All Phenotypes Rptor<tm1Rueg> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Rptor^tm1Rueg/Rptor^tm1Rueg Tg(ACTA1-cre)1Mll/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:3829872
cn2	Rictor^tm1Rueg/Rictor^tm1Rueg Rptor^tm1Rueg/Rptor^tm1Rueg Tg(ACTA1-cre)1Mll/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL	MGI:3829873
cn3	Gt(ROSA)26Sor^{tm4(Wnt7b)Flng}/Gt(ROSA)26Sor⁺ Rptor^tm1Rueg/Rptor^tm1Rueg Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0	involves: 129S1/Sv * 129X1/SvJ * CD-1	MGI:5613582
cn4	Gt(ROSA)26Sor^{tm4(Wnt7b)Flng}/Gt(ROSA)26Sor⁺ Rptor^tm1Rueg/Rptor⁺ Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0	involves: 129S1/Sv * 129X1/SvJ * CD-1	MGI:5613583
cn5	Rptor^tm1Rueg/Rptor^tm1Rueg Tg(Fabp4-cre)1Rev/0	involves: 129S1/SvImJ * C57BL/6J	MGI:3829752

Allelic Composition	Rptor^tm1Rueg/Rptor^tm1Rueg Tg(ACTA1-cre)1Mll/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rptor^tm1Rueg mutation (1 available); any Rptor mutation (115 available)
Tg(ACTA1-cre)1Mll mutation (0 available)

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

mortality/aging

premature death ( J:143748 )

• mice begin to die at 110 days and none survives beyond 190 days unlike wild-type mice

muscle

abnormal muscle morphology ( J:143748 )

• muscles are pale compared to in wild-type mice

• muscles have few intermyofibrillar mitochondrial that are localized to the subsarcolemmal space, densely packed and swollen compared to in wild-type muscles

• the EDL and soleus exhibit increased expression of slow-twitch-specific markers

increased skeletal muscle glycogen level ( J:143748 )

decreased muscle weight ( J:143748 )

• at 90 and 140 days

skeletal muscle interstitial fibrosis ( J:143748 )

dystrophic muscle ( J:143748 )

• muscles exhibit signs of dystrophy including mononuclear cells, a high number of small and large muscle fibers, active de- and re-generation, and centralized nuclei unlike in wild-type muscle

• dystrophy is severe in the diaphragm

abnormal muscle physiology ( J:143748 )

• the soleus muscle exhibits characteristics (time to peak, half time to peak and relaxation time of the twitch) of slow muscles unlike in wild-type mice

• twitch force and maximal titanic absolute force for the EDL and soleus muscles are less than in wild-type muscles

• the EDL and soleus muscles are more resistant to fatigue than in wild-type mice

• muscles exhibit a reduction in aerobic capacity compared to in wild-type muscles

abnormal muscle cell glucose uptake ( J:143748 )

• slower than in wild-type muscles

homeostasis/metabolism

impaired exercise endurance ( J:143748 )

• mice run for shorter and less frequent bouts than wild type mice with decreased top running speeds

increased skeletal muscle glycogen level ( J:143748 )

growth/size/body

increased lean body mass ( J:143748 )

• mice appear lean

decreased body weight ( J:143748 )

• at 63 days of age

adipose tissue

decreased total body fat amount ( J:143748 )

• at 140 days

skeleton

kyphosis ( J:143748 )

• mice develop severe kyphosis beginning at 2 months of age unlike wild-type mice

behavior/neurological

impaired exercise endurance ( J:143748 )

• mice run for shorter and less frequent bouts than wild type mice with decreased top running speeds

cellular

abnormal muscle cell glucose uptake ( J:143748 )

• slower than in wild-type muscles

Allelic Composition	Rictor^tm1Rueg/Rictor^tm1Rueg Rptor^tm1Rueg/Rptor^tm1Rueg Tg(ACTA1-cre)1Mll/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rictor^tm1Rueg mutation (1 available); any Rictor mutation (140 available)
Rptor^tm1Rueg mutation (1 available); any Rptor mutation (115 available)
Tg(ACTA1-cre)1Mll mutation (0 available)

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

mortality/aging

premature death ( J:143748 )

• mice exhibit a phenotype indistinguishable from 4932417H02Rik^tm1Rueg homozygotes

muscle

abnormal muscle morphology ( J:143748 )

• mice exhibit a phenotype indistinguishable from 4932417H02Rik^tm1Rueg homozygotes

abnormal muscle physiology ( J:143748 )

• mice exhibit a phenotype indistinguishable from 4932417H02Rik^tm1Rueg homozygotes

adipose tissue

abnormal adipose tissue morphology ( J:143748 )

• mice exhibit a phenotype indistinguishable from 4932417H02Rik^tm1Rueg homozygotes

growth/size/body

abnormal postnatal growth/weight/body size ( J:143748 )

• mice exhibit a phenotype indistinguishable from 4932417H02Rik^tm1Rueg homozygotes

Allelic Composition	Gt(ROSA)26Sor^{tm4(Wnt7b)Flng}/Gt(ROSA)26Sor⁺ Rptor^tm1Rueg/Rptor^tm1Rueg Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * CD-1

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm4(Wnt7b)Flng} mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)
Rptor^tm1Rueg mutation (1 available); any Rptor mutation (115 available)
Tg(Sp7-tTA,tetO-EGFP/cre)1Amc mutation (2 available)

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

skeleton

abnormal bone structure ( J:208766 )

• when cre expression is suppressed by doxycycline treatment until 1 month of age then stopped, 3 weeks later bone mass is reduced compared to mutant mice with one wild-type Rptor allele

abnormal bone marrow cavity morphology ( J:208766 )

• when cre expression is suppressed by doxycycline treatment until 1 month of age then stopped, 3 weeks later bone marrow cavity is larger than in mutant mice with one wild-type Rptor allele but still smaller than in controls not over expressing Wnt7b

increased osteoblast cell number ( J:208766 )

• when cre expression is suppressed by doxycycline treatment until 1 month of age then stopped, 3 weeks later osteoblast number is increased

• however, unlike in mice with one wild-type Rptor osteoblast hyperactivity is reduced

Allelic Composition	Gt(ROSA)26Sor^{tm4(Wnt7b)Flng}/Gt(ROSA)26Sor⁺ Rptor^tm1Rueg/Rptor⁺ 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

skeleton

abnormal bone marrow cavity morphology ( J:208766 )

• when cre expression is suppressed by doxycycline treatment until 1 month of age the marrow cavity is decreased

increased bone mass ( J:208766 )

• when cre expression is suppressed by doxycycline treatment until 1 month of age mice show very high bone mass 3 weeks after stopping doxycycline treatment

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

reproductive system

reduced female fertility ( J:143749 )

• female mice produce fewer pups per litter and the time between litters is slightly longer than in control mice that do not express cre

decreased litter size ( J:143749 )

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:143749 )

N	• despite reduced adiposity, mice exhibit normal lipolysis

decreased susceptibility to diet-induced obesity ( J:143749 )

• when fed a high fat diet, mice initially gain more weight than control mice but cease gaining weight after 2 to 3 weeks and over all weight gain is 41% of starting weight compared to 85% in control mice

decreased circulating glucose level ( J:143749 )

• when fed a standard or high fat diet

decreased circulating insulin level ( J:143749 )

• when fed a standard diet

decreased circulating leptin level ( J:143749 )

• when fed a standard or high fat diet

decreased circulating cholesterol level ( J:143749 )

• when fed a high fat diet

increased oxygen consumption ( J:143749 )

• when fed a standard or high fat diet, oxygen consumption in white adipose cells is increased compared to in control cells

improved glucose tolerance ( J:143749 )

• when fed a high fat diet

decreased adiponectin level ( J:143749 )

• when fed a standard or high fat diet

decreased liver triglyceride level ( J:143749 )

• when fed a standard diet, liver triglyceride levels are lower than in control mice

• however, mice fed a high fat diet exhibit normal liver steatosis and liver triglyceride levels

adipose tissue

decreased brown adipose tissue amount ( J:143749 )

• when fed a standard or high fat diet

decreased white fat cell number ( J:143749 )

• when fed a standard or high fat diet

decreased white fat cell size ( J:143749 )

• when fed a high fat diet

decreased total fat pad weight ( J:143749 )

• when fed a standard diet and more pronounced when fed a high fat diet

growth/size/body

increased lean body mass ( J:143749 )

• when fed a standard or high fat diet, mice are leaner than controls

decreased body weight ( J:143749 )

• when fed a standard diet, mice weight 18% less than control mice that do not express cre

decreased susceptibility to diet-induced obesity ( J:143749 )

behavior/neurological

decreased locomotor activity ( J:143749 )

• when fed a standard diet, mice are less active on a running wheel compared to control mice

• however, mice exhibit normal food intake

digestive/alimentary system

digestive/alimentary phenotype ( J:143749 )

N	• despite reduced adiposity, mice exhibit normal lipid absorption

liver/biliary system

decreased liver triglyceride level ( J:143749 )

• when fed a standard diet, liver triglyceride levels are lower than in control mice

• however, mice fed a high fat diet exhibit normal liver steatosis and liver triglyceride levels

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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