Mouse Genome Informatics
cn1
    Cd4tm1.1Tich/Cd4+
Gt(ROSA)26Sortm1(cre/ERT2)Thl/Gt(ROSA)26Sortm1(rtTA*M2)Jae

involves: 129 * 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
immune system
• derepression of Cd4 occurs in all CD4- T cells
• T cell expression of CD4 increases rapidly after cre activation

hematopoietic system
• derepression of Cd4 occurs in all CD4- T cells
• T cell expression of CD4 increases rapidly after cre activation


Mouse Genome Informatics
cn2
    Col1a1tm5(tetO-GFP/RNAi:Cdkn2a)Slowe/Col1a1+
Gt(ROSA)26Sortm1(Luc)Kael/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Krastm4Tyj/Kras+
Tg(Scgb1a1-rtTA)1Jaw/0

involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• mice treated with a cre-expressing adenovirus and treated with doxycycline exhibit reduced survival compared with control mice

tumorigenesis
• mice treated with a cre-expressing adenovirus and treated with doxycycline exhibit increased tumor incidence (size and number) in the lungs with rare noninvasive lung adenomas compared with control mice
• however, mice treated with a cre-expressing adenovirus and treated with doxycycline exhibit tumor regression after doxycycline removal
• in mice treated with a cre-expressing adenovirus and treated with doxycycline

respiratory system
• rapid shallow breathing in mice treated with a cre-expressing adenovirus and treated with doxycycline

growth/size
• in mice treated with a cre-expressing adenovirus and treated with doxycycline


Mouse Genome Informatics
cn3
    Col1a1tm1(tetO-EWSR1/ATF1)Yasu/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(EYFP)Cos
Tg(Mpz-cre)94Imeg/0

involves: 129S4/SvJae * 129X1/SvJ * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• in of all doxycycline-treated mice arising from neural crest-lineage cells


Mouse Genome Informatics
cn4
    Col1a1tm1(tetO-EWSR1/ATF1)Yasu/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(CAG-cat-lacZ)11Miya/0
Tg(Wnt1-cre)11Rth/0

involves: 129S4/SvJae * C57BL/6 * CBA/J * DBA/2
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• in of all doxycycline-treated mice arising from neural crest-lineage cells


Mouse Genome Informatics
cx5
    Col1a1tm9(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

chimera involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
reproductive system
• the founder mouse is sterile


Mouse Genome Informatics
cx6
    Cd4tm1.1Tich/Cd4+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129 * 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
immune system
• 15 days of doxycycline exposure leads to CD4 induction in all but the earliest CD4- thymocytes (not in DN1-3)
• only about 30% of peripheral CD8 cells begin expressing CD4

hematopoietic system
• 15 days of doxycycline exposure leads to CD4 induction in all but the earliest CD4- thymocytes (not in DN1-3)
• only about 30% of peripheral CD8 cells begin expressing CD4


Mouse Genome Informatics
cx7
    Cd4tm1.1Tich/Cd4tm1.1Tich
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae

involves: 129 * 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
immune system
• doxycycline treatment leads to detectable CD4+ CD8+ cells after 2 days
• levels of double positive cells reach 47% by 17 days after the start of treatment

hematopoietic system
• doxycycline treatment leads to detectable CD4+ CD8+ cells after 2 days
• levels of double positive cells reach 47% by 17 days after the start of treatment


Mouse Genome Informatics
cx8
    Col1a1tm1(tetO-Irf4)Sing/Col1a1tm1(tetO-Irf4)Sing
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Irf4tm1Mak/Irf4+

involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
hematopoietic system
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination

immune system
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination


Mouse Genome Informatics
cx9
    Col1a1tm1(tetO-Irf4)Sing/Col1a1tm1(tetO-Irf4)Sing
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Irf4tm1Mak/Irf4tm1Mak

involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
hematopoietic system
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4tm1Mak
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4tm1Mak

immune system
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4tm1Mak
• doxycycline-treated mice exhibit enhanced plasma cell generation at the expense of class switch recombination but not as severe as in mice heterozygous for Irf4tm1Mak


