All Phenotypes Gt(ROSA)26Sor<tm7(Pik3ca*,-EGFP)Rsky> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Gt(ROSA)26Sor^{tm7(Pik3ca,-EGFP)Rsky}/Gt(ROSA)26Sor⁺ Tg(CAG-cre/Esr1)5Amc/0	B6.Cg-Gt(ROSA)26Sor^{tm7(Pik3ca,-EGFP)Rsky} Tg(CAG-cre/Esr1)5Amc	MGI:6197269
cn2	Egr2^tm2(cre)Pch/Egr2⁺ Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky}/? Ptpn11^tm1.1Wbm/Ptpn11^tm1.1Wbm	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6	MGI:5588148
cn3	Gt(ROSA)26Sor^{tm7(Pik3ca,-EGFP)Rsky}/Gt(ROSA)26Sor^{tm13(CAG-MYC,-CD2)Rsky} Ighg1^tm1(cre)Cgn/Ighg1⁺	involves: 129P2/OlaHsd * C57BL/6	MGI:5463978
cn4	Erbb3^tm3Cbm/Erbb3^tm3Cbm Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky}/? Tg(Dhh-cre)1Mejr/0	involves: 129P2/OlaHsd * C57BL/6 * FVB/N	MGI:5588164
cn5	Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky}/? Ptpn11^tm1.1Wbm/Ptpn11^tm1.1Wbm Tg(Dhh-cre)1Mejr/0	involves: 129P2/OlaHsd * C57BL/6 * FVB/N	MGI:5588151
cn6	Gt(ROSA)26Sor^{tm7(Pik3ca,-EGFP)Rsky}/Gt(ROSA)26Sor⁺ Gt(ROSA)26Sor^{tm4(ACTB-tdTomato,-EGFP)Luo}/Gt(ROSA)26Sor⁺ Tg(ACTA1-cre/Esr1)2Kesr/0	involves: 129S1/Sv * 129X1/SvJ * C3H * C57BL/6J	MGI:8268434
cn7	Egr2^tm2(cre)Pch/Egr2⁺ Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky}/?	involves: 129S2/SvPas * C57BL/6	MGI:5588141
cn8	Gt(ROSA)26Sor^{tm7(Pik3ca,-EGFP)Rsky}/Gt(ROSA)26Sor^{tm7(Pik3ca,-EGFP)Rsky} Tg(Cr2-cre)3Cgn/0	involves: C57BL/6	MGI:4430556

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

mortality/aging

premature death ( J:264410 )

• mice administered a single low dose (4 mg/kg) of tamoxifen to induce cre recombination survive 2 months and then die with multiple abnormalities

• tamoxifen-administered mice treated with rapamycin show improved survival but no improvement in organ abnormalities such as liver and spleen disorganization with aberrant vascularization

postnatal lethality, incomplete penetrance ( J:264410 )

• mice start to rapidly die after 40 mg/kg tamoxifen administration, with 50% of mortality at day 9

• tamoxifen-administered mice treated with BYL719 are alive after 40 days, however interruption of BYL719 treatment 40 days after tamoxifen-administration leads to rapid death

• tamoxifen-administered mice treated with rapamycin show improved survival but no improvement in organ abnormalities such as liver and spleen disorganization with aberrant vascularization

growth/size/body

kidney cyst ( J:264410 )

• kidney cysts in tamoxifen-administered mice

visceromegaly ( J:264410 )

• organomegaly is seen in mice administered a single low dose of tamoxifen

cardiovascular system

abnormal blood vessel morphology ( J:264410 )

• vessel abnormalities in tamoxifen-administered mice

• tamoxifen-administered mice treated with BYL719 show normal vessels

abnormal vein morphology ( J:264410 )

• ecstatic venous channels with a thin endothelial cell lining, surrounded by sparse, erratically distributed vascular smooth muscle cells and a disorganized extracellular matrix are seen in mice administered a low dose of tamoxifen

dilated vasculature ( J:264410 )

• severe vessel dilation in tamoxifen-administered mice

internal hemorrhage ( J:264410 )

• intra-abdominal hemorrhages in tamoxifen-administered mice

liver hemorrhage ( J:264410 )

• hepatic hemorrhages in tamoxifen-administered mice

cellular

increased cell proliferation ( J:264410 )

• high number of proliferating cells in affected organs of tamoxifen-administered mice

• however, no changes in apoptosis are seen

• tamoxifen-administered mice treated with BYL719 show a reduction in proliferation

hematopoietic system

abnormal spleen morphology ( J:264410 )

• loss of spleen microarchitecture integrity in tamoxifen-administered mice

immune system

abnormal spleen morphology ( J:264410 )

• loss of spleen microarchitecture integrity in tamoxifen-administered mice

enlarged lymphatic vessel ( J:264410 )

• expansion of lymphatic vessels in tamoxifen-administered mice

limbs/digits/tail

abnormal limb morphology ( J:264410 )

• mice administered a single low dose of tamoxifen progressively develop asymmetrical overgrowth of extremities, disseminated voluminous tumors and subcutaneous vascular abnormalities

