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.
The better performance of the E53K variant suggests an improved antitoxin activity against Hha, although the possibility that TomB has some residual toxicity that is reduced in the E53K mutant cannot be ruled out.
The mutant did not grow on xylose and lost fermenting ability gradually, indicating that the RD mutant cannot maintain a good fermenting ability on xylose as a sole carbon source.
Importantly, endogenous hBest1 P274R could not be co-immunoprecipitated with virally expressed WT hBest1 or any of the A1 A4 mutants, suggesting that the P274R mutant cannot interfere with the assembly of the pentameric WT/A1 A4 channels (Supplementary Figure 5).
Further, in the scenario where there is cooperation but no competition, we note that while the complex phenotype can arise as an emerging property, the m-hit mutant cannot invade because it does not have a fitness advantage over the "collection of cooperators".
If a mutant cannot be distinguished from the original, it is called equivalent.
For example, the auxin biosynthesis-defective yuc2 yuc6 double mutant cannot produce grains (Cheng et al. 2006).
This result correlates with the finding that ErbB1 ΔNLS mutant cannot interact with nucleolin.
This indicates that this mutant cannot perform at least one of Lhp1's original functions.
β-arrestin1 S412D mutant cannot target receptors to clathrin-coated pits, thus disturbs β-arrestin1 mediated receptor endocytosis.