Mouse Genome Informatics
cx10
    Col1a1tm1(tetO-Yod1*)Hpl/Col1a1tm1(tetO-Yod1*)Hpl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Tap1tm1Arp/Tap1tm1Arp

involves: 129S2/SvPas * 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
immune system
• APCs from doxycycline-treated mice exhibit enhanced antigen cross-presentation compared with control cells


Mouse Genome Informatics
cx11
    Col1a1tm2(tetO-Pou5f1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• mice with doxycycline-induced ectopic Oct4 expression become morbid after 3-5 days of treatment and usually die after 5-10 days of treatment
• however, if doxycycline treatment is stopped after 5 days mice completely recover

digestive/alimentary system
• after doxycline treatment, dysplastic cells are found in the entire epithelium; cells have structural and cytological dysplasia which mimics adenocarcinoma
• the proximal part of the small intestine is most severely affected by doxycycline treatment with abnormal cells often almost obstructing the lumen
• after 5 days of doxycycline treatment, proliferative zone expands; postmitotic, differentiated cells lining the villus are replaced
• upon cessation of treatment, cells migrate to final destinations and differentiate resulting in restoration of normal morphology
• in doxycycline treated mice, cells in the forestomach show a marked atypia and increased mitotic activity
• pyloric mucosa contains lesions resembling high grade-dysplasia in doxycycline treated mice
• hyperplastic fundic glands are seen in doxycycline treated mice
• in doxycycline treated mice, forestomach epithelium is thickened and stomach shows lack of differentiation into granular and cornified cell layers compared to control mice
• the thickened epithelium consists of atypical cells with enlarged nuclei and prominent nucleoli
• after doxycycline treatment, mice display severe dysplasia and increased proliferation
• cells show atypia and increased mitotic activity throughout the squamous epithelial layer in doxycycline treated mice

homeostasis/metabolism
• after 3-5 days of doxycycline treatment, animals display severe dehydration

cellular
• abnormal cell proliferation is observed in several organs after 2 days of Oct4-induction
• however, complete reversion is seen with withdrawal of doxycycline treatment

behavior/neurological
• animals become lethargic with doxycycline treatment within 3-5 days

hematopoietic system
• atrophy and absence of CD4, CD8 double positive cells in doxycycline treated mice
• in doxycycline treated mice

immune system
• atrophy and absence of CD4, CD8 double positive cells in doxycycline treated mice
• in doxycycline treated mice

tumorigenesis
• in doxycycline treated mice, tumors originating from the outer-root-sheath progenitors and invading the subcutaneous layer are seen

integument
• increased numbers of immature cells in the hair follicles of the skin are seen after 5-10 days of doxycycline
• after 5-10 days of doxycycline treatment, mice show mild to moderate epidermal dysplasia with a decrease in differentiation in dysplastic cells
• in doxycycline treated mice, tumors originating from the outer-root-sheath progenitors and invading the subcutaneous layer are seen

endocrine/exocrine glands
• atrophy and absence of CD4, CD8 double positive cells in doxycycline treated mice


Mouse Genome Informatics
cx12
    Col1a1tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae/Col1a1tm3(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
normal phenotype
• mice exhibit no tumors or health problems up to 31 weeks


Mouse Genome Informatics
cx13
    Col1a1tm4(tetO-Pou5f1,-Sox2,-Klf4,-Myc)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
phenotype not analyzed


Mouse Genome Informatics
cx14
    Col1a1tm5(tetO-Pou5f1,-Klf4,-Myc)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
phenotype not analyzed