• low-dose tamoxifen administered mice treated with BYL719 show improvement of the overgrowth of extremities, however, withdrawal of BYL719 leads to the development of asymmetric extremity hypertrophy within 4 weeks

liver/biliary system

liver hemorrhage ( J:264410 )

• hepatic hemorrhages in tamoxifen-administered mice

hepatic steatosis ( J:264410 )

• severe liver steatosis with vessel disorganization in tamoxifen-administered mice

muscle

skeletal muscle hypertrophy ( J:264410 )

• muscle hypertrophy in tamoxifen-administered mice

• mice treated with BYL719 7 days after cre induction show improved muscle hypertrophy

neoplasm

increased classified tumor incidence ( J:264410 )

• low dose tamoxifen-administered mice develop tumors that are lipomatous tumors and severe vascular lesions mixing venous and arterial vessels

• low-dose tamoxifen administered mice treated with BYL719 show reduced and disappearance of visible tumors within 2 weeks

• withdrawal of BYL719 from the low-dose tamoxifen administered mice leads to recurrence of tumors

• low-dose tamoxifen-administered mice treated with rapamycin show no effect on tumor growth

renal/urinary system

kidney cyst ( J:264410 )

• kidney cysts in tamoxifen-administered mice

renal fibrosis ( J:264410 )

• fibrosis of the kidney with aberrant vessels in tamoxifen-administered mice

skeleton

scoliosis ( J:264410 )

• scoliosis in tamoxifen-administered mice

• mice treated with BYL719 7 days after cre induction show improved scoliosis

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
CLOVES syndrome		DOID:0080351	OMIM:612918	J:264410

Allelic Composition	Egr2^tm2(cre)Pch/Egr2⁺ Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky}/? Ptpn11^tm1.1Wbm/Ptpn11^tm1.1Wbm
Genetic Background	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Egr2^tm2(cre)Pch mutation (2 available); any Egr2 mutation (32 available)
Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky} mutation (1 available); any Gt(ROSA)26Sor mutation (1058 available)
Ptpn11^tm1.1Wbm mutation (1 available); any Ptpn11 mutation (43 available)

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

nervous system

abnormal myelination ( J:207470 )

• myelination defects are more pronounced than in single conditional Ptpn11^tm1.1Wbm homozygotes

Allelic Composition	Gt(ROSA)26Sor^{tm7(Pik3ca,-EGFP)Rsky}/Gt(ROSA)26Sor^{tm13(CAG-MYC,-CD2)Rsky} Ighg1^tm1(cre)Cgn/Ighg1⁺
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm13(CAG-MYC,-CD2*)Rsky} mutation (1 available); any Gt(ROSA)26Sor mutation (1058 available)
Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky} mutation (1 available); any Gt(ROSA)26Sor mutation (1058 available)
Ighg1^tm1(cre)Cgn mutation (4 available); any Ighg1 mutation (30 available)

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

mortality/aging

premature death ( J:191824 )

• when bone marrow is used to reconstitute Rag2 and Il2rg null mice stimulated with sheep red blood cells, median survival is 227 days

immune system

abnormal class switch recombination ( J:191824 )

• impaired

increased germinal center B cell number ( J:191824 )

• in the Peyer's patches and spleen

neoplasm

increased B cell derived lymphoma incidence ( J:191824 )

• of germinal center B cell origin when bone marrow is used to reconstitute Rag2 and Il2rg null mice stimulated with sheep red blood cells

hematopoietic system

abnormal class switch recombination ( J:191824 )

• impaired

increased germinal center B cell number ( J:191824 )

• in the Peyer's patches and spleen

Allelic Composition	Erbb3^tm3Cbm/Erbb3^tm3Cbm Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky}/? Tg(Dhh-cre)1Mejr/0
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Erbb3^tm3Cbm mutation (0 available); any Erbb3 mutation (44 available)
Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky} mutation (1 available); any Gt(ROSA)26Sor mutation (1058 available)
Tg(Dhh-cre)1Mejr mutation (1 available)

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

nervous system

abnormal myelination ( J:207470 )

• myelination is not seen

Allelic Composition	Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky}/? Ptpn11^tm1.1Wbm/Ptpn11^tm1.1Wbm Tg(Dhh-cre)1Mejr/0
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky} mutation (1 available); any Gt(ROSA)26Sor mutation (1058 available)
Ptpn11^tm1.1Wbm mutation (1 available); any Ptpn11 mutation (43 available)
Tg(Dhh-cre)1Mejr mutation (1 available)

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

nervous system

abnormal myelination ( J:207470 )

• mice show myelination defects similar to single conditional Ptpn11^tm1.1Wbm homozygotes

Allelic Composition	Gt(ROSA)26Sor^{tm7(Pik3ca,-EGFP)Rsky}/Gt(ROSA)26Sor⁺ Gt(ROSA)26Sor^{tm4(ACTB-tdTomato,-EGFP)Luo}/Gt(ROSA)26Sor⁺ Tg(ACTA1-cre/Esr1)2Kesr/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C3H * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm4(ACTB-tdTomato,-EGFP)Luo} mutation (10 available); any Gt(ROSA)26Sor mutation (1058 available)
Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky} mutation (1 available); any Gt(ROSA)26Sor mutation (1058 available)
Tg(ACTA1-cre/Esr1*)2Kesr mutation (2 available)

