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However, the mutant shows a different orientation in the hinge region that connects two domains of the protein.

The C266M mutant shows a displacement of E306 away from the relevant residue S90 to accommodate the bulky methionine introduced.

The 3D structure of the substrate-free mutant shows a conformation similar to the closed one found in the substrate-bound wild type enzyme, but with a higher degree of disorder in the region of the G-helix and F-G loop.

TGA2's repressor activity overlaps with SNI1 because the tga2-2 sni1-1 double mutant shows a synergistic effect on PR gene expression.

The nal2/nal3 double mutant shows a complex phenotype, with altered development of different parts of the plant and, notably, a strong reduction of the density of lateral roots.

The D32N mutant shows a Km of 87.7 µM for DCoA, almost 2.54-times the WT.

The single myb28 mutant shows a strong reduction of MAM3 expression.

The ubc4Δ mutant shows a shift in peak fluorescence after the arrest that is comparable to wild type (Figure 3C).

The tm3004 mutant shows a decrease in uptake of fatty acid specifically into triglyceride, while the uptake into other phospholipids was not affected.

Only one of the five mutants isolated (the m8 mutant) shows a toxic phenotype strong enough to allow a further characterization.

This mutant shows a weak Daf-c phenotype when treated with RNAi targeted for the strong Daf-c genes daf-2 and daf-19.