Mouse Genome Informatics
cx15
    Col1a1tm6(tetO-MSI2)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 die within 14 days due to rapid and lethal myeloproliferative disease

hematopoietic system
• at 6 weeks, but not 16 weeks, in wild-type mice reconstituted with bone marrow and treated with doxycyline
• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• at 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1
• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 die within 14 days due to rapid and lethal myeloproliferative disease
• wild-type mice reconstituted with bone marrow and treated with doxycycline exhibit a decrease in myeloid progenitor and myeloid erythrocroid progenitor cells compared with mice reconstituted with wild-type bone marrow
• at 6 weeks, but not 16 weeks, in wild-type mice reconstituted with bone marrow and treated with doxycyline
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1
• doxycycline-treated mice exhibit an expansion of hematopoietic stem cells (HSCs) due to preferential expansion of short term HSC compared with wild-type mice
• wild-type mice reconstituted with bone marrow and treated with doxycycline exhibit an increase in HSCs, hematopoietic progenitor cells, and long term HSCs compared with mice reconstituted with wild-type bone marrow
• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 exhibit increased liver size compared with similarly treated mice reconstituted with wild-type bone marrow
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1
• modestly in doxycycline-treated wild-type mice reconstituted with bone marrow
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

liver/biliary system
• modestly in doxycycline-treated wild-type mice reconstituted with bone marrow
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1

tumorigenesis
• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 exhibit an increase in the number of leukemic blasts and infiltration with immature myeloid cells compared with similarly treated wild-type mice reconstituted with wild-type bone marrow

immune system
• at 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• at 6 and 16 weeks in wild-type mice reconstituted with bone marrow and treated with doxycyline
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1
• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 die within 14 days due to rapid and lethal myeloproliferative disease
• wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1 exhibit increased liver size compared with similarly treated mice reconstituted with wild-type bone marrow
• modestly in doxycycline-treated wild-type mice reconstituted with bone marrow
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1
• in wild-type mice reconstituted with bone marrow, treated with doxycyline, and transduced with BCR-ABL1


Mouse Genome Informatics
cx16
    Col1a1tm1(tetO-GFP/RNAi:luc)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
normal phenotype
• doxycycline-treated mice are normal


Mouse Genome Informatics
cx17
    Col1a1tm2(tetO-GFP/RNAi:Trp53)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
phenotype not analyzed


Mouse Genome Informatics
cx18
    Col1a1tm3(tetO-GFP/RNAi:Apc)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• doxycycline-treated mice with lymphoma exhibit median survival of 7.4 months

skeleton
• at E14.5 and E18.5, mice treated with doxycycline at E8.5 exhibit severely delayed or absent endochondral ossification of multiple skeletal elements (spine, ribs, and limbs) compared with wild-type mice
• mice transiently treated with doxycycline between E8.5 and E12.5 exhibit some reduced bone growth (ribs, spine, and skull) compared with wild-type mice
• at E14.5 and E18.5, mice treated with doxycycline at E8.5 exhibit severely delayed or absent endochondral ossification of multiple skeletal elements (spine, ribs, and limbs) compared with wild-type mice
• mice transiently treated with doxycycline between E8.5 and E12.5 exhibit some reduced bone growth (ribs, spine, and skull) compared with wild-type mice

integument
• mice treated with doxycycline for 6 weeks (either initiated at birth or 4 to 6 weeks of age) exhibit excessive hair growth compared with wild-type mice
• in mice treated with doxycycline beyond 20 weeks
• however, reactivation after 4 weeks by doxycycline withdrawal prevents hair loss
• in mice treated with doxycycline beyond 20 weeks

homeostasis/metabolism
• in mice treated with doxycycline at E8.5
• however, mice transiently treated with doxycycline between E8.5 and E12.5 do not exhibit edema

limbs/digits/tail
• mice transiently treated with doxycycline between E8.5 and E12.5 exhibit extra digits (total 5 to 9) that are largely unsegmented and duplicated along their length compared with wild-type mice
• mice transiently treated with doxycycline between E8.5 and E12.5 exhibit severely stunted hind- and forelimb development compared with wild-type mice
• mice transiently treated with doxycycline between E8.5 and E12.5 exhibit severely stunted hind- and forelimb development compared with wild-type mice

growth/size
• in mice treated with doxycycline 1 to 2 days prior to birth
• reactivation after 4 weeks of doxycycline treatment does not rescue stunted snout
• runting in mice treated with doxycycline 1 to 2 days prior to birth
• in mice treated with doxycycline 1 to 2 days prior to birth
• at E14.5 and E18.5 in mice treated with doxycycline at E8.5

tumorigenesis
• in mice treated with doxycycline from 4 to 6 weeks of age
• in the thymus and lymph nodes of mice treated with doxycycline from 4 to 6 weeks of age
• in mice treated with doxycycline from 4 to 6 weeks of age

craniofacial
• reactivation after 4 weeks of doxycycline treatment does not rescue stunted snout
• in mice treated with doxycycline 1 to 2 days prior to birth


