Dead cells release a ‘necrosignal’ that activates antibiotic survival pathways in bacterial swarms
Nature Communications, ISSN: 2041-1723, Vol: 11, Issue: 1, Page: 4157
2020
- 51Citations
- 179Captures
- 5Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations51
- Citation Indexes51
- 51
- CrossRef28
- Captures179
- Readers179
- 179
- Mentions5
- News Mentions5
- 5
Most Recent News
'Death screams' of swarming bacteria help their comrades survive antibiotic attacks
Swarming bacteria "scream" when they die, warning neighboring bacteria of danger. These death shrieks aren't audible; rather, they are chemical alarms that the bacteria broadcast
Article Description
Swarming is a form of collective bacterial motion enabled by flagella on the surface of semi-solid media. Swarming populations exhibit non-genetic or adaptive resistance to antibiotics, despite sustaining considerable cell death. Here, we show that antibiotic-induced death of a sub-population benefits the swarm by enhancing adaptive resistance in the surviving cells. Killed cells release a resistance-enhancing factor that we identify as AcrA, a periplasmic component of RND efflux pumps. The released AcrA interacts on the surface of live cells with an outer membrane component of the efflux pump, TolC, stimulating drug efflux and inducing expression of other efflux pumps. This phenomenon, which we call ‘necrosignaling’, exists in other Gram-negative and Gram-positive bacteria and displays species-specificity. Given that adaptive resistance is a known incubator for evolving genetic resistance, our findings might be clinically relevant to the rise of multidrug resistance.
Bibliographic Details
Springer Science and Business Media LLC
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