All Phenotypes Tg(Aqp2-cre)1Dek MGI Mouse

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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

10 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Cldn4^tm1.1Jhou/Cldn4^tm1.1Jhou Tg(Aqp2-cre)1Dek/0	B6.Cg-Cldn4^tm1.1Jhou Tg(Aqp2-cre)1Dek	MGI:5609166
cn2	Cldn8^tm1.1Jhou/Cldn8^tm1.1Jhou Tg(Aqp2-cre)1Dek/0	B6.Cg-Cldn8^tm1.1Jhou Tg(Aqp2-cre)1Dek	MGI:5803713
cn3	Edn1^tm1Ywa/Edn1^tm1Ywa Tg(Aqp2-cre)1Dek/0	involves: 129S6/SvEvTac * C57BL/6 * SJL	MGI:3714388
cn4	Ednra^tm2Ywa/Ednra^tm2Ywa Tg(Aqp2-cre)1Dek/0	involves: 129S7/SvEvBrd * C57BL/6 * SJL	MGI:3714397
cn5	Pparg^tm1.1Gonz/Pparg^tm1.1Gonz Tg(Aqp2-cre)1Dek/0	involves: 129X1/SvJ * C57BL/6 * SJL	MGI:5437733
cn6	Adcy6^tm1.1Dek/Adcy6^tm1.1Dek Tg(Aqp2-cre)1Dek/0	involves: 129X1/SvJ * C57BL/6 * SJL	MGI:5490605
cn7	Kctd1^{tm1c(EUCOMM)Wtsi}/Kctd1^{tm1c(EUCOMM)Wtsi} Tg(Aqp2-cre)1Dek/0	involves: C57BL/6 * C57BL/6N * SJL	MGI:7657840
cn8	Kctd15^{tm1c(EUCOMM)Wtsi}/Kctd15^{tm1c(EUCOMM)Wtsi} Tg(Aqp2-cre)1Dek/0	involves: C57BL/6 * C57BL/6N * SJL	MGI:7657841
cn9	Kctd1^{tm1c(EUCOMM)Wtsi}/Kctd1^{tm1c(EUCOMM)Wtsi} Kctd15^{tm1c(EUCOMM)Wtsi}/Kctd15^{tm1c(EUCOMM)Wtsi} Tg(Aqp2-cre)1Dek/0	involves: C57BL/6 * C57BL/6N * SJL	MGI:7657842
tg10	Tg(Aqp2-cre)1Dek/0	involves: C57BL/6 * SJL	MGI:3714393

Allelic Composition	Cldn4^tm1.1Jhou/Cldn4^tm1.1Jhou Tg(Aqp2-cre)1Dek/0
Genetic Background	B6.Cg-Cldn4^tm1.1Jhou Tg(Aqp2-cre)1Dek

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cldn4^tm1.1Jhou 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

decreased mean systemic arterial blood pressure ( J:216399 )

• 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

increased circulating bicarbonate level ( J:216399 )

• arterial bicarbonate levels are higher

increased circulating aldosterone level ( J:216399 )

• mice fed a low-salt diet exhibit higher plasma aldosterone levels than those on a regular diet

increased circulating potassium level ( J:216399 )

• plasma potassium shows a trend toward hyperkalemia however, renal handling of potassium is normal

decreased circulating chloride level ( J:216399 )

• 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

increased urine chloride ion level ( J:216399 )

• 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

abnormal renal sodium reabsorption ( J:216399 )

• the reduction of urinary sodium excretion is slower in mutants from regular to low-salt diet, indicating defects in low-salt-induced renal reabsorption

increased urine sodium level ( J:216399 )

• 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

alkalosis ( J:216399 )

• arterial bicarbonate levels are higher, however arterial pH is maintained at similar levels to controls, indicating compensated metabolic alkalosis

renal/urinary system

increased urine chloride ion level ( J:216399 )

• 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

increased urine sodium level ( J:216399 )

• 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

abnormal renal reabsorption ( J:216399 )

• 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

abnormal renal sodium reabsorption ( J:216399 )

• the reduction of urinary sodium excretion is slower in mutants from regular to low-salt diet, indicating defects in low-salt-induced renal reabsorption

polyuria ( J:216399 )

• 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

decreased body weight ( J:216399 )

