About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gt(ROSA)26Sortm1(rtTA)Awu
targeted mutation 1, Anton Wutz
MGI:3664736
Summary 6 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sor+
Hif1atm3Rsjo/Hif1atm3Rsjo
Tg(tetO-cre)LC1Bjd/0
involves: 129P2/OlaHsd * 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:4418526
cx2
Tsixtm1.1Awu/Tsixtm1.1Awu
Tg(CAG-EGFP)50Osb/0
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sortm1(rtTA)Awu
involves: 129P2/OlaHsd * 129S4/SvJae * C3H/HeSlc * C57BL/6J * C57BL/6Slc MGI:5285846
cx3
Tsixtm1.1Awu/Y
Tg(CAG-EGFP)50Osb/0
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sortm1(rtTA)Awu
involves: 129P2/OlaHsd * 129S4/SvJae * C3H/HeSlc * C57BL/6J * C57BL/6Slc MGI:5285847
cx4
Tsixtm1.1Awu/Tsix+
Tg(CAG-EGFP)50Osb/0
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sortm1(rtTA)Awu
involves: 129P2/OlaHsd * 129S4/SvJae * C3H/HeSlc * C57BL/6J * C57BL/6Slc MGI:5285848
cx5
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sortm1(rtTA)Awu
Xisttm1Awu/Y
involves: 129S4/SvJae MGI:3664738
cx6
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sortm1(rtTA)Awu
Xisttm1Awu/Xisttm1Awu
involves: 129S4/SvJae MGI:3664739


Genotype
MGI:4418526
cn1
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sor+
Hif1atm3Rsjo/Hif1atm3Rsjo
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)26Sortm1(rtTA)Awu mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Hif1atm3Rsjo 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
• hypoxic primary tubular epithelial cells from doxycycline treated mice fails to migrate unlike similarly treated cells from Hif1atm3Rsjo/Hif1atm3Rsjo Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sor+ mice




Genotype
MGI:5285846
cx2
Allelic
Composition
Tsixtm1.1Awu/Tsixtm1.1Awu
Tg(CAG-EGFP)50Osb/0
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sortm1(rtTA)Awu
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C3H/HeSlc * C57BL/6J * C57BL/6Slc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA)Awu mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(CAG-EGFP)50Osb mutation (1 available)
Tsixtm1.1Awu mutation (0 available); any Tsix mutation (57 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• uninduced mice are normal and fertile




Genotype
MGI:5285847
cx3
Allelic
Composition
Tsixtm1.1Awu/Y
Tg(CAG-EGFP)50Osb/0
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sortm1(rtTA)Awu
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C3H/HeSlc * C57BL/6J * C57BL/6Slc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA)Awu mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(CAG-EGFP)50Osb mutation (1 available)
Tsixtm1.1Awu mutation (0 available); any Tsix mutation (57 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• uninduced mice are normal and fertile




Genotype
MGI:5285848
cx4
Allelic
Composition
Tsixtm1.1Awu/Tsix+
Tg(CAG-EGFP)50Osb/0
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sortm1(rtTA)Awu
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C3H/HeSlc * C57BL/6J * C57BL/6Slc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA)Awu mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(CAG-EGFP)50Osb mutation (1 available)
Tsixtm1.1Awu mutation (0 available); any Tsix mutation (57 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• when Tsixtm1.1Awu is inherited paternally, female mice treated with doxycycline from E0.5 exhibit severe developmental defect at E7.5 compared with control mice
• however, no developmental defect is observed when the allele is maternally inherited or when doxycycline treated blastocysts with paternally inherited Tsixtm1.1Awu are transplanted into wild-type recipients
• when Tsixtm1.1Awu is inherited maternally, female mice treated with doxycycline from E6.5 exhibit reduced density of fetal capillaries in the placental labyrinth compared with control mice
• when Tsixtm1.1Awu is inherited paternally, female mice treated with doxycycline from E6.5 exhibit a severe defect in fetal capillaries compared with control mice
• in severely affected female mice treated with doxycycline from E6.5 when Tsixtm1.1Awu is inherited paternally
• at E13.5 in female mice treated with doxycycline from E6.5 or E7.5 when Tsixtm1.1Awu is inherited paternally
• mild at E13.5 in female mice treated with doxycycline from E8.5 when Tsixtm1.1Awu is inherited paternally
• however, female mice treated with doxycycline from E9.5 exhibit normal placenta size at E13.5 when the allele is inherited paternally
• when Tsixtm1.1Awu is inherited paternally, female mice treated with doxycycline from E6.5 exhibit a severe defect in all trophoblast cell types compared with control mice
• when Tsixtm1.1Awu is inherited paternally, female mice treated with doxycycline from E6.5 exhibit overabundant and massively enlarged compared to in control mice
• in severely affected female mice treated with doxycycline from E6.5 when Tsixtm1.1Awu is inherited paternally
• absent in severely affected female mice treated with doxycycline from E6.5 when Tsixtm1.1Awu is inherited paternally

cellular
• increased in female mice treated with doxycycline from E6.5 when Tsixtm1.1Awu is inherited paternally
• in female mice treated with doxycycline from E6.5 when Tsixtm1.1Awu is inherited paternally
• when Tsixtm1.1Awu is inherited paternally, female mice treated with doxycycline from E0.5 fail to imprint and inactivated the paternal X chromosome unlike in control mice

cardiovascular system
• when Tsixtm1.1Awu is inherited maternally, female mice treated with doxycycline from E6.5 exhibit reduced density of fetal capillaries in the placental labyrinth compared with control mice
• when Tsixtm1.1Awu is inherited paternally, female mice treated with doxycycline from E6.5 exhibit a severe defect in fetal capillaries compared with control mice

growth/size/body
• when Tsixtm1.1Awu is inherited paternally, female mice treated with doxycycline from E0.5 exhibit severe developmental defect at E7.5 compared with control mice
• however, no developmental defect is observed when the allele is maternally inherited or when doxycycline treated blastocysts with paternally inherited Tsixtm1.1Awu are transplanted into wild-type recipients




Genotype
MGI:3664738
cx5
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sortm1(rtTA)Awu
Xisttm1Awu/Y
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA)Awu mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Xisttm1Awu mutation (0 available); any Xist mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in mice where doxycycline treatment begins at 4 weeks of age most mice die between 5 to 6 weeks after initiation of treatment with none surviving more than 10 weeks
• mice exposed to doxycycline for 4 days beginning at E12.5 die within 1 day after birth probably as a result of hematopoietic failure
• treatment with doxycycline before E9.5 results in death of the embryo within 3 days

hematopoietic system
• 6 weeks after initiation of doxycycline treatment (started at 4 weeks of age)the thymus is severely reduced in size or absent
• all T cell subsets rapidly decline after initiation of doxycycline treatment (started at 4 weeks of age) producing a strong reduction in overall cellularity
• all T cell subsets rapidly decline in the thymus after initiation of doxycycline treatment (started at 4 weeks of age)
• doxycycline treatment initiated at 4 weeks of age results in rapid loss of lineage committed immature cells; however populations of progenitor cells that include hematopoietic stem cells and pre-pro B cells are expanded 20- and 10-fold, respectively, after 2 weeks of treatment
• a transient expansion of Ter119+ erythroid cells is seen 7 days after initiation of doxycycline treatment (started at 4 weeks of age); however erythroid progenitors are significantly reduced at the same time
• severely reduced in the bone marrow at 5 and 7 days after initiation of doxycycline treatment (started at 4 weeks of age)
• however, mature B cells in the bone marrow and spleen are only slightly affected at 5 and 7 days after initiation of doxycycline treatment (started at 4 weeks of age)
• 2-fold reduction in the bone marrow at 5 and 7 days after initiation of doxycycline treatment (started at 4 weeks of age)
• most rapidly lost of the all the T-cell subsets in the thymus after initiation of doxycycline treatment (started at 4 weeks of age)
• reduction in red cell markers indicates loss of red cells in neonates treated for 4 days with doxycycline beginning at E12.5
• seen 4 weeks after initiation of doxycycline treatment when treatment is started at 4 weeks of age
• seen 6 weeks after initiation of doxycycline treatment (started at 4 weeks of age)
• severe decrease in neonates treated for 4 days with doxycycline beginning at E12.5
• in mice where doxycycline treatment begins at 4 weeks of age hematocrit decreases to 1/10 of untreated controls
• doxycycline treatment-induced loss is more gradual than for macrophages but still significant
• nearly absent in the bone marrow at 5 and 7 days after initiation of doxycycline treatment (started at 4 weeks of age)
• most rapidly lost cell type of the myeloid lineages after doxycycline treatment (started at 4 weeks of age)

embryo
• treatment with doxycycline at E9.5 results in a severely deformed embryo at E13.5

immune system
• 6 weeks after initiation of doxycycline treatment (started at 4 weeks of age)the thymus is severely reduced in size or absent
• all T cell subsets rapidly decline after initiation of doxycycline treatment (started at 4 weeks of age) producing a strong reduction in overall cellularity
• all T cell subsets rapidly decline in the thymus after initiation of doxycycline treatment (started at 4 weeks of age)
• severely reduced in the bone marrow at 5 and 7 days after initiation of doxycycline treatment (started at 4 weeks of age)
• however, mature B cells in the bone marrow and spleen are only slightly affected at 5 and 7 days after initiation of doxycycline treatment (started at 4 weeks of age)
• 2-fold reduction in the bone marrow at 5 and 7 days after initiation of doxycycline treatment (started at 4 weeks of age)
• most rapidly lost of the all the T-cell subsets in the thymus after initiation of doxycycline treatment (started at 4 weeks of age)
• doxycycline treatment-induced loss is more gradual than for macrophages but still significant
• nearly absent in the bone marrow at 5 and 7 days after initiation of doxycycline treatment (started at 4 weeks of age)
• most rapidly lost cell type of the myeloid lineages after doxycycline treatment (started at 4 weeks of age)

behavior/neurological
• 2 weeks after initiation of doxycycline treatment (started at 4 weeks of age) mice appear weak

endocrine/exocrine glands
• 6 weeks after initiation of doxycycline treatment (started at 4 weeks of age)the thymus is severely reduced in size or absent
• all T cell subsets rapidly decline after initiation of doxycycline treatment (started at 4 weeks of age) producing a strong reduction in overall cellularity
• all T cell subsets rapidly decline in the thymus after initiation of doxycycline treatment (started at 4 weeks of age)




Genotype
MGI:3664739
cx6
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA)Awu/Gt(ROSA)26Sortm1(rtTA)Awu
Xisttm1Awu/Xisttm1Awu
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA)Awu mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Xisttm1Awu mutation (0 available); any Xist mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in mice where doxycycline treatment begins at 4 weeks of age most mice die between 5 to 6 weeks after initiation of treatment with none surviving more than 10 weeks

hematopoietic system
• 6 weeks after initiation of doxycycline treatment (started at 4 weeks of age)the thymus is severely reduced in size or absent
• seen 6 weeks after initiation of doxycycline treatment (started at 4 weeks of age)
• in mice where doxycycline treatment begins at 4 weeks of age hematocrit decreases to 1/10 of untreated controls

immune system
• 6 weeks after initiation of doxycycline treatment (started at 4 weeks of age)the thymus is severely reduced in size or absent

behavior/neurological
• 2 weeks after initiation of doxycycline treatment (started at 4 weeks of age) mice appear weak

endocrine/exocrine glands
• 6 weeks after initiation of doxycycline treatment (started at 4 weeks of age)the thymus is severely reduced in size or absent





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)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
11/12/2024
MGI 6.24
The Jackson Laboratory