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The fibrinolytic activities of Harobin mutants were completely inhibited by PMSF and SBTI, but not by EDTA, EGTA, DTT, indicating that Harobin is a serine protease.

Biochemical and live cell imaging experiments demonstrated that single acylated mutants were completely deacylated with similar kinetic in both cell types.

After root lengthening 2 to 3 d post-IR, radiosensitive atm mutants were completely arrested, whereas WT roots had restarted growth [46].

Whereas wild type MT1 reduced forskolin-stimulated cAMP levels by 30%, MT1-I49N MT1-I212T212T mutants were completely inactive and MT1-G166E MT1-K334N334N were significantly less active compared to wild type receptors (Figure 3A, 3B).

As expected from the combination of defects in several major virulence factors, the mpk1Δ mutants were completely eliminated from the murine lungs by day 4 of the infection (Figure 8).

Using a similar approach we constructed three mutant P particles (R347A, D376A and G441A) of MOH, each with a single residue change in the three GII conserved sites deduced from VA387 (Fig. 3B) and the binding to HBGAs of all three mutants were completely (R347A and D376A) or nearly completely (G441A) lost (Fig. 5 and Table 4).

Interestingly, the two Ala mutants are completely devoid of enzymatic activity.

Each of these mutants was completely defective in NaCl chemotaxis (Fig. 3A).

In EGS, Lys132Ala and Lys132Gln mutants are completely inactive, whereas the Lys132Arg mutant retains partial (71%) activity (Table 2).

Not only that the activity of Δ6 and Δ7 mutants is completely lost, but very low or no recovery is found at 31°C.

As expected, we found that the axon guidance phenotype of lin-23 ot1) lin-23 ot1s comutantsy suppressed by the bar-1(ga80) null allele (Fig. 6C).