Bacterial Cell Walls Are Much More Resilient Than Previously Thought
Bacterial cells are much more resilient than previously thought, a new study suggests, and the findings have implications for fighting disease such as cholera, according to researchers at Stamford University's School of Engineering. Their study, published online Monday in the Proceedings of the National Academy of Sciences represents a 'paradigm shift' in understanding how bacterial cells grow, and may lead to new strategies for fighting bacterial disease.
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A molecular biologist uninvolved in the work hailed the discovery as "a paradigm shift that provides a new molecular understanding of bacterial cell growth." Gurol Suel, PhD, an associate professor at the University of California-San Diego, told the International Science Times, "It was believed that turgor pressure was a driving force for bacterial growth, but the authors present a different mechanism."
Biologists have long believed that it was the growth of a cell's inner mass pressing on its outer membrane that caused cell walls to grow. But the bioengineers at Stamford found that cell wall growth occurrs regardless of internal or external pressures exerted on the cell. They demonstrated this by bathing isolated cells, first in highly concentrated sugars to trigger high osmotic pressure, and then in normal solutions to trigger low osmotic pressure. They then watched as the cells contracted and expanded in reaction to these prods.
Cell walls are porous and subject to the pressure of osmosis, and thus responsive to the amount of solid materials dissolved in a liquid solution. The more solids in the liquid, the greater the osmotic pressure, forcing the cell to flush liquid out through its porous membranes to create equilibrium. If the cell flushes out enough liquid, the cell membrane shrivels up, compacting the cell. Biologists have long supposed that this kind of pressure dynamic retarded cell wall growth. But the researchers found that putting the same cell back into a normal solution, its porous cell wall allowed water to seep back in, causing the cell to swell and resume its former size. "What we observed was not what we had expected," K.C. Huang, PhD, assistant professor of bioengineering and the senior author of the study said in a press release. "The cells just didn't seem to care that they had been subjected to frequent and large osmotic insults in the chamber."
The Stanford team initially looked at cell wall growth in E. coli, but te surprising resilience of cell wall growth spurred lead author Enrique Rojas, PhD, a postdoctoral scholar in bioengineering, to travel to Bangladesh to investigate how bacterial pathogens such as Vibrio cholerae respond to rapidly changing fluid environments.
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