Mouse Genome Informatics
cx19
    Col1a1tm4(tetO-GFP/RNAi:Apc)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• doxycycline-treated mice with lymphoma exhibit median survival or 5.3 months

tumorigenesis
• in mice treated with doxycycline from 4 to 6 weeks of age
• in the thymus and lymph nodes of mice treated with doxycycline from 4 to 6 weeks of age
• in mice treated with doxycycline from 4 to 6 weeks of age

integument
• mice treated with doxycycline for 6 weeks (either initiated at birth or 4 to 6 weeks of age) exhibit excessive hair growth compared with wild-type mice
• in mice treated with doxycycline beyond 20 weeks
• however, reactivation after 4 weeks of doxycycline prevents hair loss
• in mice treated with doxycycline beyond 20 weeks

craniofacial
• in mice treated with doxycycline 1 to 2 days prior to birth
• reactivation after 4 weeks of doxycycline treatment does not rescue stunted snout

growth/size
• in mice treated with doxycycline 1 to 2 days prior to birth
• reactivation after 4 weeks of doxycycline treatment does not rescue stunted snout
• runting in mice treated with doxycycline 1 to 2 days prior to birth
• in mice treated with doxycycline 1 to 2 days prior to birth


Mouse Genome Informatics
cx20
    Col1a1tm5(tetO-GFP/RNAi:Cdkn2a)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
phenotype not analyzed


Mouse Genome Informatics
cx21
    Col1a1tm6(tetO-GFP/RNAi:Cdkn2a)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
phenotype not analyzed


Mouse Genome Informatics
cx22
    Col1a1tm7(tetO-GFP/RNAi:rluc)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
phenotype not analyzed


Mouse Genome Informatics
cx23
    Col1a1tm8(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• most mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size
• in doxycycline-treated mice

cellular
• doxycycline-treated mice exhibit cell cycle arrest unlike control mice


Mouse Genome Informatics
cx24
    Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• when treated in utero with doxycycline, mice die shortly after birth

cellular
• doxycycline-treated mouse embryonic fibroblasts arrest in S phase with increased DNA content compared with untreated cells
• doxycycline-treated mouse embryonic fibroblasts exhibit early cellular replicative senescence compared with untreated cells
• however, withdrawal of doxcycline restores proliferation

normal phenotype
• mice treated with doxycycline during adulthood exhibit no abnormal phenotype


Mouse Genome Informatics
cx25
    Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• all mice treated with doxycycline between 5 and 10 weeks of age die prematurely

digestive/alimentary system
• doxycycline-treated adult mice exhibit atrophy of intestinal epithelium unlike control mice
• however, withdrawal of doxycycline reverses villus atrophy
• doxycycline-treated adult mice exhibit decreased proliferation and cell cycle arrest in the intestinal epithelium unlike control mice

hematopoietic system
• doxycycline-treated adult mice exhibit decreased erythroid precursors in the bone marrow unlike in control mice

growth/size
• in doxycycline-treated adult mice
• however, mice regain weight after withdrawal of doxycycline

cellular
• doxycycline-treated adult mice exhibit decreased proliferation and cell cycle arrest in the intestinal epithelium unlike control mice


Mouse Genome Informatics
cx26
    Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• when treated in utero with doxycycline, mice die shortly after birth

cellular
• doxycycline-treated mouse embryonic fibroblasts arrest in S phase with increased DNA content compared with untreated cells
• doxycycline-treated mouse embryonic fibroblasts exhibit early cellular replicative senescence compared with untreated cells
• however, withdrawal of doxcycline restores proliferation

normal phenotype
• mice treated with doxycycline during adulthood exhibit no abnormal phenotype


