The energy consumption was then altered so as to produce mutant models with different relative swarming fitness values.
In the present study we used the high growth (hg) mouse mutant model in combination with chromosome 2 (MMU2) congenic and subcongenic strains to map genes that affect body composition, and genes that may interact with the Growth Hormone/IGF signaling pathways [ 5- 7].
Consistently, motif analysis showed that binding sites of several important transcription factors for retinal physiology were hypermethylated in the mutant model, which also correlated with transcriptional silencing of their respective target genes.
As shown in Figure 6 the cAMP and PKAa levels of the mutant model simulations are in agreement with experimentally observed phenotypes.
During the revision of our manuscript, another Lmod3 mutant mouse model with NM was generated by TALEN mutagenesis (Cenik et al., 2015).
In this study, by using a mutant mouse model with oocyte-specific deletion of Tsc1, we found that the tumor suppressor Tsc1 functions in oocytes to suppress follicular activation.
In order to examine the potential involvement of gangliosides in AD (Alzheimer's disease), we compared the ganglioside compositions of the brains of a double-transgenic (Tg) mouse model [APP (amyloid precursor protein)/PSEN1 (presenilin)] of AD and a triple mutant mouse model with an additional deletion of the GD3S (GD3-synthase) gene (APP/PSEN1/GD3S−/−).
We use a mutant mouse model with altered mechanical stimulation due to the absence of limb skeletal muscle (Splotch-delayed) where muscle-less embryos show specific defects in skeletal elements including delayed ossification, changes in the size and shape of cartilage rudiments and joint fusion.
In addition, two mutant models have been established with inactivated tumor suppressor genes.
However, as previous examples have shown, evolutionary mutant models can be combined with established laboratory models for functional and translational studies, e.g. by expressing the gene of interest from the evolutionary model as a transgene in zebrafish and medaka, or by knocking down the zebrafish or medaka homolog (Schartl et al., 2010; Yergeau et al., 2005).
