Theoretical models explain the biological phenomena that keep the shape of bacteria

Review by Emily Henderson, Bachelor of ScienceOctober 7, 2020

Fat bacteria? Skinny bacteria? From a height point of view, they all seem to be about the same size. In fact, they are.

According to Rice University chemist Anatoly Koromeiski, who currently holds the theory, exactly why it was an open question.

The main mechanism of bacteria is to keep them in the individual Goldilocks zone (that is, just right). It seems to rely on growth and division, two random regulators that cancel each other out. The same mechanism may give researchers a new perspective on diseases, including cancer.

The “minimum model” by Rice’s postdoctoral researcher and lead author Hamid Teimouri and Rupusha Mukelzy, a former research assistant at Rice at the Indian Institute of Technology Gandhinagar, has been published in the American Chemical Society. Journal of Physical Chemistry Letters..

Wherever we see bacteria, they are more or less the same size and shape. The same is true for the cells of our tissue. This is a characteristic of homeostasis, where the system attempts to bring in nearly the same physiological parameters such as body temperature, blood pressure, and blood sugar... “

Rice University Chemist Anatoly Koromeiski

“Nature prefers to put these parameters in a very narrow range so that the living system can function most efficiently,” he said. “Deviations from these parameters are a sign of illness.”

Bacteria are a model of homeostasis, sticking to a narrow distribution of size and shape. “But the explanation so far is not good,” said Koromeiski. “As we know, science doesn’t like magic, but something magical-threshold-is suggested to explain it.”

For bacteria, he said, there is no threshold. “In essence, it’s not necessary,” he said. “There are many underlying biochemical processes, but they can be broadly divided into two probabilistic chemical processes: growth and division. Both are random, so these random phenomena are very deterministic. The problem was to explain why it led to good results. “

Rice Labs specializes in theoretical modeling that describes biological phenomena such as genome editing, antibiotic resistance, and cancer growth. Teimouri said the highly efficient chemical bonds between bacterial growth and division are much easier to model.

“Under typical growth conditions, we assumed that the number of division and growth protein precursors was always proportional to cell size,” he said.

This model predicts when bacteria will divide and allows them to optimize their function. The researchers said it was in good agreement with observations, and that manipulating the formula to knock out bacteria from homeostasis proved their point. They said that increasing the theoretical length of post-mitotic bacteria would reduce their size and simply lead to a faster rate of division.

“For short lengths, growth is dominant and keeps the bacteria in the right size,” Kolomeisky said.

He said the same theory does not always apply to large creatures. “The problem is more complicated because we know that humans have many other biochemical pathways that can regulate homeostasis.”

However, this study may give researchers a new perspective on the growth of diseased cells and, for example, the mechanisms that force cancer cells to vary in shape and size.

“One way to determine cancer is to look at deviations from the norm,” Kolomeisky said. “Are there mutations that lead to faster cell growth or faster division? This mechanism, which helps maintain the size and shape of the bacteria, may help us understand what is happening there. . “