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Importantly, we showed that the protein levels of the p62 K13R mutant, but not wild-type p62 or the p62 K420R mutant, were not reduced in the presence of wild-type parkin (Fig. 5I).
While levels of starch in both the WT and the mutant were not different (Fig. 6h), significant differences in the sugar levels were determined till 20 days after heading (DAH) (Fig. 6a-e), where the mutant showed higher sucrose and lower hexose levels until 10 DAH (Fig. 6a-d).
The effects of the mutations when combined in the P2P3Shift mutant were not additive (Figure 6B).
As expected, revertants of the lysA deletion mutant were not detected after plating up to 108 particles on a control strain.
Importantly, H3 and H4 acetylation levels in the Δrpd3 mutant were not diminished upon deletion of SET2 (Fig. 3 and Fig. S4).
Since the PilC1 mutant were not found at the respiratory mucosa, but crossed the BBB, it is likely that the mechanisms by which N. meningitidis interacts with these two cellular barriers are different.
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Notably, a S. cerevisiae tkl1 deletion mutant is not able to grow in synthetic complete medium lacking AAAs.
Cheng et al. (2007) demonstrated that NAAT1 mutant was not able to produce DMA and take up Fe(III) efficiently.
The C52 ΔprfA mutant was not available.
As rescue of ΔNLS mutant was not complete, its phenotype was not analysed further.
Moreover, the gemin5 Δ25) mutant was not specifically labeled by the capped RNA.
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