Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A/J inbred strain is widely used in cancer and immunology research. It is highly susceptible to cortisone-induced congenital cleft palate. It has a high incidence of spontaneous lung adenomas, and lung tumors readily develop in response to carcinogens. A high percentage of mammary adenocarcinomas (a large proportion of acinar-type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A/J are much less responsive to LPR than are C57BL/6J, generating less IL10 and having lower mortality. Fulton et al. (2006) mapped this trait to an interval containing Msr1 and found lower MSR1 expression on A/J peritoneal macrophages. Compared with MRS1 from C57BL/6J, A/J MRS1 has a faster electrophoretic mobility and polymorphisms that impact N-linked glycosylation. A/J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid, and 15% fat) fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. <a href="https://www.jax.org/strain/000664">000664</a>; C57L/J, Stock No. <a href="https://www.jax.org/strain/000668">000668</a>, C57BR/cdJ, Stock No. <a href="https://www.jax.org/strain/000667">000667</a>, and SM/J, Stock No. <a href="https://www.jax.org/strain/000687">000687</a>). In addition to atherosclerosis resistance, A/J mice are resistant to diabetes, obesity, insulin resistance and glucose intolerance. On either chow or high fat diet, A/J mice maintain low glucose and insulin levels. A/J mice develop cigarette smoke-induced emphysema in approximately half the time when compared with C57BL/6J mice. Structural lung damage caused by induced asthma mimics the phenotype found in asthma patients more closely than does the induced damage in BALB/c mice. A strain characteristic of A/J is a late onset (four to five months) progressive muscular dystrophy as a result of a homozygous retrotransposon insertion in the dysferlin (Dysf) gene. Myofibers in Dysfprmd homozygotes undergo degeneration and regeneration, and their nuclei are placed centrally. Proximal muscles are more severely affected than distal muscles (Ho M, et al. 2004). Sequencing of the mitochondrial genome of A/J reveals 10 adenines in a polymorphic adenine repeat sequence in the mt-Tr sequence. This repeat contains nine adenines in NOD/ShiLtJ, A/HeJ, A/WySnJ, and SKH2/J and 10 adenines in A/J, and NZB/B1NJ, and likely enhances the hearing loss associated with the Cdh23ahl allele (Johnson et al. 2001). A/J mice are challenging breeders, exhibiting reduced productivity and high incidence of non-productive matings. They may require some special maintenance. A/J mice tend to be very docile and easy to work with. A 2022 study found vaginal septa in &lt;2% of females.

A/J inbred mice are widely used to model cancer and for carcinogen testing given their high susceptibility to carcinogen-induced tumors. Other uses include hybridoma production for immunology applications, cardiovascular research, developmental biology (low background incidence of cleft palate; high susceptibility to cortisone-induced cleft palate) and sensorineural given their early hearing loss. Our preclinical efficacy testing services offer scientific expertise and an array of target-based and phenotype-based outcome measures, both in vivo and at endpoint, for flexible study designs and assay development in mouse models of muscular dystrophy. <a href="https://www.jax.org/jax-mice-and-services/in-vivo-pharmacology/neurobiology-services/muscular-dystrophy-efficacy-studies">See our full service platform</a>.