Thursday, July 11, 2024

Team discovers a new defense mechanism in bacteria

Good news! How many more tricks have bacteria "up their sleeves"?

"When confronted with an antibiotic, toxic substance, or other source of considerable stress, bacteria are able to activate a defense mechanism using cell-to-cell communication to "warn" unaffected bacteria, which can then anticipate, shield themselves and spread the warning signal.
This mechanism has just been described for the first time by a team of scientists ... It paves the way for the development of new, more effective antibiotic treatments that can target this bacterial communication system. ..."

"... Indeed, when a source of stress is perceived by a bacterium, it will become activated: the expression of some of its genes changes and modifies its physiology in order to make it less sensitive to the lethal substance encountered. It will also adorn its surface with small "alarmone" type proteins  which will allow it to activate, by contact and randomly, other neighboring bacteria. However, a sufficient quantity of alarmones is required in contact with non-stressed bacteria to make them change state. Thus, only a source of stress captured by several bacteria triggers a propagation of this activation.
This mechanism offers bacteria several advantages: it limits unnecessary energy expenditure, it allows a rapid and coordinated reaction of the bacterial population and, since the activation of bacteria is progressive, it is a source of diversity within the bacterial population over time, thus increasing its chances of survival. ..."

From the abstract:
"Competence for natural transformation is a central driver of genetic diversity in bacteria. In the human pathogen Streptococcus pneumoniae, competence exhibits a populational character mediated by the stress-induced ComABCDE quorum-sensing (QS) system. Here, we explore how this cell-to-cell communication mechanism proceeds and the functional properties acquired by competent cells grown under lethal stress. We show that populational competence development depends on self-induced cells stochastically emerging in response to stresses, including antibiotics. Competence then propagates through the population from a low threshold density of self-induced cells, defining a biphasic Self-Induction and Propagation (SI&P) QS mechanism. We also reveal that a competent population displays either increased sensitivity or improved tolerance to lethal doses of antibiotics, dependent in the latter case on the competence-induced ComM division inhibitor. Remarkably, these surviving competent cells also display an altered transformation potential. Thus, the unveiled SI&P QS mechanism shapes pneumococcal competence as a health sensor of the clonal population, promoting a bet-hedging strategy that both responds to and drives cells towards heterogeneity."

Team discovers a new defense mechanism in bacteria



Fig. 1: Pneumococcal competence development.


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