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Conidiation in 10-day-old cultures of the ΔpdeL mutant was markedly reduced to approximately 8% of the wild-type strain, while conidia in the ΔpdeH mutant were only reduced approximately 80% (Table 2).
The respective percentages for p40Metcaspase and the K1108A mutant were only ~5 and 2%.
Surprisingly, we found that Tim9 levels in the temperature-sensitive tim9C2,3S mutant were only slightly enhanced at 37°C by deletion of the Yme1 protease (lane 9 compared with 12), but the levels of its partner protein Tim10 were significantly restored in the same mutant.
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The third leaf sheath of slr1 was 123% longer than that of wild type, whereas that of the pla1/slr1 double mutant was only 53% that of the pla1 single mutant (Figure 1C).
TSHR mutant D633A increases the constitutive activity by 13.6-fold compared to the wild type (Table 4), even though the cell surface expression of the mutant is only 26% of that of the wild-type TSHR.
As expected the double mutant was only detected as a monomer (Fig. 2C, lane 8).
Normal growth of the mutant was only restored when CDM was supplemented with potassium at high concentration.
In fact, this mutant was only found to form polymers, detectable by electron microscopy, when ZapA was added.
As clearly shown in Figure 3, the ribH1-ribH2 mutant is only viable at very high concentrations of exogenous flavins.
The rck2Δ mutant is more sensitive to tBOOH and cadmium than WT whereas the rck1Δ mutant is only slightly more sensitive to tBOOH [16].
The A65E mutant is only detected by the H28 anti-AnxA2 antibody, and will be referred to in the paper as AnxA2H28.
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