Secrets of shape-shifting bacteria decoded

Scientists have found how bacteria lose the cell walls that define their shapes, become less visible to the immune system, then revert to original form and regain full infectious potential.
Using time-lapse microscopy and other new techniques, Stanford University bioengineering professor KC Huang and colleagues have created a forensic account detailing exactly how bacteria pull off their shape-shifting trick.
The experiments they described in the journal Molecular Microbiology also shed light on one of the ways bacteria may develop antibiotic resistance.
Huang's team experimented with E coli, one of the bacteria that can cause food poisoning.
Their experiments focused on the rigid cell wall that gives E coli its characteristic rod-like shape. When the rigid cell wall is dissolved, the bacterium becomes a shapeless blob called an L-form.

Huang's team used high-resolution microscopes to record time-lapse images of rod-shaped E coli cells becoming L-form blobs and then reverting to rod-shaped again.

E coli's cell wall is knitted together by proteins. Research has shown that one protein, MreB, acts like the conductor, coordinating the efforts of several other proteins.
The researchers grew E coli cells dosed with the antibiotic cefsulodin that prevents E coli from building cell walls. The cefsulodin did not kill the E coli, but as the cells divided and created successive generations, the bacteria lost their rod-shaped walls and became blob-like L-forms.
The bioengineers let the L-forms grow and reproduce for a few hours before flushing out the cefsulodin. As the cells continued to reproduce, the time-lapse images showed that later generations slowly regained their rod-like shape.

To demonstrate the link between the rod shape and MreB, the engineers performed a variation on this experiment. After adding cefsulodin and letting the rod-shaped E coli reproduce to become shapeless L-forms, they again flushed out the antibiotic.
They added a different antibiotic that specifically suppressed MreB function. Two hours later, the cell walls returned, as a rigid structure protecting the cell.
But this time the cells were still shaped like blobs, and eventually all of these misshapen cells died.
"What we found was very stark: MreB was critical for this reversion process to occur, and without MreB what would happen is that the cells would just expand in size without any notion of their normal shape," Huang said.

Huang said the findings could help researchers understand how some bacteria adapt to stressful environments.
Many antibiotics, including penicillin, target the cell wall. But bacteria can lose their cell walls and then later recover their shapes.
This process of reversion might explain how bacteria develop resistance to bacteria and establish chronic infections.