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

growth/size/body

abnormal body weight ( J:370764 )

• mice administered alpelisib, a PIK3CA inhibitor, daily starting 48 hours after cre induction (preventative alpelisib) exhibit a normal appearance during the 22 weeks of treatment and a body weight increase similar to that of controls

• mice administered alpelisib 2 weeks after cre induction when global muscle hypertrophy is already prominent for 20 additional weeks (therapeutic alpelisib), show a rapid body weight decrease

• 6-week-old mice treated with tamoxifen for 5 days show progressive weight gain starting at 3 weeks after treatment which is not seen in wild-type mice and around 11 weeks after induction in males and 24 weeks in females, body weight becomes lower than in wild-type mice

muscle

abnormal skeletal muscle morphology ( J:370764 )

• mitochondrial mass is reduced in striated muscle cells of tamoxifen-treated mice

skeletal muscle hypertrophy ( J:370764 )

• mice show skeletal muscle hypertrophy at 15 weeks after tamoxifen, with hypertrophic striated cells

• mice administered alpelisib, a PIK3CA inhibitor, daily starting 48 hours after cre induction (preventative alpelisib) exhibit no skeletal muscle overgrowth 8 weeks after alpelisib initiation indicating that alpelisib prevents skeletal muscle overgrowth

• mice treated with therapeutic alpelisib show a reduction in muscular volume and striated muscle is conserved indicating that alpelisib reverses skeletal muscle overgrowth

abnormal muscle physiology ( J:370764 )

• striated muscle cells from tamoxifen-treated mice show an alteration in the mitochondrial transmembrane potential

increased muscle cell glucose uptake ( J:370764 )

• tamoxifen-treated mice show higher fluoro-D-glucose muscular uptake

adipose tissue

decreased total body fat amount ( J:370764 )

• tamoxifen-treated mice show reduced fat content

behavior/neurological

increased grip strength ( J:370764 )

• tamoxifen-treated mice show a gain in muscle strength

cellular

increased muscle cell glucose uptake ( J:370764 )

• tamoxifen-treated mice show higher fluoro-D-glucose muscular uptake

abnormal mitochondrial physiology ( J:370764 )

• striated muscle cells from tamoxifen-treated mice show an alteration in the mitochondrial transmembrane potential

homeostasis/metabolism

abnormal blood homeostasis ( J:370764 )

• plasma metabolites metabolomics analysis of tamoxifen-treated mice show metabolic changes with increases in acetyl-aspartate, acetyl-glutamine, acetyl-lysine, aminoadipate, ATP, camosine, citrate, creatinine, cytidine, decanoic acid, dodecanoyl-carnitine, dodecanoic acid/lauric acid, docosahexaenoic acid, hexanoic acid, hexanoyl-carnitine, linoleic acid, linolenic acid, methyl-lysine, myristic acid, myristoyl-carnitine, octanoyl-carnitine, oleic acid, O-phosphoethanolamine, palmitic acid, palmitoyl-carnitine, palmitoleic acid, phosphocreatine, riboflavin, S-adenosyl-L-homocysteine, and taurine, and decreases in glutamate, glucose, L-alanine, lysine, methionine, ornithine, threonine, tryptophan, and tyrosine

• alpelisib treatment results in partial correction of the different metabolic anomalies

hypoglycemia ( J:370764 )

• tamoxifen-treated mice are hypoglycemic

• mice treated with preventative alpelisib show normal 12-h fasted glycemia

• mice treated with therapeutic alpelisib show increased blood glucose levels

decreased circulating insulin level ( J:370764 )

• mice treated with therapeutic alpelisib show increased insulin levels

• however, mice show conserved insulin secretion in the oral glucose tolerance test

• mice treated with preventative alpelisib show corrected circulating insulin levels

• tamoxifen-treated mice exhibit low insulin levels

decreased circulating insulin-like growth factor I level ( J:370764 )

• tamoxifen-treated mice show low IGF1 levels

• mice treated with preventative alpelisib show corrected IGF1 levels

• mice treated with therapeutic alpelisib show increased circulating IGF1 levels

Allelic Composition	Egr2^tm2(cre)Pch/Egr2⁺ Gt(ROSA)26Sor^{tm7(Pik3ca*,-EGFP)Rsky}/?
Genetic Background	involves: 129S2/SvPas * C57BL/6

Find Mice

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

nervous system

abnormal myelination ( J:207470 )

• myelination is impaired

Allelic Composition	Gt(ROSA)26Sor^{tm7(Pik3ca,-EGFP)Rsky}/Gt(ROSA)26Sor^{tm7(Pik3ca,-EGFP)Rsky} Tg(Cr2-cre)3Cgn/0
Genetic Background	involves: C57BL/6

Find Mice

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

mortality/aging

neonatal lethality, complete penetrance ( J:157297 )

• mice die soon after birth

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