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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Hoxb7-cre)13Amc
transgene insertion 13, Andrew P McMahon
MGI:2675121
Summary 20 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Ift140tm1b(KOMP)Wtsi/Ift140tm1c(KOMP)Wtsi
Tg(Hoxb7-cre)13Amc/?
B6J.B6-Ift140tm1b(KOMP)Wtsi/Ift140tm1c(Komp)Wtsi Tg(Hoxb7-cre)13Amc MGI:5311855
cn2
Lin7ctm2Dsb/Lin7ctm2Dsb
Tg(Hoxb7-cre)13Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:3804963
cn3
Itgb1tm1Ross/Itgb1tm1Ross
Tg(Hoxb7-cre)13Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:5289691
cn4
Shhtm1Amc/Shhtm2Amc
Tg(Hoxb7-cre)13Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:5441067
cn5
Spry1tm1Jdli/Spry1tm1Jdli
Tg(Hoxb7-cre)13Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J MGI:3574644
cn6
Pkd1tm2Ggg/Pkd1tm2Ggg
Tg(Hoxb7-cre)13Amc/0
involves: 129S4/SvJae * C57BL/6 MGI:6188648
cn7
Ift20tm1.1Gjp/Ift20tm1.1Gjp
Tg(Hoxb7-cre)13Amc/0
involves: 129S4/SvJaeSor * 129S7/SvEvBrd * C57BL/6 MGI:3817270
cn8
Gt(ROSA)26Sortm1Sor/?
Wnt7btm2Amc/Wnt7btm2.1Amc
Tg(Hoxb7-cre)13Amc/0
involves: 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 MGI:3829882
cn9
Lhx1tm2.1Bhr/Lhx1tm1Tmj
Tg(Hoxb7-cre)13Amc/0
involves: 129S/SvEv * C57BL/6 MGI:3580500
cn10
Scnn1atm1.1Hum/Scnn1atm1.1Hum
Tg(Hoxb7-cre)13Amc/0
involves: 129/Sv * C57BL/6 MGI:4460805
cn11
Aqp2tm1Nlsn/Aqp2tm1Nlsn
Tg(Hoxb7-cre)13Amc/0
involves: 129/Sv * C57BL/6 MGI:3626345
cn12
Gt(ROSA)26Sortm1(RARA*)Clmd/Gt(ROSA)26Sortm1(RARA*)Clmd
Tg(Hoxb7-cre)13Amc/0
Tg(Hoxb7-EGFP)33Cos/0
involves: 129/SvEv * C57BL/6 * CBA * Swiss Webster MGI:4431231
cn13
Gt(ROSA)26Sortm1(RARA*)Clmd/Gt(ROSA)26Sor+
Tg(Hoxb7-cre)13Amc/0
Tg(Hoxb7-EGFP)33Cos/0
involves: 129/SvEv * C57BL/6 * CBA * Swiss Webster MGI:4431229
cn14
Gt(ROSA)26Sortm1(RARA*)Clmd/Gt(ROSA)26Sortm1(RARA*)Clmd
Tg(Hoxb7-cre)13Amc/0
involves: 129/SvEv * C57BL/6 * Swiss Webster MGI:4431228
cn15
Wnt7btm2Amc/Wnt7btm2.1Amc
Tg(Hoxb7-cre)13Amc/0
involves: 129X1/SvJ * C57BL/6 MGI:3829881
cn16
Ctnnb1tm1Mmt/Ctnnb1+
Tg(Hoxb7-cre)13Amc/0
involves: 129X1/SvJ * C57BL/6 MGI:5289781
cn17
Gfra1tm2Jmi/Gfra1tm3Jmi
Tg(Hoxb7-cre)13Amc/0
involves: 129X1/SvJ * C57BL/6 MGI:5514419
cn18
Gt(ROSA)26Sortm2(Wnt1/GFP)Amc/Gt(ROSA)26Sor+
Tg(Hoxb7-cre)13Amc/0
Wnt9btm1.1Amc/Wnt9btm1.1Amc
involves: 129X1/SvJ * C57BL/6 * CBA MGI:3716215
cn19
Cyp2c23tm1.1Jhc/Cyp2c23tm1.1Jhc
Tg(Hoxb7-cre)13Amc/0
involves: C57BL/6 MGI:5695613
cn20
Ctdnep1tm3Ryn/Ctdnep1tm3Ryn
Tg(Hoxb7-cre)13Amc/0
involves: C57BL/6 MGI:5548191


Genotype
MGI:5311855
cn1
Allelic
Composition
Ift140tm1b(KOMP)Wtsi/Ift140tm1c(KOMP)Wtsi
Tg(Hoxb7-cre)13Amc/?
Genetic
Background
B6J.B6-Ift140tm1b(KOMP)Wtsi/Ift140tm1c(Komp)Wtsi Tg(Hoxb7-cre)13Amc
Cell Lines EPD0073_5_F01
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ift140tm1b(KOMP)Wtsi mutation (0 available); any Ift140 mutation (49 available)
Ift140tm1c(KOMP)Wtsi mutation (0 available); any Ift140 mutation (49 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• either very short or no cilia are present in collecting ducts at birth
• cilia continue to be present in decreasing numbers at 10 and 20 days of age
• only very short cilia are assembled
• at birth
• stumpy cilia present at at 10 and 20 days of age
• extensive cysts throughout the kidney by 20 days of age
• present at 10 days of age
• present at 5 and 10 days of age
• cystic kidneys are fibrotic
• increased interstitial cell smooth muscle actin
• increased collagen
• at 20 days of age in non-collecting duct cells
• percentage of mitotic cells is elevated and remains high in collecting ducts
• during the third week of life

cellular
N
• normal orientation of mitotic spindles in precystic collecting ducts of the kidney
• either very short or no cilia are present in collecting ducts at birth
• cilia continue to be present in decreasing numbers at 10 and 20 days of age
• at 20 days of age in non-collecting duct cells
• percentage of mitotic cells is elevated and remains high in collecting ducts




Genotype
MGI:3804963
cn2
Allelic
Composition
Lin7ctm2Dsb/Lin7ctm2Dsb
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lin7ctm2Dsb mutation (0 available); any Lin7c mutation (6 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype




Genotype
MGI:5289691
cn3
Allelic
Composition
Itgb1tm1Ross/Itgb1tm1Ross
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itgb1tm1Ross mutation (0 available); any Itgb1 mutation (14 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• ~5% of mice failed to survive either birth or the first week of life due to complete bilateral renal agenesis
• all others survived into adulthood (8 weeks), indicating at least one functioning kidney

renal/urinary system
• a significant increase in apoptotic (TUNEL+) cells was observed in the cortex
• a significant increase in apoptotic (TUNEL+) cells was associated with the dilated tubules in the medulla
• a significant increase in proliferative (Ki67+) cells was noted in the cortex, probably associated with proximal tubular structures, but not in the medulla
• adult mice displayed an increased urinary AVP-to-creatinine ratio (as a surrogate for plasma AVP levels)
• adult mice exhibited a severe decrease in urine osmolarity relative to control mice
• mice exhibited a wide range of kidney abnormalities ranging from bilateral agenesis to grossly normal-sized kidneys
• mice with polyuria and renal failure showed a severely disturbed kidney architecture
• adult renal medullary collecting ducts exhibited hypoplasia, increased apoptosis, dilation (ectasia) and cyst formation
• adult renal medullary collecting ducts exhibited ectasia
• in adult mice, normal renal cortex areas containing clustered glomeruli were separated by larger areas with multiple cystic structures, likely to be dilated cortical collecting ducts
• a significant increase in apoptotic (TUNEL+) cells was observed in the cortex
• a significant increase in proliferative (Ki67+) cells was noted in the cortex, probably associated with proximal tubular structures, but not in the medulla
• in adult mice, the renal medulla exhibited tubular ectasia
• a significant increase in apoptotic (TUNEL+) cells was associated with the dilated tubules in the medulla
• adult renal medullary collecting ducts exhibited cyst formation
• late-stage developing kidneys displayed a reduced inner medulla size
• at both 1 and 2 wks of age, mutant kidneys were smaller than control kidneys
• at both 1 and 2 weeks of age
• at E18-P1, eleven of 25 mice showed gross renal hypoplasia, with mutant kidneys being less than 2/3 of normal size
• 2 of 45 mice (~5%) displayed complete bilateral renal agenesis
• at E18-P1, one of 25 mice displayed unilateral renal agenesis
• adult kidneys exhibited a reduced capacity to clear the contrast agent DPTA from blood
• in adult mice, renal uptake of labeled PAH was reduced ~85% relative to that of control kidneys
• mutant urine remained relatively isosmotic with blood plasma
• in mice with polyuria and severely disturbed kidney architecture
• at 8 weeks of age, mice had >10 times the urine output seen in control mice
• water deprivation for 12 hrs failed to reduce the urine output, unlike in control mice
• polyuria is likely due to an inability to respond to AVP within the kidney

homeostasis/metabolism
• adult mice displayed increased plasma urea levels
• adult mice displayed an increased urinary AVP-to-creatinine ratio (as a surrogate for plasma AVP levels)
• adult mice exhibited a severe decrease in urine osmolarity relative to control mice

hematopoietic system
• adult mice displayed a significantly lower blood hematocrit than control mice (42% in vs. 52%)

cellular
• a significant increase in apoptotic (TUNEL+) cells was observed in the cortex
• a significant increase in apoptotic (TUNEL+) cells was associated with the dilated tubules in the medulla
• a significant increase in proliferative (Ki67+) cells was noted in the cortex, probably associated with proximal tubular structures, but not in the medulla




Genotype
MGI:5441067
cn4
Allelic
Composition
Shhtm1Amc/Shhtm2Amc
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Shhtm1Amc mutation (1 available); any Shh mutation (23 available)
Shhtm2Amc mutation (1 available); any Shh mutation (23 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• at the newborn stage, cortical glomerular density is increased by 24% while glomerular density of the whole kidney is increased by 26% relative to that in wild-type controls
• however, no gross differences in glomerular size are observed
• newborn mice exhibit a 40% reduction in glomerular number
• at the newborn stage, cortical volume is reduced by 51%
• at 4 months of age, most of the inner medulla is lost in hydronephric kidneys
• at 4 months of age, most of the inner stripe of the outer medulla is lost in hydronephric kidneys
• at the newborn stage, medullary volume is reduced by 46%
• at 4 months of age, 50% of mice exhibit hydronephrosis
• however, no hydronephrosis is detected in newborn pups
• neonatal kidneys are 52% smaller than wild-type kidneys
• at E14.5, fewer mesenchymal cells line the ureteral epithelium relative to wild-type controls
• at E14.5, the mitotic index of the proximal and distal ureter mesenchyme is ~50% of that in wild-type controls, indicating reduced cell proliferation
• however, no differences in ureteral mesenchyme apoptosis are observed by TUNEL analysis
• a delay in smooth muscle differentiation is observed along the proximodistal axis of the ureter
• at E15.0, no smooth muscle alpha-actin protein (SMA), an early marker of smooth muscle differentiation, is detected at any axial level of the ureter, unlike in wild-type embryos where SMA is detected in the proximal ureter
• at the newborn stage, SMA is detected in the proximal ureter but, in contrast to wild-type controls, almost no SMA is detected in the distal-most part of the ureter, closest to the bladder
• in addition, mesenchymal cells in the distal ureter are not as condensed as those in wild-type controls
• newborn mice exhibit prominent hydroureter, usually more severe in the proximal region
• at E14.5, ureter length is ~21% shorter than in wild-type controls




Genotype
MGI:3574644
cn5
Allelic
Composition
Spry1tm1Jdli/Spry1tm1Jdli
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Spry1tm1Jdli mutation (1 available); any Spry1 mutation (9 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• neonatal kidneys are highly disorganized as revealed by ectopic renal nodules
• 11 of 15 newborn mice display ureter abnormalities (multiple ureters or hydoureter) similar to Spry1tm1.1Jdli homozygotes
• extra ureters attach to the vas deferens in newborn males




Genotype
MGI:6188648
cn6
Allelic
Composition
Pkd1tm2Ggg/Pkd1tm2Ggg
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pkd1tm2Ggg mutation (1 available); any Pkd1 mutation (101 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• apoptosis is increased in kidneys in P7 and P15 mice
• cell proliferation is increased in kidneys in both early and late stage of cystogenesis
• newborn mice exhibit microscopic kidney cysts derived from both cortical and medullary collecting ducts
• P7 kidneys have more and larger cysts, with less parenchyma compared to those in newborns
• by P15, mice present with huge bilateral masses on their flanks and kidneys are grossly cystic with very little normal renal parenchyma
• early and late stage of cystogenesis is associated with increased cell proliferation and increased Cux1 expression while late stage cystogenesis is associated with increased apoptosis and increased Cux1 expression

cellular
• apoptosis is increased in kidneys in P7 and P15 mice
• cell proliferation is increased in kidneys in both early and late stage of cystogenesis

homeostasis/metabolism
• BUN levels are increased at P7 and P15

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
polycystic kidney disease 1 DOID:0110858 OMIM:173900
J:171619




Genotype
MGI:3817270
cn7
Allelic
Composition
Ift20tm1.1Gjp/Ift20tm1.1Gjp
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129S4/SvJaeSor * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ift20tm1.1Gjp mutation (1 available); any Ift20 mutation (5 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• progressive bilateral kidney enlargement beginning by P10
• by P23, kidney weight is about 10 times that of controls

renal/urinary system
• by P23, collecting duct cells lacking cilia show increased rates of proliferation
• by P23 most of the kidney is replaced by collecting duct epithelium, fluid filled cysts, and fibrotic material
• at E18 collecting duct epithelial cells almost completely lack cilia
• progressive bilateral kidney enlargement beginning by P10
• by P23, kidney weight is about 10 times that of controls
• at E18 collecting duct epithelial cells almost completely lack cilia
• at P5 in non-dilated tubules, mitotic spindle orientation is randomized rather than being parallel to the long axis of the tubule
• at P5 the centrosome remains at the apical end of the cell but can be located anywhere from the lateral junction to the center of the cell rather than at the center of the cell
• dilation is first seen at P5
• cells lining cysts lack primary cilia
• cystic expansion of the collecting ducts
• cells lining cysts may be flat with prominent microvilli or domed with less pronounced microvilli

homeostasis/metabolism
• about 3 times higher than in controls

cellular
• at E18 collecting duct epithelial cells almost completely lack cilia
• by P23, collecting duct cells lacking cilia show increased rates of proliferation




Genotype
MGI:3829882
cn8
Allelic
Composition
Gt(ROSA)26Sortm1Sor/?
Wnt7btm2Amc/Wnt7btm2.1Amc
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129S4/SvJaeSor * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (540 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
Wnt7btm2.1Amc mutation (0 available); any Wnt7b mutation (11 available)
Wnt7btm2Amc mutation (1 available); any Wnt7b mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• at E15.5 the collecting ducts are dilated and branch points are less evident




Genotype
MGI:3580500
cn9
Allelic
Composition
Lhx1tm2.1Bhr/Lhx1tm1Tmj
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129S/SvEv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lhx1tm1Tmj mutation (0 available); any Lhx1 mutation (14 available)
Lhx1tm2.1Bhr mutation (0 available); any Lhx1 mutation (14 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• hypoplastic metanephroi with reduced number of glomeruli
• however, morphologically normal medulla and glomeruli
• neonates had small metanephroi that were functional at birth
• observed in 40% of mutants
• greatly reduced numbers of developing nephrons at birth
• the distal ureter was closed in both sexes
• the distal ureter ended abnormally in the uterus in some females
• observed in 40% of mutants
• delayed induction of the ureteric bud

reproductive system
• 57.1% of mutant females had completely or partially absent uteri with residual uterine tissue discontinuously present
• posterior uterus was more frequently absent compared to the anterior region
• 57.1% of mutant females had completely or partially absent uteri
• absent epididymis in all mutant males

embryo
• loss of caudal mesonephric tubules; however, the cranial mesonephros was present
• exhibited Mullerian duct aplasia, impaired posterior elongation of the Mullerian duct and Mullerian duct degeneration adjacent to where the Wolffian duct was lost
• degeneration of the nephric (Wolffian) duct epithelium that resulted in the absence of most parts of the reproductive tract in all mutant males, except for some residual tissue




Genotype
MGI:4460805
cn10
Allelic
Composition
Scnn1atm1.1Hum/Scnn1atm1.1Hum
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Scnn1atm1.1Hum mutation (1 available); any Scnn1a mutation (20 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• when mice are fed a normal sodium diet, cortical collecting ducts exhibit no significant sodium, chloride, or potassium ion transport unlike wild-type ducts from similarly treated wild-type mice
• when mice are fed a sodium-depleted diet, cortical collecting ducts absorb sodium without forming a lumen-negative transepithelial voltage unlike ducts from similarly treated wild-type mice




Genotype
MGI:3626345
cn11
Allelic
Composition
Aqp2tm1Nlsn/Aqp2tm1Nlsn
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Aqp2tm1Nlsn mutation (0 available); any Aqp2 mutation (12 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

renal/urinary system
• osmolality is only 170 +/- 19 milliosmoles/kg of water compared to 1630 +/- 135 milliosmoles/kg of water for wild-type mice
• water deprivation does not increase urine osmolality
• variable progressive papillary atrophy in those that survive past weaning
• variable progressive hydronephrosis in those that survive past weaning
• about a 10-fold increase in urine output
• water deprivation results in only a marginal decrease in urine output

homeostasis/metabolism
• osmolality is only 170 +/- 19 milliosmoles/kg of water compared to 1630 +/- 135 milliosmoles/kg of water for wild-type mice
• water deprivation does not increase urine osmolality




Genotype
MGI:4431231
cn12
Allelic
Composition
Gt(ROSA)26Sortm1(RARA*)Clmd/Gt(ROSA)26Sortm1(RARA*)Clmd
Tg(Hoxb7-cre)13Amc/0
Tg(Hoxb7-EGFP)33Cos/0
Genetic
Background
involves: 129/SvEv * C57BL/6 * CBA * Swiss Webster
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(RARA*)Clmd mutation (0 available); any Gt(ROSA)26Sor mutation (540 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
Tg(Hoxb7-EGFP)33Cos mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• severe renal hypoplasia with reduced branching at E14
• renal agenesis at E14
• barely begin to branch at E11
• severe renal hypoplasia with reduced branching at E14
• smaller ureteric bud at E10.5 than in normal embryos




Genotype
MGI:4431229
cn13
Allelic
Composition
Gt(ROSA)26Sortm1(RARA*)Clmd/Gt(ROSA)26Sor+
Tg(Hoxb7-cre)13Amc/0
Tg(Hoxb7-EGFP)33Cos/0
Genetic
Background
involves: 129/SvEv * C57BL/6 * CBA * Swiss Webster
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(RARA*)Clmd mutation (0 available); any Gt(ROSA)26Sor mutation (540 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
Tg(Hoxb7-EGFP)33Cos mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• renal hypoplasia with a 50-80% reduction in branch numbers at E14
• 50-80% reduction in branch numbers at E14




Genotype
MGI:4431228
cn14
Allelic
Composition
Gt(ROSA)26Sortm1(RARA*)Clmd/Gt(ROSA)26Sortm1(RARA*)Clmd
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129/SvEv * C57BL/6 * Swiss Webster
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(RARA*)Clmd mutation (0 available); any Gt(ROSA)26Sor mutation (540 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• few ureteric bud branches or nephrons and severe patterning abnormalities at E14
• at E14 the kidneys are greatly reduced in size than normal




Genotype
MGI:3829881
cn15
Allelic
Composition
Wnt7btm2Amc/Wnt7btm2.1Amc
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Hoxb7-cre)13Amc mutation (1 available)
Wnt7btm2.1Amc mutation (0 available); any Wnt7b mutation (11 available)
Wnt7btm2Amc mutation (1 available); any Wnt7b mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

renal/urinary system
• at P10, urine osmolality is 56% that of controls
• at P11 - P12 kidneys are grossly abnormal
• absent at P10
• by P11 - P12 kidneys are physiologically incompetent

homeostasis/metabolism
• at P10, urine osmolality is 56% that of controls




Genotype
MGI:5289781
cn16
Allelic
Composition
Ctnnb1tm1Mmt/Ctnnb1+
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm1Mmt mutation (0 available); any Ctnnb1 mutation (24 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Kidney agenesis in Ctnnb1tm1Mmt/Ctnnb1+ Tg(Hoxb7-cre)13Amc/0 mice

renal/urinary system
• mice exhit both uni- and bilateral kidney agenesis, similar to that observed in Lrp4tm2Her homozygotes
• however, formation of the Wolffian duct and distal ureters as well as bladder and adrenal glands remain intact




Genotype
MGI:5514419
cn17
Allelic
Composition
Gfra1tm2Jmi/Gfra1tm3Jmi
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gfra1tm2Jmi mutation (0 available); any Gfra1 mutation (6 available)
Gfra1tm3Jmi mutation (0 available); any Gfra1 mutation (6 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• at P0, most have bilateral kidney agenesis/aplasia (16/20)
• at P0, a few pups (3/20) have unilateral kidney agenesis and contralateral megaureter
• at P0, a few pups (3/20) have unilateral kidney agenesis and contralateral megaureter




Genotype
MGI:3716215
cn18
Allelic
Composition
Gt(ROSA)26Sortm2(Wnt1/GFP)Amc/Gt(ROSA)26Sor+
Tg(Hoxb7-cre)13Amc/0
Wnt9btm1.1Amc/Wnt9btm1.1Amc
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(Wnt1/GFP)Amc mutation (1 available); any Gt(ROSA)26Sor mutation (540 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
Wnt9btm1.1Amc mutation (0 available); any Wnt9b mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
N
• when the Wnt1:GFP fusion protein is expressed in the Wolffian duct, embryos exhibit normal mesonephric and metanephric tubule induction, as well as caudal extension of the Mullerian duct




Genotype
MGI:5695613
cn19
Allelic
Composition
Cyp2c23tm1.1Jhc/Cyp2c23tm1.1Jhc
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cyp2c23tm1.1Jhc mutation (0 available); any Cyp2c23 mutation (4 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• mutant mice fed a high K+ (5% KCl) diet for 3 days show a significantly increased body weight on HK day 2, unlike wild-type controls where increased K+ intake has no effect on body weight

cardiovascular system
• mutant mice fed a high K+ (5% KCl) diet display significantly increased systolic BP and remain hypertensive for 3 days during increased K+ intake, unlike wild-type controls
• addition of amiloride (an epithelial Na+ channel inhibitor) in drinking water abolishes high K+ intake-induced hypertension and decreases systolic BP from 146 +/- 5 to 117 +/- 3 mmHg, unlike in wild-type controls where amiloride has no effect on BP
• mutant mice fed a high-salt (4% NaCl) diet for 3 days show no significant differences in mean systolic BP relative to wild-type controls
• no differences in mean systolic BP are observed under normal salt or normal K+ (1.0% KCl) conditions relative to wild-type controls

renal/urinary system
• mutant mice fed a high K+ (5% KCl) diet display significantly decreased Na+ excretion relative to mutant mice fed a normal K+ (1.0% KCl) diet, unlike wild-type controls
• however, mutant mice exhibit no differences in Na+ intake when fed a 5% KCl diet or a normal (1.0% KCl) diet
• 10 uM of arachidonic acid (AA) fails to inhibit apical epithelial Na+ channel (ENaC) activity in the cortical collecting duct (CCD) of mutant mice fed a high K+ (5% KCl) diet, unlike in wild-type controls where channel activity (NPo) is decreased from 1.2 +/- 0.2 to 0.3 +/- 0.1
• however, addition of 100 nM 11,12-epoxyeicosatrienoic acid (11,12-EET) is still able to inhibit ENaC in the CCD of mutant mice fed a high K+ (5% KCl) diet, with NPo reduced from 2.5 +/- 0.4 to 0.2 +/- 0.1

homeostasis/metabolism
• mutant mice fed a high K+ (5% KCl) diet display significantly decreased Na+ excretion relative to mutant mice fed a normal K+ (1.0% KCl) diet, unlike wild-type controls
• however, mutant mice exhibit no differences in Na+ intake when fed a 5% KCl diet or a normal (1.0% KCl) diet




Genotype
MGI:5548191
cn20
Allelic
Composition
Ctdnep1tm3Ryn/Ctdnep1tm3Ryn
Tg(Hoxb7-cre)13Amc/0
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctdnep1tm3Ryn mutation (0 available); any Ctdnep1 mutation (14 available)
Tg(Hoxb7-cre)13Amc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice are obtained at a Mendelian frequency and survive over 1 year

renal/urinary system
N
• mice exhibit normal kidneys





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
11/10/2020
MGI 6.16
The Jackson Laboratory