Mouse Genome Informatics
cx27
    Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• all mice treated with doxycycline between 5 and 10 weeks of age die prematurely

digestive/alimentary system
• doxycycline-treated adult mice exhibit atrophy of intestinal epithelium unlike control mice
• however, withdrawal of doxycycline reverses villus atrophy
• doxycycline-treated adult mice exhibit decreased proliferation and cell cycle arrest in the intestinal epithelium unlike control mice

hematopoietic system
• doxycycline-treated adult mice exhibit decreased erythroid precursors in the bone marrow unlike in control mice

growth/size
• in doxycycline-treated adult mice
• however, mice regain weight after withdrawal of doxycycline

cellular
• doxycycline-treated adult mice exhibit decreased proliferation and cell cycle arrest in the intestinal epithelium unlike control mice


Mouse Genome Informatics
cx28
    Col1a1tm7(tetO-HIST1H2BJ/GFP)Jae/Col1a1tm7(tetO-HIST1H2BJ/GFP)Jae
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
phenotype not analyzed


Mouse Genome Informatics
cx29
    Col1a1tm1(tetO-Tcfap2c)Hsc/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype

Col1a1tm1(tetO-Tcfap2c)Hsc/Col1a1+ Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+ mice show increased proliferation and induced hepatic steatosis

mortality/aging
• within 6 to 7 days of doxycycline treatment

homeostasis/metabolism
• after doxycycline treatment, mice exhibit increased serum levels of aspartate transaminase, alanine transaminase, alkaline phosphatase, lipase, amylase, lactate dehydrogenase levels compared with control mice
• after doxycycline treatment
• after doxycycline treatment
• after doxycycline treatment
• after doxycycline treatment
• after doxycycline treatment
• after doxycycline treatment

liver/biliary system
• after doxycycline treatment
• after doxycycline treatment
• after doxycycline treatment
• after doxycycline treatment, hepatocytes exhibit abnormally bright mitochondria and increased mitophagy compared to in cells from control mice
• after doxycycline treatment, mice exhibit microvesicular steatosis unlike control mice
• after doxycycline treatment

digestive/alimentary system
• after doxycycline treatment, the proliferative zone is expanded to cover crypt and villus compared to in control mice
• after doxycycline treatment, the number of terminally differentiated intestinal cells (absorptive enterocytes, goblet cells, Paneth, cells and enteroendocrine cells) is reduced compared to in control mice
• after doxycycline treatment
• after doxycycline treatment, the ratio of crypt length to villus length in the duodenum, jejunum, and ileum is increased compared to in control mice

endocrine/exocrine glands
• after doxycycline treatment, mice exhibit pancreatic injury unlike control mice

behavior/neurological
• after doxycycline treatment

growth/size
• after doxycycline treatment

immune system
N
• doxycycline-treated mice do not exhibit induction of inflammatory processes (J:174049)

cellular
• after doxycycline treatment
• after doxycycline treatment, the proliferative zone is expanded to cover crypt and villus compared to in control mice
• after doxycycline treatment


Mouse Genome Informatics
cx30
    Col1a1tm1(tetO-RNAi:Rps19)Karl/Col1a1tm1(tetO-RNAi:Rps19)Karl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• most mice die within 2 months following doxycycline treatment

hematopoietic system
• seven weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• seven weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• decrease in the frequency of bipotential megakaryocytic-erythroid cells and preGM/GMP progenitor cells at 7 weeks after doxycycline treatment
• decrease in the frequency or proerythroblasts in the bone marrow by 10 days after doxycycline treatment
• seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• by 10 days after doxycycline treatment
• absolute numbers of all hematopoietic stem and progenitor cells are reduced at 7 weeks after doxycycline treatment
• seven weeks after doxycycline treatment
• preMegE and preCFU-E/CFU-E progenitors show impaired proliferation and increased apoptosis following doxycycline treatment

growth/size
• following doxycycline treatment

digestive/alimentary system
• occasional dilated glands in the large intestine and colon

immune system
• seven weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment

Mouse Models of Human Disease
OMIM IDRef(s)
Diamond-Blackfan Anemia 1; DBA1 105650 J:179085


Mouse Genome Informatics
cx31
    Col1a1tm1(tetO-RNAi:Rps19)Karl/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
N
• unlike homozygous mice, heterozygotes survive at least 3 months following doxycycline treatment (J:179085)

hematopoietic system
• seven weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• decrease in the frequency of bipotential megakaryocytic-erythroid cells and preGM/GMP progenitor cells at 7 weeks after doxycycline treatment
• decrease in the frequency or proerythroblasts in the bone marrow by 10 days after doxycycline treatment
• two weeks after doxycycline treatment
• by 10 days after doxycycline treatment
• absolute numbers of all hematopoietic stem and progenitor cells are reduced at 7 weeks after doxycycline treatment
• seven weeks after doxycycline treatment
• preMegE and preCFU-E/CFU-E progenitors show impaired proliferation and increased apoptosis following doxycycline treatment

immune system
• two and seven weeks after doxycycline treatment

growth/size
• following doxycycline treatment
• less pronounced than in homozygous mice

Mouse Models of Human Disease
OMIM IDRef(s)
Diamond-Blackfan Anemia 1; DBA1 105650 J:179085


Mouse Genome Informatics
cx32
    Col1a1tm2(tetO-RNAi:Rps19)Karl/Col1a1tm2(tetO-RNAi:Rps19)Karl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• most mice die within 2 months following doxycycline treatment

hematopoietic system
• seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• seven weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• seven weeks after doxycycline treatment

growth/size
• following doxycycline treatment

immune system
• seven weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment

Mouse Models of Human Disease
OMIM IDRef(s)
Diamond-Blackfan Anemia 1; DBA1 105650 J:179085


Mouse Genome Informatics
cx33
    Col1a1tm2(tetO-RNAi:Rps19)Karl/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
N
• unlike homozygous mice, heterozygotes survive at least 3 months following doxycycline treatment (J:179085)

hematopoietic system
• seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• two weeks after doxycycline treatment
• two and seven weeks after doxycycline treatment
• seven weeks after doxycycline treatment

growth/size
• following doxycycline treatment
• less pronounced than in homozygous mice

immune system
• two and seven weeks after doxycycline treatment

Mouse Models of Human Disease
OMIM IDRef(s)
Diamond-Blackfan Anemia 1; DBA1 105650 J:179085


Mouse Genome Informatics
cx34
    Col1a1tm1(tetO-YAP1*)Fcam/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• mice become ill and must be euthanized 4-6 days after doxycycline treatment

digestive/alimentary system
• increased proliferation of epithelium cells in the crypt regions, villus regions and at the tip of the villi of undifferentiated progenitor cells in doxycycline-treated mice
• dipenzazepine administration decreases cell proliferation in the intestine of mice treated with doxycycline
• however, proliferation of undifferentiated cells is reversed by doxycycline-withdrawal
• in doxycycline-treated mice
• ductal metaplasia in doxycycline-treated mice
• severe dysplasia in doxycycline-treated mice
• Paneth cells are absent 5 days after doxycycline treatment
• however, the absence of Paneth cells is reversed by doxycycline-withdrawal
• mature goblet cells are absent 5 days after doxycycline treatment
• however, the absence of mature goblet cells is reversed by doxycycline-withdrawal and administration of dipenzazepine increased goblet cell numbers

endocrine/exocrine glands
• in doxycycline-treated mice
• ductal metaplasia in doxycycline-treated mice
• Paneth cells are absent 5 days after doxycycline treatment
• however, the absence of Paneth cells is reversed by doxycycline-withdrawal
• in doxycycline-treated mice

cellular
• increased proliferation of epithelium cells in the crypt regions, villus regions and at the tip of the villi of undifferentiated progenitor cells in doxycycline-treated mice
• dipenzazepine administration decreases cell proliferation in the intestine of mice treated with doxycycline
• however, proliferation of undifferentiated cells is reversed by doxycycline-withdrawal
• in the epidermis of doxycycline-treated mice

homeostasis/metabolism
• absent in the small intestine 5 days after doxycycline treatment

integument
• in doxycycline-treated mice


Mouse Genome Informatics
cx35
    Col1a1tm1(tetO-Yap1*)Lrsn/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• all mice die 10 days after treatment with doxycycline


