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Unlike the Δppk2 mutant, the ppk1 mutant has no survival defect under aerobic conditions [15], [16].
In PPK-KO, the ppk1 knockout mutant, the ppk1 gene was introduced under the control of the tet promoter.
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M, the molecular mass marker; lane 1, the wide-type; lane 2, the mutant K312E; lane 3, the mutant E539K; lane 4, the mutant T166A/E539K; and lane 5, the mutant K312E/E539K.
Like a met3 mutant, the met6 mutant was avirulent.
Like a met3 mutant, the met6 mutant was a methionine auxotroph.
However, relative to a met3 mutant, the met6 mutant grew very slowly and was less heat-shock resistant.
In contrast to a met3 mutant, the met6 mutant lost viability when starved of methionine, and it was deficient in capsule formation.
Similar to the hog1Δ mutant, the hrk1Δ mutant was highly resistant to fludioxonil, although the hog1Δ mutant was more resistant than the hrk1Δ mutant (Fig. 4A).
In contrast to the F3/A mutant, the W6/A and M10/A mutants did not affect AChE586-599 fibrilization properties.
The pab2 pab8 mutant, the eif3k mutant and the eif3h-1 mutant were grown in continuous light.
Transport was not restored by transfection of the P691S mutant, the P202A/F203A mutant, or NPC1L1.
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