B6.Cg-Slc2a9tm1.1Thor Albtm1(cre/ERT2)Mtz/ThorOrl
| Status | Available to order |
| EMMA ID | EM:12351 |
| International strain name | B6.Cg-Slc2a9tm1.1Thor Albtm1(cre/ERT2)Mtz/ThorOrl |
| Alternative name | B6-Albtm1(creERT2)Pch Slc2a9tm(lox/lox)Thor |
| Strain type | Targeted Mutant Strains : Knock-in |
| Allele/Transgene symbol | Albtm1(cre/ERT2)Mtz, |
| Gene/Transgene symbol | Alb |
Information from provider
| Provider | Bernard Thorens |
| Provider affiliation | Faculty of Biology and Medicine Center for Integrative Genomics, Universite de Lausanne |
| Genetic information | Full-body conditional knock-out. Exon 4 of Slc2a9 gene was flanked by two loxP sites (Preitner et al. PNAS 2009 Sep 8;106(36):15501-6), allowing its liver-specific and tamoxifen-inducible excision by cre recombinase when Slc2a9 mice are crossed with Alb-creERT2 mice (Schuler M, et al. Genesis. 2004; 39: 167-72). Generation of the liver-specific Slc2a9 knockout mice is described in detail in Preitner et al. PNAS 2009 Sep 8;106(36):15501-6. Producer: Pr Bernard Thorens, UniL, CIG, Lausanne Method of production: Cross-breeding between parental lines (Female: B6-Albtm1(creERT2)Pch; Male: B6-Slc2a9tm(lox/lox)Thor) generates AlbCre(ERT2)-Slc2a9lox/+ mice. These are further crossed with Slc2a9 breeder to generate Slc2a9 lox/lox (controls) and Alb-cre(ERT2)-Slc2a9 lox/lox (inducible mutants). Experimental cohorts are obtained by breeding controls x mutants, yielding 50% of each genotype (control and mutant), i.e. 100% breeding efficacy. |
| Phenotypic information | Homozygous:The LG9 knockout mice (Alb-creERT2;Glut9loxlox) show mild hyperuricemia (120umol/l). No phenotype before tamoxifen-induced gene deletion in Alb-creERT2;Slc2a9lox/lox mice. Mild hyperuricemia after tamoxifen induction, associated with a very mild increase in water intake (+20%) and urine volume, without any observed consequence on the housing requirements (drinking control, cage change), general behaviour, metabolic health (energy homeostasis, glucose homeostasis, blood pressure). No development of any complication with age. Degree of severity assessed retrospectively on more than 100 tamoxifen-induced mice: 0 The Alb-creERT2 transgene allows the tamoxifen-inducible expression of cre recombinase. The Slc2a9 mutation is recessive, as indicated by the absence of phenotype in heterozygous mice. Heterozygous:None |
| Breeding history | Started in 2012; 8 generations. |
| References |
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| Homozygous fertile | not known |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Institut de Transgenose, INTRAGENE, Orléans, France |
| Animals used for archiving | heterozygous C57BL/6J |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- Hereditary renal hypouricemia / Orphanet_94088
- Congenital analbuminemia / Orphanet_86816
Literature references
- Glut9 is a major regulator of urate homeostasis and its genetic inactivation induces hyperuricosuria and urate nephropathy.;Preitner Frédéric, Bonny Olivier, Laverrière Alexandra, Rotman Samuel, Firsov Dmitri, Da Costa Anabela, Metref Salima, Thorens Bernard, ;2009;Proceedings of the National Academy of Sciences of the United States of America;106;15501-6; 19706426
- No development of hypertension in the hyperuricemic liver-Glut9 knockout mouse.;Preitner Frederic, Pimentel Anabela, Metref Salima, Berthonneche Corinne, Sarre Alexandre, Moret Catherine, Rotman Samuel, Centeno Gabriel, Firsov Dmitri, Thorens Bernard, ;2015;Kidney international;87;940-7; 25565311
- Urate-induced acute renal failure and chronic inflammation in liver-specific Glut9 knockout mice.;Preitner Frederic, Laverriere-Loss Alexandra, Metref Salima, Da Costa Anabela, Moret Catherine, Rotman Samuel, Bazin Dominique, Daudon Michel, Sandt Christophe, Dessombz Arnaud, Thorens Bernard, ;2013;American journal of physiology. Renal physiology;305;F786-95; 23804456