RBRC00897, B6.Cg-Aicda<tm1Hon> (N10)/HonRbrc

RBRC No. RBRC00897
Type Targeted Mutation CongenicCartagena wks
Species Mus musculus
Strain name B6.Cg-Aicda<tm1Hon> (N10)/HonRbrc
Former Common name AID-KO C57BL/6 N10, B6-AID KO#N10, B6.Cg-Aicda<tm1Hon> (N10)/HonRbrc
H-2 Haplotype No Data
ES cell line TT2 [(C57BL/6NCrlj x CBA/JNCrlj)F1]
Donor strain (C57BL/6 x CBA)F1 via TT2 ES cell line
Background strain No Data
1 Appearance Black
Genotype a/a B/B C/C
Strain development Developed by Tasuku Honjo, Graduate School of Medicine, Kyoto University. The construct was electoroporated into TT2 ES cells derived from (C57BL/6 x CBA)F1. The mutant mice were backcrossed to C57BL/6N.
Strain description AID (Aicda, activation-induced cytidine deaminase) knockout mice. Exon 2 and part of exon 3 were replaced with a neomycin resistance cassette. Aid, Activation-Induced cytidine Deaminase is a molecule which specifically expressed in B lymphocytes after antigen stimulation. AID deficiency caused a complete defect in class switching and showed a hyper-IgM phenotype with enlarged germinal centers containing strongly activated B cells before or after immunization. Accumulation of IgM positive B cell is remarkable in the gut lamina propria. Furthermore, it is suggested that a mutation of the Aid gene was a cause of the hereditary immune deficiency disorder, type-2 hyper-IgM syndrome (HIGM2) in human. As well as class switch recombination, it was also indicated that somatic hypermutation of an immunoglobulin variable region gene and gene conversion do not occur at all in the Aid deficiency mice. Aid gene is a molecule serving as a central role in antibody gene variety acquisition mechanism of B cell.
Colony maintenance Homozygote x Homozygote. Homozygous mutant mice are viable and fertile.
Health Report
Gene Details
Promoter No Data
1 Symbol Aicda
Symbol name Activation-induced cytidine deaminase
Chromosome 6
Common name AID
Symbol description No Data
2 Symbol loxP
Symbol name phage P1 loxP
Chromosome 6
Common name No Data
Symbol description No Data
Promoter mouse phosphoglycerate kinase promoter (PGK promoter)
3 Symbol neo
Symbol name neomycin resistance gene (E. coli)
Chromosome 6
Common name neo; neomycin;
Symbol description No Data
References Cell. 2000 Sep 1;102(5):553-63.

Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme.
Research applications Cre/loxP system,
Immunology and Inflammation Research
Specific Term and Conditions The following terms and conditions will be requested by the DEPOSITOR.
1) The RECIPIENT shall use the BIOLOGICAL RESOURCE only for academic research for the purpose of publishing the research results.
2) In publishing the research results obtained by use of the BIOLOGICAL RESOURCE, an acknowledgment to the DEPOSITOR and a citation of the following literature(s) designated by the DEPOSITOR are requested. Cell 102, 553-563 (2000).
3) RECIPIENT shall notify the PROVIDER upon filing a patent application claiming modification of the BIOLOGICAL RESOURCE or method(s) of manufacture or use(s) of the BIOLOGICAL RESOURCE.
Additional information
1 Honjo Lab HP
2 Mouse of the Month Dec 2005
Genetic Background
3 Genotyping protocol <PCR>
Depositor Honjo, Tasuku (Graduate School of Medicine, Kyoto University) Honjo, Tasuku
Strain Status /
(Expected delivery)

Cryopreserved embryos : Within 1 month
Recovered litters from cryopreserved embryos : 2-4 months

Cryopreserved sperm : Within 1 month
Recovered litters from cryopreserved sperm : 2-4 months

Live mouse :
BRC mice in Publications
Title Journal
IgG and IgE Collaboratively Accelerate Expulsion of Strongyloides venezuelensis in a Primary Infection. Infect Immun.81(7): 2518-27 (2013).(23630966)
Matsumoto M, Sasaki Y, Yasuda K, Takai T, Muramatsu M, Yoshimoto T, Nakanishi K.
Class switch recombination and somatic hypermutation of virus-neutralizing antibodies are not essential for control of friend retrovirus infection. J. Virol.89(2): 1468-73 (2014).(25378499)
Kato M, Tsuji-Kawahara S, Kawasaki Y, Kinoshita S, Chikaishi T, Takamura S, Fujisawa M, Kawada A, Miyazawa M.