and TJ integrity remain intact
• significant increase in urinary volume at 10-12 weeks of age relative to control mice
• however, urinary osmotic pressure is normal

cardiovascular system
• mean arterial blood pressure (BP) in anesthetized mice is 17.6 mmHg lower than in control mice
• in vivo telemetric recording showed that the mean BP of awake and unrestrained males is consistently lower than in control males throughout the 24-h period, with statistical significance reached for each time point
• hypotension associated with renal salt wasting defects and urinary volume depletion

growth/size/body
N
• at 10-12 weeks of age, mice fed a regular salt diet show normal body weight relative to controls




Genotype
MGI:3714388
cn3
Allelic
Composition
Edn1tm1Ywa/Edn1tm1Ywa
Tg(Aqp2-cre)1Dek/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Edn1tm1Ywa mutation (1 available); any Edn1 mutation (25 available)
Tg(Aqp2-cre)1Dek mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• levels are significantly decreased in conditional mutants compared to controls during normal water diet, and levels are essentially zero during high water intake
• mice tend to have lower plasma sodium concentration and plasma osmolality than controls but differences do not reach significance
• more urinary excretion of endothelin-1 is seen in mutants over 6 hour period following water loading compared to controls
• with chronic administration (for 7 days) of 1-desamno-8-D-arginine vasopressin (DDAVP) increases urine osmolality in mutants but not in controls; elevation does not persist past 3 days of DDAVP administration

renal/urinary system
N
• mutant and control animals display similar renal function (volume of urine excreted, osmolyte secretion, plasma osmolality, or plasma sodium concentration) under normal and high water intake
• more urinary excretion of endothelin-1 is seen in mutants over 6 hour period following water loading compared to controls
• with chronic administration (for 7 days) of 1-desamno-8-D-arginine vasopressin (DDAVP) increases urine osmolality in mutants but not in controls; elevation does not persist past 3 days of DDAVP administration
• antidiuretic hormone-induced cyclic AMP accumulation is higher in mutant inner medullary collecting ducts than in control tissue
• mutants show reduced water excretion for up to 3 hours after acute water loading




Genotype
MGI:3714397
cn4
Allelic
Composition
Ednratm2Ywa/Ednratm2Ywa
Tg(Aqp2-cre)1Dek/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ednratm2Ywa mutation (1 available); any Ednra mutation (34 available)
Tg(Aqp2-cre)1Dek mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• during initial 2 days of water loading, mutants show body weight increase of 0.7 grams compared to 0.6 grams in controls, while after 6 days of water loading, mutants gain 1.1 grams compared to 1 gram for controls (no significant difference)
• plasma AVP levels are significantly greater than controls
• after acute water loading, mutants show a more rapid drop in urine osmolality in the initial 2 hours, then osmolality normalizes sooner than in control

renal/urinary system
N
• urine volume, urine or plasma osmolality, and plasma sodium concentration are similar to controls
• after acute water loading, mutants show a more rapid drop in urine osmolality in the initial 2 hours, then osmolality normalizes sooner than in control




Genotype
MGI:5490605
cn5
Allelic
Composition
Adcy6tm1.1Dek/Adcy6tm1.1Dek
Tg(Aqp2-cre)1Dek/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adcy6tm1.1Dek mutation (1 available); any Adcy6 mutation (49 available)
Tg(Aqp2-cre)1Dek mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• on a 0.3% sodium diet and free access to drinking water
• after water deprivation
• in pair-fed mice

homeostasis/metabolism
• on a 0.3% sodium diet and free access to drinking water
• after water deprivation
• in pair-fed mice




Genotype
MGI:5437733
cn6
Allelic
Composition
Ppargtm1.1Gonz/Ppargtm1.1Gonz
Tg(Aqp2-cre)1Dek/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppargtm1.1Gonz mutation (0 available); any Pparg mutation (39 available)
Tg(Aqp2-cre)1Dek mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• after a 9-day rosiglitazone (RGZ) treatment, mice fail to exhibit a significant increase in body weight gain as a result of fluid retention, unlike similarly-treated control mice

cardiovascular system
• after RGZ treatment, mice exhibit a significantly reduced plasma volume expansion relative to similarly-treated control mice, as shown by the Evans blue technique

hematopoietic system
• after RGZ treatment, mice fail to exhibit a significant fall in hematocrit levels, unlike similarly-treated control mice

homeostasis/metabolism
• after RGZ treatment, mice fail to exhibit a significant fall in plasma aldosterone levels, unlike similarly-treated control mice
• after a 9-day RGZ treatment, mice fail to exhibit a significant reduction in urinary Na excretion, unlike similarly-treated control mice where Na excretion is reduced at day 6 and returns to normal at day 8
• after RGZ treatment, mice fail to exhibit induction of a positive Na balance (where intake > excretion), unlike similarly-treated control mice
• mice are resistant to RGZ-induced fluid retention (increase in body weight and plasma volume expansion) seen in control mice
• RGZ-induced changes in sodium transport are significantly blocked in primary cultures of collecting duct (CD) cells

renal/urinary system
• after a 9-day RGZ treatment, mice fail to exhibit a significant reduction in urinary Na excretion, unlike similarly-treated control mice where Na excretion is reduced at day 6 and returns to normal at day 8
• after RGZ treatment, mice fail to exhibit induction of a positive Na balance (where intake > excretion), unlike similarly-treated control mice
• after RGZ treatment, primary cultures of mutant collecting duct (CD) cells fail to exhibit a reduction in transepithelial resistance or show an increase in transepithelial 22Na flux in an amiloride-sensitive manner, unlike similarly-treated control CD cells




Genotype
MGI:3714393
tg7
Allelic
Composition
Tg(Aqp2-cre)1Dek/0
Genetic
Background
involves: C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Aqp2-cre)1Dek mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• hemizygous mice are viabl and fertile





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory