In order to acquire robust datasets of broad based phenotypes from mouse mutants it is necessary to design and implement pipelines that incorporate standardised phenotyping platforms that are validated across diverse mouse genetics centres or mouse clinics.
Using a simple model in which molecules are classified as master, lethal and non-lethal mutants, it is possible to obtain the mutation rates of the transitions between the three regimes analytically.
Since this robust method is very sensitive for identifying positive mutants, it is also highly suitable for an automated cloning and selection platform.
If the time ever does come when the world is revealed to be full of super-powerful mutants, it is going to be no big deal, so accustomed have we become to the idea.
In the case of WHIM-associated CXCR4 mutants, it is unclear which step or steps are abnormal.
Based on the embryonic lethality of hep mutants it is obvious that Mkk4, which is expressed during embryonic development, cannot substitute for Hep function in this process.
However, in the case of the Atcrt1b single mutants, it is likely that an increased production of, for example, the tunicamycin-sensitive AtCRT1a would mask any growth phenotype.
We find that in a rols, loner double mutant fusion is completely blocked and in other double mutants it is significantly compromised.
It is interesting that in natural and experimentally created mutants it is very rare to observe inversions between individual adjacent organs.
With single gene mutants, it is more feasible to alter in vitro growth conditions, such as cell density, to take account of attenuation.
Given the similar but distinct phenotypes of the pmt1 and pmt4 mutants, it is likely that these two Pmt proteins possess different affinities for Pmt target proteins.
