While the level of horizontal activity of Clock/Clock mutants was similar to the horizontal activity of wild type mice, Clock/Clock mutants demonstrated elevated rearing activity [F[ 1, 5] = 7.65, P = 0.04], which was intermediate between that of wild type and Bmal1-/ animals.
We use mouse mutants to demonstrate that in the absence of Bace1, muscle spindle numbers are reduced and spindle maturation is impaired.
We also show that both insertion mutants demonstrate enhanced tumorigenicity in nude mice.
In contrast, mice infected with an isogenic saeR/S deletion mutant demonstrated significantly reduced pro-inflammatory cytokine levels.
These mutant mice demonstrated variation in muscle fiber size, increase in endomysial connective tissue, and ubiquitin positive sarcoplasmic and myonuclear vacuoles.
These conditional knock-out mouse mutants have been instrumental in demonstrating that miRNAs are vital for inner ear morphogenesis and development of the sensory epithelia and sensory neurons.
Initially, loss of RB had no gross effect on Sertoli cell function as the mice were fertile with normal testis weights at 6 weeks of age, but by 10 14 weeks of age, mutant mice demonstrated severe Sertoli cell dysfunction and infertility.
Analyses of Scrapper mutant mice demonstrated that SCRAPPER-dependent UPS contributes to the regulation of synaptic vesicle release probability via RIM1 [1].
Tydell et al., using mutant mice, demonstrated that also adult DN subsets such as T cell precursors sorted cells express Eva1 [21].
Analysis of these mutant mice demonstrated that loss of presenilins in mature neurons of the cerebral cortex results in progressive impairment in synaptic plasticity and learning and memory, followed by age-dependent neurodegeneration [10], [11].
