All Phenotypes Hif1a<tm3Rsjo> MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Hif1a^tm3Rsjo
targeted mutation 3, Randall S Johnson
MGI:2386679

Summary

30 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo	involves: 129S1/Sv * 129X1/SvJ	MGI:4418494
cn2	Egln1^tm2.1Fsl/Egln1^tm2.1Fsl Gt(ROSA)26Sor^{tm9(cre/ESR1)Arte}/Gt(ROSA)26Sor⁺ Hif1a^tm3Rsjo/Hif1a^tm3Rsjo	B6.Cg-Gt(ROSA)26Sor^{tm9(cre/ESR1)Arte} Egln1^tm2.1Fsl Hif1a^tm3Rsjo	MGI:5525146
cn3	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1^{Tg(Alb-cre)21Mgn}	B6.Cg-Hif1a^tm3Rsjo Speer6-ps1^{Tg(Alb-cre)21Mgn}	MGI:6275178
cn4	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0	involves: 129 * 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:4418552
cn5	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Hprt1^{tm1(Pck1-cre)Vhh}/Y Vhl^tm1Jae/Vhl^tm1Jae	involves: 129 * BALB/c * C57BL/6	MGI:3621461
cn6	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Vhl^tm1Jae/Vhl^tm1Jae Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺	involves: 129 * BALB/c * C57BL/6 * DBA	MGI:3621471
cn7	Gt(ROSA)26Sor^tm1(rtTA)Awu/Gt(ROSA)26Sor⁺ Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(tetO-cre)LC1Bjd/0	involves: 129P2/OlaHsd * 129S1/Sv * 129S4/SvJae * 129X1/SvJ	MGI:4418526
cn8	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ Hprt1^{tm1(Pck1-cre)Vhh}/Y	involves: 129P2/OlaHsd * 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ	MGI:4418525
cn9	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Lyz2^tm1(cre)Ifo/Lyz2⁺	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ	MGI:4418465
cn10	Ccl17^{tm2.1(cre)Ifo}/Ccl17⁺ Hif1a^tm3Rsjo/Hif1a^tm3Rsjo	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:5545808
cn11	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Lyz2^tm1(cre)Ifo/Lyz2⁺	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:4418500
cn12	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Myl2^tm1(cre)Krc/Myl2⁺	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6	MGI:4418481
cn13	Epas1^tm1Mcs/Epas1^tm1Mcs Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Vhl^tm1Jae/Vhl^tm1Jae Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * CD-1	MGI:5432005
cn14	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Vhl^tm1Jae/Vhl^tm1Jae Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * CD-1	MGI:5432006
cn15	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Ndor1^{Tg(UBC-cre/ERT2)1Ejb}/0	involves: 129S1/Sv * 129X1/SvJ	MGI:3710347
cn16	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Lck-cre)1Jtak/0	involves: 129S1/Sv * 129X1/SvJ	MGI:3698301
cn17	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Fabp1-cre)1Jig/0	involves: 129S1/Sv * 129X1/SvJ * BALB/c * FVB/N	MGI:4418471
cn18	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Tal1-cre/ERT)42-056Jrg/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:5464999
cn19	Egln1^tm1.1Brei/Egln1^tm1.1Brei Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(CD68-icre)1Bwlx/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:5568401
cn20	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(CD68-icre)1Bwlx/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6	MGI:5568404
cn21	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Camk2a-cre)2Szi/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA	MGI:4418484
cn22	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Camk2a-cre)1Szi/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA	MGI:4418498
cn23	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Itgax-cre)1-1Reiz/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA	MGI:5545809
cn24	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Ckmm-cre)5Khn/?	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N	MGI:3621470
cn25	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Tek-cre)1Ywa/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:4418479
cn26	Epas1^tm1Mcs/Epas1^tm1Mcs Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0	involves: 129S1/Sv * 129X1/SvJ * CD-1	MGI:5432003
cn27	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(MMTV-cre)1Mam/0	involves: 129S1/Sv * 129X1/SvJ * CD-1 * FVB	MGI:4418467
cn28	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Pax6-cre,GFP)1Pgr/0	involves: 129S1/Sv * 129X1/SvJ * FVB	MGI:4418547
cn29	Hif1a^tm1Rsjo/Hif1a^tm3Rsjo Tg(Col2a1-cre)1Rsjo/?	involves: 129S1/Sv * 129X1/SvJ * FVB/N	MGI:3621467
cn30	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Col2a1-cre)1Rsjo/?	involves: 129S1/Sv * 129X1/SvJ * FVB/N	MGI:3621466

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo
Genetic Background	involves: 129S1/Sv * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)

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

homeostasis/metabolism

decreased circulating glucose level ( J:152724 )

• following partial hepatectomy, fed or fasted mice exposed to a cre-expressing adenovirus exhibit a greater decrease in circulating glucose levels compared with similarly treated wild-type mice

abnormal gluconeogenesis ( J:152724 )

• in mice exposed to a cre-expressing adenovirus following partial hepatectomy

decreased liver glycogen level ( J:152724 )

• decreased glycogen level in the liver of fed, but not fasted, mice exposed to a cre-expressing adenovirus 72 hours after partial hepatectomy

cellular

increased cellular sensitivity to gamma-irradiation ( J:116762 )

• in adenoviral cre-treated mouse embryonic fibroblasts

decreased cell proliferation ( J:116762 )

• adenoviral cre-treated mouse embryonic fibroblasts exhibit reduced proliferation under normoxic or hypoxic conditions compared with similarly treated wild-type cells

decreased hepatocyte proliferation ( J:152724 )

• in mice exposed to a cre-expressing adenovirus following partial hepatectomy

early cellular replicative senescence ( J:116762 )

• under normoxic conditions, adenoviral cre-treated mouse embryonic fibroblasts exhibit premature replicative senescence compared with similarly treated wild-type cells

liver/biliary system

decreased hepatocyte proliferation ( J:152724 )

• in mice exposed to a cre-expressing adenovirus following partial hepatectomy

decreased liver glycogen level ( J:152724 )

• decreased glycogen level in the liver of fed, but not fasted, mice exposed to a cre-expressing adenovirus 72 hours after partial hepatectomy

delayed liver regeneration ( J:152724 )

• following exposure to a cre-expressing adenovirus, recovery from partial hepatectomy is delayed compared to in similarly treated wild-type mice

Allelic Composition	Egln1^tm2.1Fsl/Egln1^tm2.1Fsl Gt(ROSA)26Sor^{tm9(cre/ESR1)Arte}/Gt(ROSA)26Sor⁺ Hif1a^tm3Rsjo/Hif1a^tm3Rsjo
Genetic Background	B6.Cg-Gt(ROSA)26Sor^{tm9(cre/ESR1)Arte} Egln1^tm2.1Fsl Hif1a^tm3Rsjo

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Egln1^tm2.1Fsl mutation (0 available); any Egln1 mutation (22 available)
Gt(ROSA)26Sor^{tm9(cre/ESR1)Arte} mutation (2 available); any Gt(ROSA)26Sor mutation (993 available)
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)

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

hematopoietic system

increased spleen weight ( J:202737 )

• following treatment with tamoxifen

extramedullary hematopoiesis ( J:202737 )

• following treatment with tamoxifen, extramedullary hematopoiesis is observed in spleens

increased hematocrit ( J:202737 )

• following treatment with tamoxifen, mice exhibit hematocrits close to 80%

homeostasis/metabolism

increased erythropoietin level ( J:202737 )

• following treatment with tamoxifen, mice exhibit increased serum erythropoietin levels

immune system

increased spleen weight ( J:202737 )

• following treatment with tamoxifen

mortality/aging

premature death ( J:202737 )

• following treatment with tamoxifen, however, survival is improved relative to tamoxifen treated Egln1^tm2.1Fsl mice alone

growth/size/body

increased spleen weight ( J:202737 )

• following treatment with tamoxifen

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1^{Tg(Alb-cre)21Mgn}
Genetic Background	B6.Cg-Hif1a^tm3Rsjo Speer6-ps1^{Tg(Alb-cre)21Mgn}

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Speer6-ps1^{Tg(Alb-cre)21Mgn} mutation (6 available); any Speer6-ps1 mutation (4 available)

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

homeostasis/metabolism

decreased physiological sensitivity to xenobiotic ( J:211093 )

• mice subjected to oxygen-induced retinopathy and with treated dimethyloxaloylglycine fail to exhibit an improvement in percent avascular retina and tortuosity ratio compared with similarly treated wildtype mice

vision/eye

vision/eye phenotype ( J:211093 )

N	• under normoxic conditions, mice exhibit normal retinal development

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO-cre)1Jaw/0
Genetic Background	involves: 129 * 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(SFTPC-rtTA)5Jaw mutation (4 available)
Tg(tetO-cre)1Jaw mutation (6 available)

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

mortality/aging

neonatal lethality, incomplete penetrance ( J:143384 )

• all mice die within an hour of birth when exposed to doxycycline 8 days prior to parturition

• 85% of mice die within an hour of birth when exposed to doxycycline 4 of 6 days prior to parturition

respiratory system

increased lung weight ( J:143384 )

• at birth when mice are exposed to doxycycline prior to parturition

abnormal pulmonary alveolus morphology ( J:143384 )

• when mice are exposed to doxycycline prior to parturition, mice exhibit reduced alveolar airspaces unlike wild-type mice

abnormal pulmonary alveolus epithelial cell morphology ( J:143384 )

• when mice are exposed to doxycycline prior to parturition, the alveolar surface is lined with immature pneumocytes unlike in wild-type mice

abnormal type II pneumocyte morphology ( J:143384 )

• when mice are exposed to doxycycline prior to parturition, the alveolar septa has only a few scattered type II cells unlike in wild-type mice

atelectasis ( J:143384 )

• at birth when mice are exposed to doxycycline prior to parturition

thick pulmonary interalveolar septum ( J:143384 )

• at birth when mice are exposed to doxycycline prior to parturition

respiratory distress ( J:143384 )

• at birth when mice are exposed to doxycycline prior to parturition

abnormal surfactant secretion ( J:143384 )

• when mice are exposed to doxycycline prior to parturition

homeostasis/metabolism

cyanosis ( J:143384 )

• at birth when mice are exposed to doxycycline prior to parturition

growth/size/body

increased lung weight ( J:143384 )

• at birth when mice are exposed to doxycycline prior to parturition

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Hprt1^{tm1(Pck1-cre)Vhh}/Y Vhl^tm1Jae/Vhl^tm1Jae
Genetic Background	involves: 129 * BALB/c * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Hprt1^{tm1(Pck1-cre)Vhh} mutation (0 available); any Hprt1 mutation (1279 available)
Vhl^tm1Jae mutation (2 available); any Vhl mutation (18 available)

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

renal/urinary system

kidney inflammation ( J:106705 )

• pockets of inflammation

abnormal kidney morphology ( J:106705 )

• dilated lymphatic vessels

abnormal kidney vasculature morphology ( J:106705 )

• vascular ectasia

kidney cyst ( J:106705 )

• unilateral and bilateral macroscopic cysts that vary in number and size are seen in 3 of 10 mice

• multiple microscopic cysts are also seen with 3 of 10 having cysts of tubular origin and 7 of 10 having cysts of glomerular origin

• cysts of both tubular and glomerular origin may occur in the same mouse

liver/biliary system

hepatic steatosis ( J:97652 )

increased hepatic hemangioma incidence ( J:97652 )

• cavernous hepatic hemangiomas seen in mice at 2 - 6 months of age and with increased frequency in mice older than 6 months

cardiovascular system

increased vascular endothelial cell number ( J:97652 )

• proliferation of endothelial cells in hepatic blood vessels

abnormal kidney vasculature morphology ( J:106705 )

• vascular ectasia

abnormal vasodilation ( J:97652 )

• hepatic vascular angiectasia

neoplasm

increased hepatic hemangioma incidence ( J:97652 )

• cavernous hepatic hemangiomas seen in mice at 2 - 6 months of age and with increased frequency in mice older than 6 months

hematopoietic system

polycythemia ( J:97652 )

• average red blood cell count is 10.77 x 10⁶ compared to 9.3 x 10⁶ in controls

• develop erythrocytosis as indicated by reddening of paws and muzzle

increased hemoglobin content ( J:97652 )

• hemoglobin content is 19.38 g/dl compared to 13.24 g/dl in controls

immune system

kidney inflammation ( J:106705 )

• pockets of inflammation

muscle

abnormal vasodilation ( J:97652 )

• hepatic vascular angiectasia

growth/size/body

kidney cyst ( J:106705 )

• unilateral and bilateral macroscopic cysts that vary in number and size are seen in 3 of 10 mice

• multiple microscopic cysts are also seen with 3 of 10 having cysts of tubular origin and 7 of 10 having cysts of glomerular origin

• cysts of both tubular and glomerular origin may occur in the same mouse

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
von Hippel-Lindau disease		DOID:14175	OMIM:193300	J:97652 , J:106705

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Vhl^tm1Jae/Vhl^tm1Jae Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
Genetic Background	involves: 129 * BALB/c * C57BL/6 * DBA

Find Mice

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

liver/biliary system

hepatic steatosis ( J:97652 )

• severe steatosis

cardiovascular system

increased vascular endothelial cell number ( J:97652 )

• proliferation of endothelial cells in hepatic blood vessels

abnormal vasodilation ( J:97652 )

• hepatic vascular angiectasia

muscle

abnormal vasodilation ( J:97652 )

• hepatic vascular angiectasia

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
von Hippel-Lindau disease		DOID:14175	OMIM:193300	J:97652

Allelic Composition	Gt(ROSA)26Sor^tm1(rtTA)Awu/Gt(ROSA)26Sor⁺ Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(tetO-cre)LC1Bjd/0
Genetic Background	involves: 129P2/OlaHsd * 129S1/Sv * 129S4/SvJae * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^tm1(rtTA)Awu mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(tetO-cre)LC1Bjd mutation (2 available)

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

cellular

abnormal cell migration ( J:130751 )

• hypoxic primary tubular epithelial cells from doxycycline treated mice fails to migrate unlike similarly treated cells from Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Gt(ROSA)26Sor^tm1(rtTA)Awu/Gt(ROSA)26Sor⁺ mice

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ Hprt1^{tm1(Pck1-cre)Vhh}/Y
Genetic Background	involves: 129P2/OlaHsd * 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ

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)
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Hprt1^{tm1(Pck1-cre)Vhh} mutation (0 available); any Hprt1 mutation (1279 available)

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

renal/urinary system

kidney inflammation ( J:130751 )

• after ureteral ligation, mice exhibit reduced fibrosis and inflammation compared with similarly treated Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ mice

renal fibrosis ( J:130751 )

• after ureteral ligation, mice exhibit reduced fibrosis and inflammation compared with similarly treated Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ mice

cellular

abnormal cell differentiation ( J:130751 )

• hypoxic primary tubular epithelial cells fails to undergo an epithelial to mesenchyme transition unlike similarly treated cells from Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ mice

homeostasis/metabolism

decreased susceptibility to injury ( J:130751 )

• after ureteral ligation, mice exhibit reduced fibrosis and inflammation compared with similarly treated Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ mice

immune system

kidney inflammation ( J:130751 )

• after ureteral ligation, mice exhibit reduced fibrosis and inflammation compared with similarly treated Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺ mice

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Lyz2^tm1(cre)Ifo/Lyz2⁺
Genetic Background	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Lyz2^tm1(cre)Ifo mutation (14 available); any Lyz2 mutation (40 available)

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

immune system

abnormal leukocyte physiology ( J:117348 )

• CD44^hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells

abnormal macrophage physiology ( J:107682 )

• macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells

• bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice

• macrophages lack homotypic adhesion unlike wild-type cells

impaired macrophage chemotaxis ( J:107682 )

• macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells

• macrophage capacity to invade matrigel is severely defective compared with wild-type mice

• macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells

decreased tumor necrosis factor secretion ( J:107682 )

• in LPS-treated macrophages

decreased susceptibility to induced arthritis ( J:107682 )

decreased inflammatory response ( J:107682 )

• TPA-treated ears exhibit reduced inflammatory infiltration and edema compared with similarly treated wild-type cells

• following disruption of barrier function with 5% SDS (chronic cutaneous inflammation), mice fail to exhibit an inflammatory response as in similarly treated wild-type mice

homeostasis/metabolism

increased susceptibility to injury ( J:117348 )

• following oxygen-induced retinopathy, mice exhibit decreased repair of retinal damage compared with similarly treated wild-type mice

• CD44^hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells

skeleton

decreased susceptibility to induced arthritis ( J:107682 )

cellular

impaired macrophage chemotaxis ( J:107682 )

• macrophage capacity to invade matrigel is severely defective compared with wild-type mice

• macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells

• macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells

hematopoietic system

abnormal leukocyte physiology ( J:117348 )

• CD44^hi myeloid cells fail to promote repair of oxygen-induced retinopathy unlike wild-type cells

abnormal macrophage physiology ( J:107682 )

• macrophages exhibit impaired glycolysis and energy generation compared with wild-type cells

• bacteria exposed macrophages contain 7-fold more viable bacteria than similarly treated wild-type mice

• macrophages lack homotypic adhesion unlike wild-type cells

impaired macrophage chemotaxis ( J:107682 )

• macrophage capacity to invade matrigel is severely defective compared with wild-type mice

• macrophage migration through artificial extracellular matrix is decreased 60% compared with wild-type cells

• macrophage exhibit reduced directed motility in the absence of matrigel by 50% at normoxia and 75% under hypoxic conditions compared with similarly treated wild-type cells

Allelic Composition	Ccl17^{tm2.1(cre)Ifo}/Ccl17⁺ Hif1a^tm3Rsjo/Hif1a^tm3Rsjo
Genetic Background	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccl17^{tm2.1(cre)Ifo} mutation (0 available); any Ccl17 mutation (11 available)
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)

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

immune system

immune system phenotype ( J:187773 )

• bone marrow derived dendritic cells (BMDCs) cultured under hypoxic conditions (1% oxygen) show upregulation of maturation markers such as MHCII, CD86, with CD80 only slightly enhanced; control BMDCs grown in hypoxic conditions show similar enhanced maturation markers

• cytokine production is reduced in mutant and control BMDCs under hypoxic conditions; production of Il12p70, Il10, Il6, and Il23 is decreased in mutant and control BMDCs under hypoxic conditions, with Il22 upregulated compared to normoxic cells

• stimulation by LPS does not further enhance expression of maturation markers as it does in BMDCs grown under normoxic conditions

• production of Il12p70, Il10, Il6, and Il23 is decreased in mutant and control BMDCs under hypoxic conditions, with Il22 upregulated compared to normoxic cells

abnormal leukocyte migration ( J:187773 )

• fewer mutant BMDCs generated under hypoxic conditions migrate toward CCL19 in a transwell chamber assay than control cells grown under hypoxic conditions or mutant and control cells generated under normoxic conditions; migration toward CXCL12 is not different from controls under hypoxic or normoxic conditions

abnormal dendritic cell number ( J:187773 )

• bone marrow dendritic cells (BMDCs) differentiated under hypoxic conditions in culture display reduced growth (proliferation) compared to control cells grown in hypoxia or mutant cells grown under normoxic (21% oxygen) conditions

abnormal interleukin-1 beta secretion ( J:187773 )

• BMDCs produce similar levels of Il-1b under hypoxic and normoxic conditions while control cells and BMDCs with CD11c-driven Hif1a deletion show decreased production under hypoxic conditions

abnormal tumor necrosis factor secretion ( J:187773 )

• BMDCs produce similar levels of TNFalpha under hypoxic and normoxic conditions while control cells and BMDCs with CD11c-driven Hif1a deletion show decreased production under hypoxic conditions

cellular

abnormal cell physiology ( J:187773 )

• reduced amounts of ATP are detected in lysates of mutant BMDCs cultured under hypoxic conditions compared to control cells under hypoxia suggesting an energy metabolism defect with Hif1a deletion

abnormal leukocyte migration ( J:187773 )

hematopoietic system

abnormal leukocyte migration ( J:187773 )

abnormal dendritic cell number ( J:187773 )

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Lyz2^tm1(cre)Ifo/Lyz2⁺
Genetic Background	involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

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

mortality/aging

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:148597 )

• in LPS-treated mice compared with similarly treated wild-type mice

immune system

decreased interleukin-1 alpha secretion ( J:148597 )

• 4 hours after LPS treatment

decreased interleukin-1 beta secretion ( J:148597 )

• 4 hours after LPS treatment

decreased interleukin-12 secretion ( J:148597 )

• 4 hours after LPS treatment

decreased interleukin-6 secretion ( J:148597 )

• 1.5 hrs after LPS treatment

decreased tumor necrosis factor secretion ( J:148597 )

• 1.5 and 4 hrs after LPS treatment

decreased susceptibility to endotoxin shock ( J:148597 )

• LPS-treated mice exhibit less hypothermia, hypotension, and mortality; improved hemodynamic parameter, shock index, and heart rate to systolic blood pressure; and decreased macrophage cytokine production (TNF-alpha, IL6, IL12, IL1a, and IL1b) compared with similarly treated wild-type mice

homeostasis/metabolism

abnormal body temperature ( J:148597 )

• LPS-treated mice develop less hypothermia compared with similarly treated wild-type mice

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:148597 )

• in LPS-treated mice compared with similarly treated wild-type mice

cardiovascular system

abnormal systemic arterial blood pressure ( J:148597 )

• LPS-treated mice develop less hypotension compared with similarly treated wild-type mice

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Myl2^tm1(cre)Krc/Myl2⁺
Genetic Background	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Myl2^tm1(cre)Krc mutation (2 available); any Myl2 mutation (22 available)

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

cardiovascular system

abnormal coronary vessel morphology ( J:118455 )

• fewer blood vessels are present in the left ventricle compared to in wild-type mice

thick interventricular septum ( J:118455 )

• the diastolic thickness of the intraventricular septum is increased compared to in wild-type mice

cardiac hypertrophy ( J:118455 )

• mild

abnormal heart left ventricle morphology ( J:118455 )

• left ventricular end-diastolic diameter is reduced compared to in wild-type mice

increased heart left ventricle weight ( J:118455 )

increased heart left ventricle wall thickness ( J:118455 )

• the diastolic thickness of the left ventricle is increased compared to in wild-type mice

decreased cardiac muscle contractility ( J:118455 )

• mice exhibit reduced fractional shortening compared with wild-type mice

• during electrical stimulation, cardiomyocytes exhibit reduced cell shortening compared with wild-type cells

abnormal cardiac muscle relaxation ( J:118455 )

• dobutamine-treated mice exhibit increased isovolumic relaxation time, a measure of diastolic dysfunction, compared to in similarly treated wild-type mice

abnormal heart left ventricle pressure ( J:118455 )

• mice exhibit reduced maximum rates of left ventricular pressure development and pressure decline compared to in wild-type mice

abnormal myocardial fiber physiology ( J:118455 )

• cardiomyocytes exhibit prolonged time to reduce cytosolic calcium levels compared with wild-type cells

growth/size/body

cardiac hypertrophy ( J:118455 )

• mild

homeostasis/metabolism

abnormal physiological response to xenobiotic ( J:118455 )

• dobutamine-treated mice exhibit increased isovolumic relaxation time, a measure of diastolic dysfunction, compared to in similarly treated wild-type mice

muscle

decreased cardiac muscle contractility ( J:118455 )

• mice exhibit reduced fractional shortening compared with wild-type mice

• during electrical stimulation, cardiomyocytes exhibit reduced cell shortening compared with wild-type cells

abnormal cardiac muscle relaxation ( J:118455 )

• dobutamine-treated mice exhibit increased isovolumic relaxation time, a measure of diastolic dysfunction, compared to in similarly treated wild-type mice

Allelic Composition	Epas1^tm1Mcs/Epas1^tm1Mcs Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Vhl^tm1Jae/Vhl^tm1Jae Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Genetic Background	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * CD-1

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Epas1^tm1Mcs mutation (1 available); any Epas1 mutation (66 available)
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc mutation (2 available)
Vhl^tm1Jae mutation (2 available); any Vhl mutation (18 available)

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

skeleton

decreased trabecular bone volume ( J:186085 )

decreased bone trabecula number ( J:186085 )

hematopoietic system

hematopoietic system phenotype ( J:186085 )

N	• mice exhibit normal frequencies of KLS cells (hematopoietic stem cells and multipotential progenitors) numbers of red blood cells and lymphocytes and hematocrit

homeostasis/metabolism

decreased circulating erythropoietin level ( J:186085 )

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Vhl^tm1Jae/Vhl^tm1Jae Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Genetic Background	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * CD-1

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc mutation (2 available)
Vhl^tm1Jae mutation (2 available); any Vhl mutation (18 available)

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

hematopoietic system

increased hematocrit ( J:186085 )

homeostasis/metabolism

increased circulating erythropoietin level ( J:186085 )

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Ndor1^{Tg(UBC-cre/ERT2)1Ejb}/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Ndor1^{Tg(UBC-cre/ERT2)1Ejb} mutation (6 available); any Ndor1 mutation (32 available)

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

immune system

immune system phenotype ( J:119731 )

N	• hematocrit levels are normal in mutants; mutants do not develop anemia

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Lck-cre)1Jtak/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Lck-cre)1Jtak mutation (3 available)

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

immune system

increased interferon-gamma secretion ( J:117857 )

• exhibit higher IFN-gamma secretion by activated splenocytes

• both CD4+ and CD8+ T cells produce higher levels or IFN-gamma upon activation

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Fabp1-cre)1Jig/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * BALB/c * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Fabp1-cre)1Jig mutation (2 available)

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

digestive/alimentary system

abnormal digestive system physiology ( J:93476 )

• hypoxia fails to induce an increase in colonic epithelial cell resistance unlike in similarly treated wild-type cells

increased susceptibility to induced colitis ( J:93476 )

• TNBS-treated mice exhibit more severe colitis, slower weight gain during recovery, decreased colon length, and increased mortality compared with similarly treated wild-type mice

immune system

increased susceptibility to induced colitis ( J:93476 )

• TNBS-treated mice exhibit more severe colitis, slower weight gain during recovery, decreased colon length, and increased mortality compared with similarly treated wild-type mice

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Tal1-cre/ERT)42-056Jrg/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Tal1-cre/ERT)42-056Jrg mutation (2 available)

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

hematopoietic system

decreased common myeloid progenitor cell number ( J:192126 )

• in tamoxifen-treated mice

abnormal B cell differentiation ( J:192126 )

• tamoxifen-treated mice exhibit an increase in B lymphoid cells in the bone marrow compared with control mice

abnormal T cell differentiation ( J:192126 )

• tamoxifen-treated mice exhibit an increase in T lymphoid cells in the bone marrow compared with control mice

increased hematopoietic stem cell number ( J:192126 )

• in tamoxifen-treated mice

abnormal hematopoietic stem cell physiology ( J:192126 )

• long-term hematopoietic stem cells from tamoxifen-treated mice exhibit increased oxygen consumption rates and lower levels of lactate indicating decreased cytoplasmic glycolysis compared with control cells

• long-term hematopoietic stem cells from tamoxifen-treated mice exhibit loss of quiescence compared with control cells

immune system

abnormal B cell differentiation ( J:192126 )

• tamoxifen-treated mice exhibit an increase in B lymphoid cells in the bone marrow compared with control mice

abnormal T cell differentiation ( J:192126 )

• tamoxifen-treated mice exhibit an increase in T lymphoid cells in the bone marrow compared with control mice

Allelic Composition	Egln1^tm1.1Brei/Egln1^tm1.1Brei Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(CD68-icre)1Bwlx/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Egln1^tm1.1Brei mutation (0 available); any Egln1 mutation (22 available)
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(CD68-icre)1Bwlx mutation (0 available)

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

mortality/aging

postnatal lethality ( J:194598 )

• mice start dying suddenly at 5 weeks with 95% mortality by 16 weeks (mean survival time = 11 weeks)

hematopoietic system

hematopoietic system phenotype ( J:194598 )

N	• no cardiovascular complications or thromboses are observed

increased hematocrit ( J:194598 )

• not different from CD68cre/Phd2^fl mice

craniofacial

domed cranium ( J:194598 )

• 3/16 mice show this

nervous system

hydrocephaly ( J:194598 )

• mice with domed skulls show dramatic hydrocephalus

skeleton

domed cranium ( J:194598 )

• 3/16 mice show this

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(CD68-icre)1Bwlx/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(CD68-icre)1Bwlx mutation (0 available)

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

mortality/aging

mortality/aging ( J:194598 )

N	• no premature death observed

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Camk2a-cre)2Szi/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Camk2a-cre)2Szi mutation (1 available)

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

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:121971 )

• following transient middle cerebral artery occlusion

homeostasis/metabolism

abnormal physiological response to xenobiotic ( J:121971 )

• the neuroprotective effects on infarct size and neurological deficit scores of 3,4-dihydroxybenzoic acid, deferoxamine (DFO), and DP following transient middle cerebral artery occlusion is decreased compared to in similarly treated Hif1a^tm3Rsjo homozygotes

decreased susceptibility to ischemic brain injury ( J:98637 )

• following bilateral common carotid artery occlusion, mice exhibit decreased neuronal damage compared to in similarly treated Hif1a^tm3Rsjo homozygotes

increased susceptibility to ischemic brain injury ( J:121971 )

• following transient middle cerebral artery occlusion, mice exhibit increased infarct size, increased neurological deficit scores, and mortality compared with similarly treated Hif1a^tm3Rsjo homozygotes

increased cerebral infarct size ( J:121971 )

• 4 days after transient middle cerebral artery occlusion, infarct size is larger than in similarly treated Hif1a^tm3Rsjo homozygotes

• however, mice still respond to neuroprotective hypoxia with reduced infarct volume at shorter exposure periods than wild-type mice

nervous system

decreased susceptibility to ischemic brain injury ( J:98637 )

• following bilateral common carotid artery occlusion, mice exhibit decreased neuronal damage compared to in similarly treated Hif1a^tm3Rsjo homozygotes

increased susceptibility to ischemic brain injury ( J:121971 )

increased cerebral infarct size ( J:121971 )

• 4 days after transient middle cerebral artery occlusion, infarct size is larger than in similarly treated Hif1a^tm3Rsjo homozygotes

• however, mice still respond to neuroprotective hypoxia with reduced infarct volume at shorter exposure periods than wild-type mice

hydrocephaly ( J:121971 )

• uncommon

behavior/neurological

abnormal behavior ( J:121971 )

• following transient middle cerebral artery occlusion, mice exhibit increased neurological deficit scores compared with similarly treated Hif1a^tm3Rsjo homozygotes

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Camk2a-cre)1Szi/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Camk2a-cre)1Szi mutation (0 available)

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

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:121971 )

• following transient middle cerebral artery occlusion

nervous system

abnormal brain vasculature morphology ( J:121971 )

• mice exhibit a slight reduction in cerebral cortex microvascular density compared with Hif1a^tm3Rsjo homozygotes

decreased susceptibility to ischemic brain injury ( J:121971 )

• following bilateral common carotid artery occlusion, mice exhibit decreased neuronal damage compared to in similarly treated Hif1a^tm3Rsjo homozygotes

increased susceptibility to ischemic brain injury ( J:121971 )

increased cerebral infarct size ( J:121971 )

• 4 days after transient middle cerebral artery occlusion, infarct size is larger than in similarly treated Hif1a^tm3Rsjo homozygotes

• however, mice still respond to neuroprotective hypoxia with reduced infarct volume at shorter exposure periods than wild-type mice

hydrocephaly ( J:121971 )

• uncommon

homeostasis/metabolism

abnormal physiological response to xenobiotic ( J:121971 )

decreased susceptibility to ischemic brain injury ( J:121971 )

• following bilateral common carotid artery occlusion, mice exhibit decreased neuronal damage compared to in similarly treated Hif1a^tm3Rsjo homozygotes

increased susceptibility to ischemic brain injury ( J:121971 )

increased cerebral infarct size ( J:121971 )

• 4 days after transient middle cerebral artery occlusion, infarct size is larger than in similarly treated Hif1a^tm3Rsjo homozygotes

• however, mice still respond to neuroprotective hypoxia with reduced infarct volume at shorter exposure periods than wild-type mice

behavior/neurological

abnormal behavior ( J:121971 )

• following transient middle cerebral artery occlusion, mice exhibit increased neurological deficit scores compared with similarly treated Hif1a^tm3Rsjo homozygotes

cardiovascular system

abnormal brain vasculature morphology ( J:121971 )

• mice exhibit a slight reduction in cerebral cortex microvascular density compared with Hif1a^tm3Rsjo homozygotes

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Itgax-cre)1-1Reiz/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Itgax-cre)1-1Reiz mutation (4 available)

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

immune system

immune system phenotype ( J:187773 )

• stimulation by LPS does not further enhance expression of maturation markers as it does in BMDCs grown under normoxic conditions

• production of Il12p70, Il10, Il6, and Il23 is decreased in mutant and control BMDCs under hypoxic conditions, with Il22 upregulated compared to normoxic cells; mutant and control BMDCs generated under hypoxic conditions produce less TNFalpha and Il-1beta than cells under normoxic conditions

abnormal leukocyte migration ( J:187773 )

• fewer mutant BMDCs generated under hypoxic conditions migrate toward CCL19 in a transwell chamber assay than control cells grown under hypoxic conditions; migration toward CXCL12 is not different from controls under hypoxic or normoxic conditions

• mutant BMDCs generated under hypoxic conditions injected into mouse footpads show reduced migration to popliteal lymph nodes compared to control BMDCs grown under hypoxic conditions; mutant and control BMDCs generated under normoxic conditions migrate equally well to draining lymph nodes while control cells generated under hypoxia display enhanced migration relative to control cells from normoxic cultures, indicating migration under under hypoxic conditons is dependent on Hif1a

abnormal dendritic cell number ( J:187773 )

• bone marrow dendritic cells (BMDCs) differentiated under hypoxic conditions display reduced growth (proliferation) compared to control cells grown in hypoxia or mutant and control cells grown under normoxic (21% oxygen) conditions

cellular

abnormal cell physiology ( J:187773 )

• reduced amounts of ATP are detected in lysates of mutant BMDCs cultured under hypoxic conditions compared to control cells under hypoxia suggesting an energy metabolism defect with Hif1a deletion

abnormal leukocyte migration ( J:187773 )

hematopoietic system

abnormal leukocyte migration ( J:187773 )

abnormal dendritic cell number ( J:187773 )

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Ckmm-cre)5Khn/?
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Ckmm-cre)5Khn mutation (4 available)

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

muscle

abnormal muscle physiology ( J:97761 )

• increase in muscle damage following exercise

homeostasis/metabolism

increased circulating creatine kinase level ( J:97761 )

• increased serum levels of the MM isoform of creatine kinase 1 day after exercise

abnormal glucose homeostasis ( J:97761 )

• significant decrease in lactate accumulation after exercise

abnormal exercise endurance ( J:97761 )

• increased endurance in swim tests and in the first session of running uphill (concentric exercise) but decreased endurance when running downhill (eccentric exercise)

• endurance decreased over 4 consecutive days of daily treadmill running

nervous system

abnormal innervation pattern to muscle ( J:97761 )

• slight but statistically significant decrease in type IIa fibers in the soleus

Mouse Models of Human Disease	DO ID	OMIM ID(s)	Ref(s)
glycogen storage disease V	DOID:2746	OMIM:232600	J:97761
glycogen storage disease VII	DOID:11721	OMIM:232800	J:97761

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Tek-cre)1Ywa/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Tek-cre)1Ywa mutation (6 available)

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

cardiovascular system

decreased angiogenesis ( J:94773 )

• endothelial cells exhibit reduced VEGF-induced angiogenesis compared with similarly treated wild-type mice

• transplanted tumors exhibit a 50% in tumor vessel density compared with tumors transplanted into wild-type mice

• under hypoxic culture conditions, endothelial cells exhibit reduced VEGF-induced capillary structure formation compared with similarly treated wild-type cells

abnormal vascular endothelial cell migration ( J:94773 )

• endothelial cells exhibit reduced VEGF-induced migration in matrigel compared with similarly treated wild-type mice

• endothelial cells exhibit reduced VEGF-directed migration in hypoxic culture conditions compared with similarly treated wild-type cells

• however, random migration is normal

decreased vascular endothelial cell proliferation ( J:94773 )

• VEGF-induced endothelial cell proliferation in matrigel is reduced compared with wild-type mice

neoplasm

decreased tumor growth/size ( J:94773 )

• transplanted tumors are 60% lighter than those transplanted into wild-type mice with severe central necrosis due to decreased tumor angiogenesis

homeostasis/metabolism

delayed wound healing ( J:94773 )

• with reduced capillary sprouting

cellular

abnormal vascular endothelial cell migration ( J:94773 )

• endothelial cells exhibit reduced VEGF-induced migration in matrigel compared with similarly treated wild-type mice

• endothelial cells exhibit reduced VEGF-directed migration in hypoxic culture conditions compared with similarly treated wild-type cells

• however, random migration is normal

decreased vascular endothelial cell proliferation ( J:94773 )

• VEGF-induced endothelial cell proliferation in matrigel is reduced compared with wild-type mice

Allelic Composition	Epas1^tm1Mcs/Epas1^tm1Mcs Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * CD-1

Find Mice

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

hematopoietic system

hematopoietic system phenotype ( J:186085 )

N	• mice exhibit normal hematopoietic stem cell frequency

decreased erythroid progenitor cell number ( J:186085 )

• decreased frequency of CD71+/Ter119+ cells in the bone marrow

skeleton

decreased trabecular bone volume ( J:186085 )

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(MMTV-cre)1Mam/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * CD-1 * FVB

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(MMTV-cre)1Mam mutation (1 available)

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

endocrine/exocrine glands

abnormal mammary gland morphology ( J:82618 )

• at day 1 of lactation, mammary glands have fewer alveoli, fewer milk granules, and increased trapping of lipid droplets within epithelial cells compared to in wild-type mice

• during lactation, mammary gland wet weight is decreased 50% compared to in wild-type mice

abnormal mammary gland epithelium morphology ( J:82618 )

• by day 15 of pregnancy, mammary gland epithelium lack the lacy appearance of wild-type epithelium

• during lactation, epithelial cells trap milk and fat unlike in wild-type mice

• transplanted mammary epithelium fails to grow in mice expressing the wild-type protein

abnormal mammary gland alveolus morphology ( J:82618 )

• by day 15 of pregnancy, alveoli are smaller than normal with more prominent surrounding connective tissue than in wild-type mice

• alveolar differentiation during pregnancy is blocked

• alveolar lumens are small compared to in wild-type mice and fail to secret milk

• however, cell proliferation is normal

abnormal lactation ( J:82618 )

• female mice fail to secrete sufficient milk to support their offspring, most of whom are runted and die by P15

abnormal milk composition ( J:82618 )

• milk water content is decreased while milk sodium and chloride ion contents are increased at mid-lactation compared to in wild-type mice

abnormal milk sodium level ( J:82618 )

• milk sodium ion content is significantly increased at mid-lactation

homeostasis/metabolism

abnormal milk sodium level ( J:82618 )

• milk sodium ion content is significantly increased at mid-lactation

cardiovascular system

cardiovascular system phenotype ( J:82618 )

N	• microvessel patterning and vascular density in the mammary gland are normal

integument

abnormal mammary gland morphology ( J:82618 )

• at day 1 of lactation, mammary glands have fewer alveoli, fewer milk granules, and increased trapping of lipid droplets within epithelial cells compared to in wild-type mice

• during lactation, mammary gland wet weight is decreased 50% compared to in wild-type mice

abnormal mammary gland epithelium morphology ( J:82618 )

• by day 15 of pregnancy, mammary gland epithelium lack the lacy appearance of wild-type epithelium

• during lactation, epithelial cells trap milk and fat unlike in wild-type mice

• transplanted mammary epithelium fails to grow in mice expressing the wild-type protein

abnormal mammary gland alveolus morphology ( J:82618 )

• by day 15 of pregnancy, alveoli are smaller than normal with more prominent surrounding connective tissue than in wild-type mice

• alveolar differentiation during pregnancy is blocked

• alveolar lumens are small compared to in wild-type mice and fail to secret milk

• however, cell proliferation is normal

abnormal lactation ( J:82618 )

• female mice fail to secrete sufficient milk to support their offspring, most of whom are runted and die by P15

abnormal milk composition ( J:82618 )

• milk water content is decreased while milk sodium and chloride ion contents are increased at mid-lactation compared to in wild-type mice

abnormal milk sodium level ( J:82618 )

• milk sodium ion content is significantly increased at mid-lactation

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Pax6-cre,GFP)1Pgr/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * FVB

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Pax6-cre,GFP)1Pgr mutation (2 available)

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

vision/eye

increased lens fiber apoptosis ( J:141905 )

• at 1 month of age

abnormal lens morphology ( J:141905 )

• although born with normal lenses, mice exhibit lens degeneration after 1 month unlike wild-type mice

abnormal lens fiber morphology ( J:141905 )

• at 1 month of age, fiber cells are swollen and disorganized with many apoptotic nuclei unlike in wild-type mice

small lens ( J:141905 )

• at 1 month of age

cellular

increased lens fiber apoptosis ( J:141905 )

• at 1 month of age

Allelic Composition	Hif1a^tm1Rsjo/Hif1a^tm3Rsjo Tg(Col2a1-cre)1Rsjo/?
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm1Rsjo mutation (0 available); any Hif1a mutation (50 available)
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Col2a1-cre)1Rsjo mutation (0 available)

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

mortality/aging

neonatal lethality, complete penetrance ( J:72709 )

• die within a few hours of birth

respiratory system

abnormal tracheal ciliated epithelium morphology ( J:72709 )

• partially collapsed

abnormal tracheal cartilage morphology ( J:72709 )

• chondrocytes are abnormal and disorganized and the tracheal ring is malformed

respiratory failure ( J:72709 )

• fail to fully inflate the lungs

skeleton

abnormal tracheal cartilage morphology ( J:72709 )

• chondrocytes are abnormal and disorganized and the tracheal ring is malformed

abnormal long bone morphology ( J:72709 )

• the border between the chondrocytic hypertrophic zone and the primary spongiosa is irregular and disorganized

• however, cells along the proximal surface of the bone appear normal

disorganized long bone epiphyseal plate ( J:72709 )

• long bone growth plates are misshapen and wider with disrupted organization of the chondrocytes

increased long bone epiphyseal plate size ( J:72709 )

• long bone growth plates are misshapen and wider with disrupted organization of the chondrocytes

decreased length of long bones ( J:72709 )

• shorter long bones

abnormal sternum morphology ( J:72709 )

• no definable cellular structures are seen in the center of the sternebrae or at the at the chondrosternal junctions

• collagen type II and type X expression is absent from the center of the sternum and at the chondrosternal junctions at P0

abnormal sternocostal joint morphology ( J:72709 )

• no definable cellular structures are seen at the chondrosternal junctions

• collagen type II and type X expression are absent from the chondrosternal junctions at P0

abnormal thoracic cage shape ( J:72709 )

• rib cage is wider and misshapen

abnormal cartilage development ( J:72709 )

• massive cell death is seen at the center of cartilagenous elements and a subtle delay in chondrocyte differentiation is seen in the periphery

abnormal long bone epiphyseal plate proliferative zone ( J:72709 )

• in the long bones, an area in the center of the proliferative columnar layer is hypocellular or contains abnormal cells with pyknotic nuclei

abnormal long bone hypertrophic chondrocyte zone ( J:72709 )

• in the long bones, an area in the center of the upper hypertrophic zone is hypocellular or contains abnormal cells with pyknotic nuclei

cardiovascular system

abnormal angiogenesis ( J:72709 )

• ectopic angiogenesis seen in necrotic areas of long bone growth plates

embryo

decreased embryo size ( J:72709 )

limbs/digits/tail

short limbs ( J:72709 )

• short, deformed limbs

growth/size/body

decreased embryo size ( J:72709 )

Allelic Composition	Hif1a^tm3Rsjo/Hif1a^tm3Rsjo Tg(Col2a1-cre)1Rsjo/?
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1a^tm3Rsjo mutation (3 available); any Hif1a mutation (50 available)
Tg(Col2a1-cre)1Rsjo mutation (0 available)

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

mortality/aging

neonatal lethality, complete penetrance ( J:72709 )

• die within a few hours of birth

respiratory system

abnormal tracheal ciliated epithelium morphology ( J:72709 )

• partially collapsed

abnormal tracheal cartilage morphology ( J:72709 )

• chondrocytes are abnormal and disorganized and the tracheal ring is malformed

respiratory failure ( J:72709 )

• fail to fully inflate the lungs

skeleton

abnormal tracheal cartilage morphology ( J:72709 )

• chondrocytes are abnormal and disorganized and the tracheal ring is malformed

abnormal long bone morphology ( J:72709 )

• the border between the chondrocytic hypertrophic zone and the primary spongiosa is irregular and disorganized

• however, cells along the proximal surface of the bone appear normal

disorganized long bone epiphyseal plate ( J:72709 )

• long bone growth plates are misshapen and wider with disrupted organization of the chondrocytes

increased long bone epiphyseal plate size ( J:72709 )

• long bone growth plates are misshapen and wider with disrupted organization of the chondrocytes

decreased length of long bones ( J:72709 )

• shorter long bones

abnormal sternum morphology ( J:72709 )

• no definable cellular structures are seen in the center of the sternebrae or at the at the chondrosternal junctions

• collagen type II and type X expression is absent from the center of the sternum and at the chondrosternal junctions at P0

abnormal sternocostal joint morphology ( J:72709 )

• no definable cellular structures are seen at the chondrosternal junctions

• collagen type II and type X expression are absent from the chondrosternal junctions at P0

abnormal thoracic cage shape ( J:72709 )

• rib cage is wider and misshapen

abnormal cartilage development ( J:72709 )

• massive cell death is seen at the center of cartilagenous elements and a subtle delay in chondrocyte differentiation is seen in the periphery

abnormal long bone epiphyseal plate proliferative zone ( J:72709 )

• in the long bones, an area in the center of the proliferative columnar layer is hypocellular or contains abnormal cells with pyknotic nuclei

abnormal long bone hypertrophic chondrocyte zone ( J:72709 )

• in the long bones, an area in the center of the upper hypertrophic zone is hypocellular or contains abnormal cells with pyknotic nuclei

cardiovascular system

abnormal angiogenesis ( J:72709 )

• ectopic angiogenesis seen in necrotic areas of long bone growth plates

embryo

decreased embryo size ( J:72709 )

limbs/digits/tail

short limbs ( J:72709 )

• short, deformed limbs

growth/size/body

decreased embryo size ( J:72709 )

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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