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Abstract:
Many pathogenic bacteria use the type III secretion system (T3SS)
injectisome to manipulate host cells by injecting virulence-promoting
effector proteins into the host cytosol. The T3SS is activated upon host
cell contact, and its activation is accompanied by an arrest of cell
division; hence, many species maintain a T3SS-inactive sibling
population to propagate efficiently within the host. The enteric
pathogen Yersinia enterocolitica utilizes the T3SS to prevent
phagocytosis and inhibit inflammatory responses. Unlike other species,
almost all Y. enterocolitica are T3SS-positive at 37 degrees C, which
raises the question, how these bacteria are able to propagate within the
host, that is, when and how they stop secretion and restart cell
division after a burst of secretion. Using a fast and quantitative in
vitro secretion assay, we have examined the initiation and termination
of type Ill secretion. We found that effector secretion begins
immediately once the activating signal is present, and instantly stops
when this signal is removed. Following effector secretion, the bacteria
resume division within minutes after being introduced to a non-secreting
environment, and the same bacteria are able to re-initiate effector
secretion at later time points. Our results indicate that Y.
enterocolitica use their type Ill secretion system to promote their
individual survival when necessary, and are able to quickly switch their
behavior toward replication afterwards, possibly gaining an advantage
during infection.
