FOA plate show that H658Y has as few colonies as potential wildtype MSH2 control. So, H658Y has nearly-normal MMR function. The mutation occurs in ATPase domain, so maybe human MSH2-H658Y just cannot repair as efficiently as the wildtype one, even though its actual repair machinery is normal.
It is also possible that protein expression level of H658Y is lowered.
In Gammie 2007, H658Y was shown to be '-' on MMR. So, our FOA results are not consistent with Gammie07. It is possible that H658Y cells were substantially lower than wildtype MSH2.
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