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Spontaneous mutant ICR kuru2 might be another shaker-2 deaf mouse
Michiko Watanabe1, Nobutake Akiyama, Yoshinobu Manome
1Institute of DNA Sciences, 261-2 Yamate-cho, Naka-ku, Yokohama, 231-0862, Japan. J0316705@jcom.home.ne.jp
In Vivo (Athens, Greece)
|September 6, 2012
Summary
A novel mouse model, kuru(2), exhibits spontaneous deafness due to a genetic mutation. This research identifies a deletion in the myosin-15 gene as the cause of hearing loss in these mice.
Area of Science:
- Genetics
- Auditory Science
- Animal Models
Background:
- A novel mouse model, kuru(2), was developed over 10 years of sib-inbreeding to study spontaneous deafness.
- This model exhibits hereditary hearing loss, providing a valuable tool for genetic research.
Purpose of the Study:
- To identify the specific genetic mutation responsible for spontaneous deafness in the kuru(2) mouse model.
- To characterize the molecular basis of hearing loss in this unique mouse strain.
Main Methods:
- Genetic analysis involving back-crossing the kuru(2) mouse to Mus musculus castaneus (CAST).
- Gene sequencing to pinpoint the abnormality within the myosin-15 (myoXV) gene on chromosome 11.
Main Results:
- A significant deletion of 2446 base pairs was identified in the Mus musculus unconventional myosin-15 gene (NCBI accession: AF144093).
- The deletion spans a critical region of the gene, including the myosin ATP-binding site.
Conclusions:
- The identified deletion in the myoXV gene is directly linked to the hearing loss observed in the kuru(2) mouse.
- This genetic defect suggests the kuru(2) mouse represents a new variant of the shaker-2 deaf mouse model.
Related Concept Videos
01:16In-vitro Mutagenesis
To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.
01:30Spontaneous and Induced Mutations
Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).