Using BrdU incorporation as a marker of mitotic activity in RAM, the authors demonstrate that the mutant displayed a lower level of BrdU at the QC site compared to the control.
The result noted that K116R mutant displayed a stronger capability in degradation of fAβ than its wild-type (Fig. 6A), which is accompanied by observations that more lysosomal compartments were induced in microglia and HeLa cells transfected with TFEB-K116R than TFEB-WT (Figs. 6B and S6B).
As expected, the vpsR mutant displayed a low isosurface volume of biofilm.
The C. jejuni Δppk2 mutant displayed a significant dose-dependent colonization defect in chickens (Figure 8).
As shown in Fig. 3A, the wild-type strain NEM316 (WT) and the ΔpilB mutant displayed a similar survival kinetic in this phagocytic cell line.
The HncsoS4AB Km double knockout mutant displayed a strict hcr phenotype (Figure 3), showing no signs of growth for over 70 h in an ambient CO2 atmosphere.
The K14/A mutant displayed a similar fibril morphology to the ΔK14 mutant, albeit the fibrils were thinner (5.5 to 8.5 nm) and fewer (Figure 9A).
Interestingly, the Δppk2 mutant displayed a significant increase (P≤0.05) in the ability to generate poly P-dependent ATP compared to WT (Figure 1B).
Only the Δcas2 mutant displayed a weak delay in vegetative growth, and this defect was complemented by the elevation of the CO2 concentration.
As compared to its wild-type parent M. smegmatis mc2155, the MSMEG_5084 mutant displayed a significantly reduced growth rate at 37°C.
Fluorescence microscopy analysis showed that the bipD mutant displayed a high level of co-localization with LC3 at 2 h, 4 h and 6 h p.i. (Figure 5C).
