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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Cyp1a1-cre)1Dwi
transgene insertion 1, Douglas J Winton
MGI:3052655
Summary 12 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Rb1tm2Brn/Rb1tm2Brn
Tg(Cyp1a1-cre)1Dwi/0
involves: 129 * C57BL/6 * CBA MGI:5614112
cn2
Rbpjtm1Hon/Rbpjtm1Hon
Tg(Cyp1a1-cre)1Dwi/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3603009
cn3
Ascl2tm1.1Cle/Ascl2tm1.1Cle
Tg(Cyp1a1-cre)1Dwi/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3846692
cn4
Ptentm2Mak/Ptentm2Mak
Tg(Cyp1a1-cre)1Dwi/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3829438
cn5
Brf1tm1Arte/Brf1tm1Arte
Hprt1tm1(CAG-BRF1)Gu/Hprt1+
Tg(Cyp1a1-cre)1Dwi/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:6403686
cn6
Lgr4tm1.1Knis/Lgr4tm1.1Knis
Lgr5tm2.1Cle/Lgr5tm2.1Cle
Tg(Cyp1a1-cre)1Dwi/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:5285826
cn7
Lgr4tm1.1Knis/Lgr4tm1.1Knis
Tg(Cyp1a1-cre)1Dwi/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:5285827
cn8
Lgr5tm2.1Cle/Lgr5tm2.1Cle
Tg(Cyp1a1-cre)1Dwi/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:5285828
cn9
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Cyp1a1-cre)1Dwi/0
involves: C57BL/6 * CBA MGI:3052684
cn10
Brf1tm1Arte/Brf1tm1Arte
Tg(Cyp1a1-cre)1Dwi/0
involves: C57BL/6 * CBA MGI:6403685
cn11
Apctm1Tno/Apc+
Brf1tm1Arte/Brf1tm1Arte
Tg(Cyp1a1-cre)1Dwi/0
involves: C57BL/6 * CBA MGI:6403689
cn12
Orc1tm1.1Gle/Orc1tm1.1Gle
Tg(Cyp1a1-cre)1Dwi/0
involves: C57BL/6 * CBA * SJL MGI:7408229


Genotype
MGI:5614112
cn1
Allelic
Composition
Rb1tm2Brn/Rb1tm2Brn
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm2Brn mutation (3 available); any Rb1 mutation (106 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• increased proliferation of columnar epithelial cells of the villi

digestive/alimentary system
• increased proliferation of columnar epithelial cells of the villi




Genotype
MGI:3603009
cn2
Allelic
Composition
Rbpjtm1Hon/Rbpjtm1Hon
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rbpjtm1Hon mutation (2 available); any Rbpj mutation (193 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 3 and 5 days after injection with beta-naphthoflavone the number of goblet cells is increased in the small intestine and colon
• 5 days after injection with beta-naphthoflavone, essentially all epithelial cell division has stopped in the small intestine and colon, but no significant increase in apoptosis is seen
• 5 days after injection with beta-naphthoflavone, in the small intestine and colon the rapidly dividing transit amplifying compartment is completely replaced by post-mitotic goblet cells
• however, in the small intestine Paneth cell morphology is normal

endocrine/exocrine glands
• 5 days after injection with beta-naphthoflavone, in the small intestine and colon the rapidly dividing transit amplifying compartment is completely replaced by post-mitotic goblet cells
• however, in the small intestine Paneth cell morphology is normal

cellular
• 3 and 5 days after injection with beta-naphthoflavone the number of goblet cells is increased in the small intestine and colon




