This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: New research from Indiana University has uncovered a previously unknown vulnerability in how bacteria build the whip-like tails they use to move. The researchers found that building these tails can put stress on the protective wall surrounding a bacterial cell and uncovered systems bacteria use to keep that stress from becoming destructive.
The discovery, published in the Proceedings of the National Academy of Sciences, reveals an unexpected connection between the way bacteria move and the way they maintain the wall that keeps their cells intact. The findings could help scientists find new ways to fight bacterial infections, especially at a time when drug-resistant bacteria are a growing public health threat. The study comes from the laboratory of Daniel Kearns, professor of biology in the College of Arts and Sciences at IU Bloomington, and was co-led by two researchers in the biology department, Caroline Dunn and Kehinde Adebiyi.
Their experiments focused on Bacillus subtilis, a harmless soil bacterium that scientists have long used as a stand-in for studying how bacteria build complex structures, including structures used by bacteria that cause disease. Many disease-causing bacteria, including strains of E. coli, Salmonella and Listeria, rely on a spinning tail called a flagellum to swim through fluids in the body, reach tissue and spread infection. To build that tail, a bacterium has to push a series of parts through its own cell wall, a tough, mesh-like layer made of a material called peptidoglycan.
That wall keeps water from rushing in and bursting the cell open, and it is also the same structure that many existing antibiotics, including penicillin, are designed to attack. Learning exactly what happens to that wall while a flagellum is being built helps scientists understand how bacteria overcome the challenge of getting various structures through their cell wall. It could also reveal a new vulnerability that future drugs might exploit, potentially stopping infections before they start.
Scientists had proposed that bacteria solve this problem because the cell wall isn't perfectly uniform. It naturally contains gaps of different sizes scattered across its surface, and the flagellum's building blocks are thought to search until they find a gap wide enough to fit through. Dunn and Adebiyi set out to directly test that idea.
The researchers removed a cell wall-building protein called PBP1, which might normally repair small gaps in the wall, expecting that fewer patches might create more open holes through which flagella might fit. Instead, something unexpected happened. Without PBP1, the bacteria began dying in large numbers, and the deaths lined up directly with flagellum construction.
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