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In keeping with this notion, we found that the pri2(C4343A) mutant allele exhibited synthetic growth defect with sod1Δ; the double mutant is lethal at 30°C while each single mutant showed only mild growth defect (Fig. 7C).

Since the LinBUT I134V/A247H (=mutantmutant showed only weak LinBMI-type activity in our previous study (Ito et al. [2007]), cumulative mutations at the positions A112, I138, and M253 were introduced into the M2-1 mutant.

Interestingly, fadD1 mutant showed only increased swarming motility.

Mortality assays performed with the bscN mutant showed only a partial difference with K56-2 wild-type (Figure 5C).

In the latter species, even a ppsApckA double mutant showed only a marginal degree of attenuation indicating that gluconeogenesis plays, at most, a minor role for Salmonella virulence.

We found that the apc1 mutant showed only a 1.7-fold difference in centrosome and spindle misorientation (Figure 4C), indicating that the apc1 mutant is partially defective in the centrosome orientation checkpoint.

Further, the C48A/C139A double mutant shows only monomeric behaviour.

In contrast with I323T, the TEA-insensitive Y294V (mSlo) mutant shows only one open level with a long open duration, indicating that its subunits have full cooperativity.

Despite shielding the active site in the apoenzyme and PAD·Ca(10mM 2+, R347 does not prevent calcium binding at Ca2 because the R347A mutant shows only a small effect on the concentration of calcium required for half maximal activity (i.e., K0.5; Table 1).

Lys166 and Gln169 mutants showed only minor changes in substrate specificity profiles.

Interestingly, we found that DLC1 Y442F and S440A mutants showed only a partial reduction in tensin2 binding.