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

hematopoietic system

increased hematocrit ( J:216399 )

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

Allelic Composition	Cldn8^tm1.1Jhou/Cldn8^tm1.1Jhou Tg(Aqp2-cre)1Dek/0
Genetic Background	B6.Cg-Cldn8^tm1.1Jhou Tg(Aqp2-cre)1Dek

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cldn8^tm1.1Jhou mutation (0 available); any Cldn8 mutation (32 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 Cldn8^tm1.1Jhou/Cldn8^tm1.1Jhou Tg(Aqp2-cre)1Dek/0 kidney collecting duct

homeostasis/metabolism

increased circulating bicarbonate level ( J:220813 )

• significantly increased arterial HCO3^- level (P_HCO3) at 10-12 weeks of age

• however, arterial pH is normal

increased circulating aldosterone level ( J:220813 )

• plasma aldosterone level is significantly increased by 1.48-fold relative to controls

decreased circulating potassium level ( J:220813 )

• significantly reduced plasma K⁺ level (P_K) at 10-12 weeks of age, indicating hypokalemia

hypokalemia ( J:220813 )

decreased circulating chloride level ( J:220813 )

• significantly reduced plasma Cl^- level (P_Cl) at 10-12 weeks of age

• however, plasma Na⁺ level (P_Na) is normal

increased urine chloride ion level ( J:220813 )

• 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

increased urine potassium level ( J:220813 )

• significant renal wasting of K⁺, with fractional excretion increased by 1.75-fold and absolute excretion increased by 1.67-fold relative to controls

increased urine sodium level ( J:220813 )

• 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

alkalosis ( J:220813 )

• metabolic alkalosis due renal loss of Cl^- at 10-12 weeks of age

renal/urinary system

increased urine chloride ion level ( J:220813 )

• 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

increased urine potassium level ( J:220813 )

• significant renal wasting of K⁺, with fractional excretion increased by 1.75-fold and absolute excretion increased by 1.67-fold relative to controls

increased urine sodium level ( J:220813 )

• 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

abnormal kidney collecting duct morphology ( J:220813 )

• 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

polyuria ( J:220813 )

• significant increase in urinary volume at 10-12 weeks of age relative to control mice

• however, urinary osmotic pressure is normal

cardiovascular system

decreased mean systemic arterial blood pressure ( J:220813 )

• 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 ( J:220813 )

• hypotension associated with renal salt wasting defects and urinary volume depletion

growth/size/body

growth/size/body region phenotype ( J:220813 )

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

Allelic Composition	Edn1^tm1Ywa/Edn1^tm1Ywa 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:
Edn1^tm1Ywa mutation (1 available); any Edn1 mutation (26 available)
Tg(Aqp2-cre)1Dek mutation (1 available)

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

homeostasis/metabolism

decreased circulating antidiuretic hormone level ( J:104785 )

• levels are significantly decreased in conditional mutants compared to controls during normal water diet, and levels are essentially zero during high water intake

decreased circulating sodium level ( J:104785 )

• mice tend to have lower plasma sodium concentration and plasma osmolality than controls but differences do not reach significance

abnormal urine homeostasis ( J:104785 )

• more urinary excretion of endothelin-1 is seen in mutants over 6 hour period following water loading compared to controls

increased urine osmolality ( J:104785 )

• 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

renal/urinary system phenotype ( J:104785 )

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

abnormal urine homeostasis ( J:104785 )

• more urinary excretion of endothelin-1 is seen in mutants over 6 hour period following water loading compared to controls

increased urine osmolality ( J:104785 )

abnormal kidney physiology ( J:104785 )

• antidiuretic hormone-induced cyclic AMP accumulation is higher in mutant inner medullary collecting ducts than in control tissue

oliguria ( J:104785 )

• mutants show reduced water excretion for up to 3 hours after acute water loading

Allelic Composition	Ednra^tm2Ywa/Ednra^tm2Ywa 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:
Ednra^tm2Ywa mutation (1 available); any Ednra mutation (35 available)
Tg(Aqp2-cre)1Dek mutation (1 available)

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

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:101241 )

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)

increased circulating antidiuretic hormone level ( J:101241 )

• plasma AVP levels are significantly greater than controls

abnormal urine osmolality ( J:101241 )

• 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

renal/urinary system phenotype ( J:101241 )

N	• urine volume, urine or plasma osmolality, and plasma sodium concentration are similar to controls

abnormal urine osmolality ( J:101241 )

• 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

Allelic Composition	Pparg^tm1.1Gonz/Pparg^tm1.1Gonz 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:
Pparg^tm1.1Gonz mutation (0 available); any Pparg mutation (41 available)
Tg(Aqp2-cre)1Dek mutation (1 available)

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

growth/size/body

abnormal body weight ( J:99873 )

• 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

abnormal blood volume ( J:99873 )

• 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

abnormal hematocrit ( J:99873 )

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

homeostasis/metabolism

abnormal circulating aldosterone level ( J:99873 )

• after RGZ treatment, mice fail to exhibit a significant fall in plasma aldosterone levels, unlike similarly-treated control mice

abnormal urine sodium level ( J:99873 )

• 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

abnormal physiological response to xenobiotic ( J:99873 )

• 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

abnormal urine sodium level ( J:99873 )

• after RGZ treatment, mice fail to exhibit induction of a positive Na balance (where intake > excretion), unlike similarly-treated control mice

abnormal renal sodium ion transport ( J:99873 )

• 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

Allelic Composition	Adcy6^tm1.1Dek/Adcy6^tm1.1Dek 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:
Adcy6^tm1.1Dek mutation (1 available); any Adcy6 mutation (50 available)
Tg(Aqp2-cre)1Dek mutation (1 available)

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

renal/urinary system

decreased urine osmolality ( J:180012 )

• on a 0.3% sodium diet and free access to drinking water

• after water deprivation

• in pair-fed mice

homeostasis/metabolism

decreased urine osmolality ( J:180012 )

• on a 0.3% sodium diet and free access to drinking water

• after water deprivation

• in pair-fed mice

Allelic Composition	Kctd1^{tm1c(EUCOMM)Wtsi}/Kctd1^{tm1c(EUCOMM)Wtsi} Tg(Aqp2-cre)1Dek/0
Genetic Background	involves: C57BL/6 * C57BL/6N * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kctd1^{tm1c(EUCOMM)Wtsi} mutation (0 available); any Kctd1 mutation (39 available)
Tg(Aqp2-cre)1Dek mutation (1 available)

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

renal/urinary system

renal/urinary system phenotype ( J:344153 )

N	• at 2-4 months of age, mice exhibit no alterations in blood urea nitrogen (BUN) levels relative to controls, indicating normal kidney function

Allelic Composition	Kctd15^{tm1c(EUCOMM)Wtsi}/Kctd15^{tm1c(EUCOMM)Wtsi} Tg(Aqp2-cre)1Dek/0
Genetic Background	involves: C57BL/6 * C57BL/6N * SJL
Cell Lines	EPD0177_1_E09

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kctd15^{tm1c(EUCOMM)Wtsi} mutation (0 available); any Kctd15 mutation (26 available)
Tg(Aqp2-cre)1Dek mutation (1 available)

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

renal/urinary system

renal/urinary system phenotype ( J:344153 )

• at 2-4 months of age, mice exhibit normal kidney morphology with no alterations in blood urea nitrogen (BUN) levels relative to controls, indicating normal kidney function

Allelic Composition	Kctd1^{tm1c(EUCOMM)Wtsi}/Kctd1^{tm1c(EUCOMM)Wtsi} Kctd15^{tm1c(EUCOMM)Wtsi}/Kctd15^{tm1c(EUCOMM)Wtsi} Tg(Aqp2-cre)1Dek/0
Genetic Background	involves: C57BL/6 * C57BL/6N * SJL
Cell Lines	EPD0177_1_E09

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kctd15^{tm1c(EUCOMM)Wtsi} mutation (0 available); any Kctd15 mutation (26 available)
Kctd1^{tm1c(EUCOMM)Wtsi} mutation (0 available); any Kctd1 mutation (39 available)
Tg(Aqp2-cre)1Dek mutation (1 available)

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

renal/urinary system

renal/urinary system phenotype ( J:344153 )

• adult mice exhibit normal kidney morphology relative to controls

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

no abnormal phenotype detected ( J:104785 )

• hemizygous mice are viabl and fertile

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