B6.Cg-Cyp1a1tm1.1Dwn Cyp1a2tm1Dwn Cyp1b1tm1Gonz/H

Status

Available to order

EMMA IDEM:11097
Citation informationRRID:IMSR_EM:11097 

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International strain nameB6.Cg-Cyp1a1tm1.1Dwn Cyp1a2tm1Dwn Cyp1b1tm1Gonz/H
Alternative nameTriple Cyp
Strain typeTargeted Mutant Strains : Knock-out
Allele/Transgene symbolCyp1a1tm1.1Dwn, Cyp1a2tm1Dwn, Cyp1b1tm1Gonz
Gene/Transgene symbolCyp1a1, Cyp1a2, Cyp1b1

Information from provider

ProviderBrigitta Stockinger
Provider affiliationMill Hill Laboratory, The Francis Crick Institute
Genetic informationStock that is homozygous for three knock-outs: Cyp1a1tm1.1Dwn, Cyp1a2tm1Dwn and Cyp1b1tm1Gonz. Stock described as being fully backcrossed to C57BL/6 (initially with C57BL/6J, but latterly with two generations of backcrossing to C57BL/6Nimr).
Phenotypic informationHomozygous:
Mice homozygous for all three knock-out alleles at Cyp1a1, Cyp1a2 and Cyp1b1 have an increased risk of death before embryonic day 11, and exhibit (with reduced penetrance) hydrocephalus, hermaphroditism and cystic ovaries. They also show slower weight gain, but are also prone to develop spontaneous obesity. The activity of many genes has been shown to be perturbed including those involved in: lipid, steroid and cholesterol biosynthesis and metabolism; metal-ion binding; nucleosome and chromatin assembly (see Dragin et al., 2008, Mol Pharmacol 73, (6), 1844-56).

Heterozygous:
Not known; probably no overt phenotype.
Breeding historyStock described as being fully backcrossed to C57BL/6 (initially with C57BL/6J, but latterly with two generations of backcrossing to C57BL/6Nimr). Strain has been bred to homozygosity.
References
  • Feedback control of AHR signalling regulates intestinal immunity.;Schiering Chris, Wincent Emma, Metidji Amina, Iseppon Andrea, Li Ying, Potocnik Alexandre J, Omenetti Sara, Henderson Colin J, Wolf C Roland, Nebert Daniel W, Stockinger Brigitta, ;2017;Nature;542;242-245; 28146477
Homozygous fertileyes
Homozygous viableyes
Homozygous matings requiredno
Immunocompromisedno

Information from EMMA

Archiving centreMary Lyon Centre at MRC Harwell, Oxford, United Kingdom
Animals used for archivinghomozygous C57BL/6 males
Breeding at archiving centreC57BL/6 background

Disease and phenotype information

Orphanet associated rare diseases, based on orthologous gene matching

MGI phenotypes (allele matching)
  • decreased hematocrit / MGI
  • increased neutrophil cell number / MGI
  • abnormal liver physiology / MGI
  • increased circulating alanine transaminase level / MGI
  • increased liver weight / MGI
  • decreased spleen weight / MGI
  • decreased thymus weight / MGI
  • decreased lymphocyte cell number / MGI
  • increased circulating aspartate transaminase level / MGI
  • abnormal hemoglobin content / MGI
  • increased hemoglobin content / MGI
  • increased physiological sensitivity to xenobiotic / MGI
  • decreased physiological sensitivity to xenobiotic / MGI
  • abnormal xenobiotic pharmacokinetics / MGI
  • decreased sensitivity to xenobiotic induced morbidity/mortality / MGI
  • increased susceptibility to weight loss / MGI
  • decreased leukocyte cell number / MGI
  • enlarged liver / MGI
  • small spleen / MGI
  • small thymus / MGI
  • abnormal iridocorneal angle / MGI
  • hypoplastic trabecular meshwork / MGI
  • abnormal canal of Schlemm morphology / MGI
  • decreased incidence of tumors by chemical induction / MGI
  • absent Schlemm's canal / MGI
  • abnormal trabecular meshwork morphology / MGI
  • anterior iris synechia / MGI
MGI phenotypes (gene matching)
  • decreased hematocrit / MGI
  • increased neutrophil cell number / MGI
  • decreased leukocyte cell number / MGI
  • enlarged liver / MGI
  • abnormal liver physiology / MGI
  • small spleen / MGI
  • small thymus / MGI
  • no abnormal phenotype detected / MGI
  • increased circulating alanine transaminase level / MGI
  • increased liver weight / MGI
  • no phenotypic analysis / MGI
  • decreased spleen weight / MGI
  • decreased thymus weight / MGI
  • decreased lymphocyte cell number / MGI
  • increased circulating aspartate transaminase level / MGI
  • homeostasis/metabolism phenotype / MGI
  • cardiovascular system phenotype / MGI
  • abnormal hemoglobin content / MGI
  • increased hemoglobin content / MGI
  • abnormal physiological response to xenobiotic / MGI
  • increased physiological sensitivity to xenobiotic / MGI
  • decreased physiological sensitivity to xenobiotic / MGI
  • abnormal xenobiotic pharmacokinetics / MGI
  • decreased sensitivity to xenobiotic induced morbidity/mortality / MGI
  • increased susceptibility to weight loss / MGI
  • abnormal liver physiology / MGI
  • abnormal lung development / MGI
  • atelectasis / MGI
  • cyanosis / MGI
  • respiratory distress / MGI
  • postnatal lethality / MGI
  • abnormal pulmonary alveolar duct morphology / MGI
  • abnormal type II pneumocyte morphology / MGI
  • no phenotypic analysis / MGI
  • decreased incidence of tumors by chemical induction / MGI
  • abnormal surfactant secretion / MGI
  • liver/biliary system phenotype / MGI
  • endocrine/exocrine gland phenotype / MGI
  • cardiovascular system phenotype / MGI
  • decreased body temperature / MGI
  • abnormal physiological response to xenobiotic / MGI
  • decreased physiological sensitivity to xenobiotic / MGI
  • abnormal xenobiotic pharmacokinetics / MGI
  • absent gastric milk in neonates / MGI
  • enhanced behavioral response to xenobiotic / MGI
  • neonatal lethality, incomplete penetrance / MGI
  • abnormal iridocorneal angle / MGI
  • hypoplastic trabecular meshwork / MGI
  • absent Schlemm's canal / MGI
  • decreased incidence of tumors by chemical induction / MGI
  • abnormal trabecular meshwork morphology / MGI
  • abnormal canal of Schlemm morphology / MGI
  • decreased physiological sensitivity to xenobiotic / MGI
  • anterior iris synechia / MGI

Literature references

  • Feedback control of AHR signalling regulates intestinal immunity.;Schiering Chris, Wincent Emma, Metidji Amina, Iseppon Andrea, Li Ying, Potocnik Alexandre J, Omenetti Sara, Henderson Colin J, Wolf C Roland, Nebert Daniel W, Stockinger Brigitta, ;2017;Nature;542;242-245; 28146477

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