Mouse Genome Informatics
cx36
    Col1a1tm2(tetO-Ctnnb1*)Hoch/Col1a1tm2(tetO-Ctnnb1*)Hoch
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
• decreased cell division in colonic cells
• after doxycycline treatment of adults
• number of intestinal stem cells is increased
• crypt fission and budding is normalized after treatment with notch inhibitors
• crypt fission is often observed in the large intestine
• crypt fission is often observed in the small intestine
• suppressed cellular differentiation toward goblet cells

endocrine/exocrine glands
• crypt fission and budding is normalized after treatment with notch inhibitors
• crypt fission is often observed in the large intestine
• crypt fission is often observed in the small intestine


Mouse Genome Informatics
cx37
    Col1a1tm1(tetO-Yod1*)Hpl/Col1a1tm1(tetO-Yod1*)Hpl
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sortm1(rtTA*M2)Jae

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
immune system
N
• doxycycline-treated mice exhibit normal T cell distribution in lymphoid organs (J:194608)
• CD8+ T cells from doxycycline-treated mice exhibit enhanced response to immunization with viral infection and improved viral growth control compared with control cells
• following exposure to ovalbumin, antigen presenting cells (APCs) from doxycycline-treated mice exhibit enhanced antigen cross-production with increased induction of proliferation and IL2 production in OT-I cells compared with control cells
• following infection with MHV-68 and irradiation, bone marrow derived dendritic cells from doxycycline-treated mice prime more effective CD8+ T cell response compared with control cells
• APCs from doxycycline-treated mice exhibit prolonged antigen retention compared with control cells
• cross-presentation in doxycycline-treated mice requires acidification and is insensitive to brefeldin compared to in control cells
• however, antigen presentation in doxycycline-treated mice is normal

hematopoietic system
• CD8+ T cells from doxycycline-treated mice exhibit enhanced response to immunization with viral infection and improved viral growth control compared with control cells


Mouse Genome Informatics
cx38
    Col1a1tm1(tetO-EWSR1/ATF1)Yasu/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• after 3 to 10 months of doxycycline-treated mice with median survival of 20 weeks

tumorigenesis
• in doxycycline-treated mice following withdrawal of doxycycline
• in the trunks, heads, limbs, and whisker pads of all doxycycline-treated mice after 3 months arising from neural crest-lineage cells

cellular
• in doxycycline-treated mouse embryonic fibroblasts


Mouse Genome Informatics
cx39
    Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda/?
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
reproductive system
• in doxycycline-treated neonates


Mouse Genome Informatics
cx40
    ApcMin/Apc+
Col1a1tm9(tetO-Dnmt3b_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apcmin heterozygotes
• doxycycline-treated mice exhibit increased size of microadenomas compared with Apcmin heterozygotes
• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apcmin heterozygotes

cellular
• doxycycline-treated mice exhibit loss of imprinting and increased expression of Igf2 compared with control mice
• doxycycline-treated mice exhibit biallelic methylation of H19 differentially methylated region in tumors and normal colon epithelial cells compared with control mice
• doxycycline-treated mice exhibit hypermethylation of Sfrp2, Sfrp4 and Sfrp5 in tumors and normal colon epithelial cells unlike control mice
• however, mice exhibit normal methylation of of Snrpn differentially methylated region in tumors and normal colon epithelial cells, and global DNA methylation


Mouse Genome Informatics
cx41
    ApcMin/Apc+
Col1a1tm10(tetO-Dnmt3b_i3)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes (J:127808)


Mouse Genome Informatics
cx42
    ApcMin/Apc+
Col1a1tm11(tetO-Dnmt3b_i6)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes (J:127808)


Mouse Genome Informatics
cx43
    ApcMin/Apc+
Col1a1tm12(tetO-Dnmt3a_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes (J:127808)


Mouse Genome Informatics
cx44
    Col1a1tm1(tetO-Deptor)Dmsa/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/?

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
homeostasis/metabolism
• doxycycline treated mice gain more weight on a high fat diet; not caused by a difference in food intake or locomotion
• in doxycycline treated mice on a high fat diet
• MEFs treated with doxycycline and differentiated in adipocytes show increased triglyceride accumulation

adipose tissue
• in doxycycline treated mice on a high fat diet

liver/biliary system
• in doxycycline treated mice on a high fat diet
• in doxycycline treated mice on a high fat diet

growth/size
• doxycycline treated mice gain more weight on a high fat diet; not caused by a difference in food intake or locomotion


Mouse Genome Informatics
cx45
    Col1a1tm1(tetO-CTNNB1)Tcd/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
N
• doxycycline-treated mice exhibit normal villus compartment (J:193365)
• docycycline-treated mice exhibit apoptosis all along the enlarged crypt axis instead of being restricted to the bottom of the crypt as in control mice
• upon withdrawal of doxycycline
• increased in the crypt compartment of doxycycline-treated mice
• doxycycline-treated mice exhibit partially altered intestinal differentiation compared with control mice
• enlarged crypts in doxycycline-treated mice
• however, withdrawal of doxycycline leads to a rapid regression of the crypt compartment

growth/size
• in docycycline-treated mice

endocrine/exocrine glands
• enlarged crypts in doxycycline-treated mice
• however, withdrawal of doxycycline leads to a rapid regression of the crypt compartment

cellular
• docycycline-treated mice exhibit apoptosis all along the enlarged crypt axis instead of being restricted to the bottom of the crypt as in control mice
• upon withdrawal of doxycycline
• increased in the crypt compartment of doxycycline-treated mice


Mouse Genome Informatics
cx46
    Col1a1tm2(tetO-LIN28B)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * CD-1
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
growth/size
• following doxycycline treatment mice gain less weight when fed a high fat diet compared to wild-type mice

homeostasis/metabolism
• following doxycycline treatment mice gain less weight when fed a high fat diet compared to wild-type mice
• following doxycycline treatment average fasting glucose is less than 50 mg/dL
• following doxycycline treatment on a normal or high fat diet
• following doxycycline treatment


Mouse Genome Informatics
cx47
    Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * CD-1
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
growth/size
• following doxycycline treatment
• following doxycycline treatment

homeostasis/metabolism
• in the fed state following doxycycline treatment
• during a glucose tolerance test in doxycycline treated mice
• however, no difference in insulin sensitivity is detected following doxycycline treatment
• following doxycycline treatment on a normal or high fat diet


Mouse Genome Informatics
cx48
    Col1a1tm2(tetO-LIN28B)Gqda/Col1a1tm3(tetO-Mirlet7g/Mir21)Gqda
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * CD-1
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
homeostasis/metabolism
N
• following doxycycline treatment responses in a glucose tolerance test are similar to controls (J:177113)


Mouse Genome Informatics
cx49
    Col1a1tm8(tetO-GFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(CMV-rtTA)4Bjd/0

involves: 129S4/SvJae * C57BL/6 * NMRI
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• half of mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size
• in doxycycline-treated mice

cellular
• doxycycline-treated mice exhibit cell cycle arrest in the liver, spleen, and intestine unlike control mice


Mouse Genome Informatics
cx50
    Col1a1tm10(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(CMV-rtTA)4Bjd/0

involves: 129S4/SvJae * C57BL/6 * NMRI
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• most mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size
• in doxycycline-treated mice


Mouse Genome Informatics
cx51
    Col1a1tm11(tetO*-RFP/RNAi:Rpa3)Slowe/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Tg(CMV-rtTA)4Bjd/0

involves: 129S4/SvJae * C57BL/6 * NMRI
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• most mice treated with doxycycline between 5 and 10 weeks of age die prematurely

growth/size
• in doxycycline-treated mice