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The time course of spontaneous mutation frequency from middle to late adulthood was measured in four different tissues of the mouse. [8] Mutation frequencies in the cerebellum (90% neurons) and male germ cells were lower than in liver and adipose tissue.
The availability of hundreds of mutations affecting almost every tissue and aspect of development. Mice may not be an ideal model for breast cancer. This is mainly due to the lack of precision in many of the models. When looking at metastasis, it is difficult to determine the precise location as well as its frequency.
The human germline mutation rate is approximately 0.5×10 −9 per basepair per year. [1] In genetics, the mutation rate is the frequency of new mutations in a single gene, nucleotide sequence, or organism over time. [2] Mutation rates are not constant and are not limited to a single type of mutation; there are many different types of mutations.
The shiverer mutation is an autosomal recessive loss-of-function mutation. It was generated by a 20-kilobase deletion within the MBP gene, [1] resulting in the failure of oligodendrocytes to form compact myelin in the central nervous system. Axons in shiverer mice fail to attain a normal diameter and exhibit altered cytoskeleton structure. [2]
The validation status list the categories of evidence that support a variant. These include: (1) multiple independent submissions; (2) frequency or genotype data; (3) submitter confirmation; (4) observation of all alleles in at least two chromosomes; (5) genotyped by HapMap ; and (6) sequenced in the 1000 Genomes Project .
The discovery of the athymic mouse, commonly known as the nude mouse, and that of the SCID mouse were major events that paved the way for humanized mice models. The first such mouse model was derived by backcrossing C57BL/Ka and BALB/c mice, featuring a loss of function mutation in the PRKDC gene.
A comparison of a mouse unable to produce leptin thus resulting in obesity (left) and a normal mouse (right) The ob/ob or obese mouse is a mutant mouse that eats excessively due to mutations in the gene responsible for the production of leptin and becomes profoundly obese. It is an animal model of type II diabetes.
Treatment of this mouse model with the procarcinogen azoxymethane (AOM) leads to formation of dysplastic microadenomas in the proximal but not in the distal colon. Thus the K-ras G12D mutant is a valuable mouse model of proximal colon carcinogenesis. Mutation in the Muc2 gene causes adenomas and adenocarcinomas in the intestine of mice. [24]