The next challenge is to determine exactly how RUNX1 mutations work together with the loss of the tumor-suppressing protein to drive breast cancer development.
The discussion of animal models highlights a question discussed briefly above, that of whether the mutations work as gain-of- (potentially novel) toxic function or as a dominant-negative.
We now show that these mutations work by counteracting an increase in the cellular levels of reactive oxygen species (ROS) originating from the electron transport pathway, which occurs in wall-deficient cells.
In the past two decades, scientists have investigated how the genes revealed through such mutations work in normal flowers.
We don't know enough about how specific genes and mutations work to understand how they may be advantageous or disadvantageous at the population level.
It has recently been argued that clinical presenilin mutations work as loss-of-function but not toxic gain-of-function.
Cases where multiple mutations work collectively to give resistance, while of clear importance, are not well understood, in part because the range of mutations that can increase a particular bacterium's antibiotic tolerance is rarely known.
Class 1 mutations work to generate excess membrane synthesis [ 7].
These issues are important to resolve, as, without understanding how mutations work, it is hard to develop clear ideas about mechanisms of neurodegeneration.
To find out if the gene mutations worked, we extracted pure starch granules from cassava roots, stained them with an iodine solution and looked at them under a microscope.