Genotype
MGI:3846692
cn3
Allelic
Composition
Ascl2tm1.1Cle/Ascl2tm1.1Cle
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ascl2tm1.1Cle mutation (0 available); any Ascl2 mutation (15 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• cre induction leads to an increase in crypt cell apoptosis
• five days after cre-induction, the elongated Olfm4+ stem cells at the base of crypts are absent
• by 15 days after cre-induction, stem cells that have escaped recombination of the floxed allele have completely repopulated the crypts

endocrine/exocrine glands
• five days after cre-induction, the elongated Olfm4+ stem cells at the base of crypts are absent
• by 15 days after cre-induction, stem cells that have escaped recombination of the floxed allele have completely repopulated the crypts

cellular
• cre induction leads to an increase in crypt cell apoptosis




Genotype
MGI:3829438
cn4
Allelic
Composition
Ptentm2Mak/Ptentm2Mak
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2Mak mutation (4 available); any Pten mutation (81 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• in mice induced with beta-naphthoflavonein mice induced with beta-naphthoflavonein mice induced with beta-naphthoflavone
• in mice induced with beta-naphthoflavone
• in one mouse induced with beta-naphthoflavone

neoplasm
• in one mouse induced with beta-naphthoflavone
• in mice induced with beta-naphthoflavone

reproductive system
• mice induced with beta-naphthoflavone exhibit atypical endometrial hyperplasia

behavior/neurological
• in mice induced with beta-naphthoflavone leading to euthanasia

digestive/alimentary system
N
• mice induced with beta-naphthoflavone exhibit normal crypt-villus architecture and physiology

growth/size/body
• in mice induced with beta-naphthoflavonein mice induced with beta-naphthoflavonein mice induced with beta-naphthoflavone




Genotype
MGI:6403686
cn5
Allelic
Composition
Brf1tm1Arte/Brf1tm1Arte
Hprt1tm1(CAG-BRF1)Gu/Hprt1+
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brf1tm1Arte mutation (0 available); any Brf1 mutation (23 available)
Hprt1tm1(CAG-BRF1)Gu mutation (0 available); any Hprt1 mutation (1273 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
N
• mice exhibit normal circulating liver enzyme, liver size, and liver cell proliferation




Genotype
MGI:5285826
cn6
Allelic
Composition
Lgr4tm1.1Knis/Lgr4tm1.1Knis
Lgr5tm2.1Cle/Lgr5tm2.1Cle
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr4tm1.1Knis mutation (0 available); any Lgr4 mutation (94 available)
Lgr5tm2.1Cle mutation (0 available); any Lgr5 mutation (57 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in beta-napthoflavone-treated mice

digestive/alimentary system
• after 5 days, beta-napthoflavone-treated mice exhibit a loss of crypt width with loss of crypt stem cells and proliferating progenitors compared with control mice
• however, wild-type crypt stem cell escapers exhibit proliferation
• in beta-napthoflavone-treated mice

cellular
• after 5 days, beta-napthoflavone-treated mice exhibit a loss of crypt width with loss of crypt stem cells and proliferating progenitors compared with control mice
• however, wild-type crypt stem cell escapers exhibit proliferation




Genotype
MGI:5285827
cn7
Allelic
Composition
Lgr4tm1.1Knis/Lgr4tm1.1Knis
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr4tm1.1Knis mutation (0 available); any Lgr4 mutation (94 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in beta-napthoflavone-treated mice

digestive/alimentary system
• beta-napthoflavone-treated mice exhibit a loss of crypt width with loss of crypt stem cells and proliferating progenitors compared with control mice
• in beta-napthoflavone-treated mice

cellular
• beta-napthoflavone-treated mice exhibit a loss of crypt width with loss of crypt stem cells and proliferating progenitors compared with control mice




Genotype
MGI:5285828
cn8
Allelic
Composition
Lgr5tm2.1Cle/Lgr5tm2.1Cle
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lgr5tm2.1Cle mutation (0 available); any Lgr5 mutation (57 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• beta-napthoflavone-treated mice exhibit normal crypt width and crypt stem cell proliferation




Genotype
MGI:3052684
cn9
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (49 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 4 days after BNF treatment increased apoptosis is seen in crypt epithelium
• 4 days after BNF treatment the number of crypts is reduced however by 5 days post treatment surviving crypts with unrecombined cells are enlarged and show increased proliferation
• the number of Paneth cells is reduced within the crypt 4 days after BNF treatment
• Paneth cells are in abnormal locations within the crypt 4 days after BNF treatment

endocrine/exocrine glands
• 4 days after BNF treatment the number of crypts is reduced however by 5 days post treatment surviving crypts with unrecombined cells are enlarged and show increased proliferation
• the number of Paneth cells is reduced within the crypt 4 days after BNF treatment
• Paneth cells are in abnormal locations within the crypt 4 days after BNF treatment




Genotype
MGI:6403685
cn10
Allelic
Composition
Brf1tm1Arte/Brf1tm1Arte
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brf1tm1Arte mutation (0 available); any Brf1 mutation (23 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• at P8

homeostasis/metabolism
• reduce in polysome loading at P4 in the liver due to shortage of tRNA
• absent polysome at P8

immune system

cellular
• reduce in polysome loading at P4 in the liver due to shortage of tRNA
• absent polysome at P8




Genotype
MGI:6403689
cn11
Allelic
Composition
Apctm1Tno/Apc+
Brf1tm1Arte/Brf1tm1Arte
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Tno mutation (6 available); any Apc mutation (154 available)
Brf1tm1Arte mutation (0 available); any Brf1 mutation (23 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop similar tumor number and size as in Apctm1aTno Tg(Cyp1a1-cre)1Dwi heterozygotes

endocrine/exocrine glands
• mice develop similar tumor number and size as in Apctm1aTno Tg(Cyp1a1-cre)1Dwi heterozygotes




Genotype
MGI:7408229
cn12
Allelic
Composition
Orc1tm1.1Gle/Orc1tm1.1Gle
Tg(Cyp1a1-cre)1Dwi/0
Genetic
Background
involves: C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Orc1tm1.1Gle mutation (0 available); any Orc1 mutation (60 available)
Tg(Cyp1a1-cre)1Dwi mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• the number of cleaved CASPASE-3-positive small intestine crypt cells is increased at 0, 2, 4, and 7 days after beta-napthoflavone (betaNF) treatment
• the number of BrdU-positive small intestine crypt cells is reduced at day 2 but increased by day 4 post-betaNF treatment
• similarly, the number of BrdU/Krt8-double positive crypt cells per small intestine length is reduced at day 2 but increased by day 4 post-betaNF treatment
• at day 2 after the last of 5 consecutive beta-napthoflavone (betaNF) injections, small intestine architecture is severely disrupted, with fewer and smaller crypts and shorter, hypocellular and progressively disorganized villi
• however, by day 4 after the last betaNF injection, ORC1 protein levels are restored to nearly normal levels and a 4- to 5-day repopulation period ensues with enhanced DNA replication, progenitor cell proliferation and crypt hypertrophy such that crypt-villus integrity is fully restored at day 7 post-treatment
• at day 2 post-betaNF treatment, fewer and smaller crypts are observed in the small intestine
• however, crypt integrity is fully restored at day 7 post-betaNF treatment
• at day 2 post-betaNF treatment, small intestine villi are shorter, hypocellular and progressively disorganized
• however, villus integrity is fully restored at day 7 post-betaNF treatment
• small intestine villi are shorter at day 2 but not at day 7 post-betaNF treatment

endocrine/exocrine glands
• at day 2 post-betaNF treatment, fewer and smaller crypts are observed in the small intestine
• however, crypt integrity is fully restored at day 7 post-betaNF treatment

cellular
• the number of cleaved CASPASE-3-positive small intestine crypt cells is increased at 0, 2, 4, and 7 days after beta-napthoflavone (betaNF) treatment
• the number of BrdU-positive small intestine crypt cells is reduced at day 2 but increased by day 4 post-betaNF treatment
• similarly, the number of BrdU/Krt8-double positive crypt cells per small intestine length is reduced at day 2 but increased by day 4 post-betaNF treatment
• DNA replication is enhanced during the 4- to 5-day repopulation period that follows after acute disruption of intestinal integrity

homeostasis/metabolism
• DNA replication is enhanced during the 4- to 5-day repopulation period that follows after acute disruption of intestinal integrity





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory