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A possible explanation is that the K residue of the mutant cannot present its side chain to the molecular surface.
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Many of these, e.g. the B3 TFs, have not yet been assigned a specific biological function (Table 3), and the significance of their down-regulation in the ashh2 mutant cannot be evaluated at present.
In contrast, the transactivation-dead p5325,26,53,54 mutant cannot induce senescence or inhibit tumorigenesis, like p53 nullizygosity.
The first mutant cannot invade because patches with type 1 cells and type 2+ mutants are outgrown by patches with type 1 cells and ancestral type 2 cells.
For example, the auxin biosynthesis-defective yuc2 yuc6 double mutant cannot produce grains (Cheng et al. 2006).
If a mutant cannot be distinguished from the original, it is called equivalent.
One cannot present all statistics.
This has been called "stochastic tunneling 4 and is likely to occur in larger populations where deleterious mutants cannot reach fixation.
Within-dimer mutants cannot form dimers and have no activity.
Therefore, bidirectionally incompatible mutants cannot spread under these "sympatric" circumstances.
These results indicate that cohesin ATPase mutants cannot be acetylated.
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