Exact(48)
These findings highlight how cell sorting can be used to separate different infection fates and distinguish gene-expression signatures within populations of host and pathogen cells.
Concerning M. phaseolina: i penetration sites of the antagonist and j lysis of the pathogen cells.
They explained their findings due to the presence of viable but non-culturable pathogen cells.
Lipovsky et al. [184] attribute the key role in the pathogen cells inactivation to ROS, particularly to hydroxyl radicals as agents that induce the cell envelope damages.
Hence, our dispersal coefficient D has the same value for hosts and free-living pathogen cells (i.e., pathogen cells disperse to the same extent as the hosts that carry them).
The few mucosal vaccines currently in the marketplace are all based on the use of live-attenuated or dead pathogen cells [3], [5], [6], [7].
Similar(12)
Avraham, R. et al. Pathogen cell-to-cell variability drives heterogeneity in host immune responses.
One mechanism responsible for such resistance involves active removal of the antibiotic from the pathogen cell by MDTs (multidrug transporters).
This effect was observed up to a pathogen cell density of about 5×108 CFU/g stem (Figure 3A, left).
Defense genes in H7996 were noticeably induced even at lower pathogen cell densities (1×107 CFU of GMI1000/gm stem and 3×108 CFU of UW551/gm stem).
H7996 resistance was characterized by a faster response kinetic; the ET and SA pathways were activated at much lower threshold pathogen cell densities in H9776 xylem than in susceptible Bonny Best.
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