To counteract the defects that are an unavoidable part of aging, bacteria simply proliferate. They grow and divide, grow and divide.

Until now, researchers weren't sure how a dividing cell distributed its defects.

"We wanted to investigate whether the bacteria divided symmetrically with an equal number of defects in both new individuals or whether divided asymmetrically with more defects in one new bacteria than the other," Ala Trusina, an associate professor in biocomplexity at the University of Copenhagen's Niels Bohr Institute, said in a news release.

Researchers combined lab experiments and computer models to determine which strategy is most beneficial.

When bacteria colonies were left alone and undisturbed in a lab setting, proliferating cells shared the burden of aging rather evenly. When stress was introduced, such as heat or a bacteriostatic agent, defects were distributed asymmetrically.

A few individual cells carried consequences of aging, and as a result, grew much more slowly. Their sacrifice allows other divided cells to carry on defect-free, and thus better able to persevere in the face of hardship.

"What we have found is that the asymmetry of cell division is not controlled genetically. It is a process that is controlled by the physical environment," Trusina explained.

"Through collective behavior, the bacterial colony that is exposed to stress can stay young, produce more offspring and keep the colony healthier. This is completely new knowledge that has never been observed before."

How cells regrow after being chopped in half
Orlando, Fla. (UPI) Jul 13, 2016 - New research reveals how cells repair themselves and maintain their shape in the wake of an injury, like being sliced in half.

Scientists wanted to understand the differences in how a cell repairs itself and how it replicates. In other words, how do the methods of maintenance and propagation differ?

To answer the question, researchers focused on the regenerative properties of Stentor, or trumpet animalcules, a genus of filter-feeding protists commonly found along the bottoms of freshwater ponds, streams and lakes.

"I'm interested in understanding how single cells maintain their proper shape," lead researcher Athena Lin, a grad student at the University of California, San Francisco, said in a news release. "Stentor cells are unique because if you cut them in half, removing the mouth, they will regenerate it."

In the lab, researchers sliced off the mouth of Stentor cells and watched them regrow.

A closer look at the regenerative method revealed a two-phase process. First, the cell material that will become new mouth moves into position within the cell. Second, the cell's nucleus -- where its DNA is stored -- shifts its shape.

Scientists noticed the nucleus shape-shift during regeneration is similar to the shape-shift during cell division, and hypothesized the similar mechanisms underlie each process.

To determine which enzymes play a vital role in regeneration, Lin and her fellow researchers began manipulating enzymes previously found to halt or alter cell division -- enzymes that are sometimes used in cancer treatments to slow or stop tumor growth.

They found that a group of enzymes called Aurora kinase play an important role in Stentor cell regeneration.

"These observations were not enough evidence to say that cell division and regeneration have similar pathways, but it gave us a hypothesis to start testing," Lin said.

Aurora kinase enzymes play several roles in the cell division process, but when it comes to cell regeneration, it appears some of those roles are unnecessary. Cell division is a more careful process, and must happen slowly. One type of Aurora kinase serves as a sort of step-by-step roadblock -- vital to healthy cell division, but prohibitive to regeneration.

When researchers inhibited the enzyme, the regeneration process was sped up.

"The cell puts up a stop sign on the regeneration pathway that serves as a 'wait, I'm not ready yet' sign," Lin said.

When the enzyme was inhibited, these stop signs came down. But when another type of Aurora kinase enzyme was inhibited, the whole regenerative process came to a halt.

The latest findings -- presented at the Allied Genetics Conference in Orlando, Florida, this week -- are just an initial step. Lin hopes further research will lead to new insights into the regenerative processes of Stentor cells.