New insights into how Mycobacterium tuberculosis develops antibiotic resistance could have implications for developing more effective treatments for the infection – genetics news

According to a study published today in eLife.

As with other types of bacteria, Mycobacterial tuberculosis (Mr. tuberculosis) is able to form complex structures called biofilms that allow bacterial cells to resist stressors such as antibiotics and immune cells. For this study, the research team developed populations of Mr. tuberculosis In the lab they found that it can form thick biofilms due to mutations in genetic regions that cause multiple changes simultaneously. These findings could benefit the development of antibiotics that target biofilm growth.

As the second leading cause of death from infectious diseases worldwide, tuberculosis is a major public health threat and there is an urgent need for new infection diagnosis, treatment and control strategies.

“Tuberculosis remains a difficult infection to treat due to the bacteria’s ability to persist in the face of antibiotic and immune stress, and to acquire new drug resistance,” says Madison Youngblum, a graduate student in the lead author’s lab. Caitlin Pepperell, University of Wisconsin-Madison, USA, and first co-author of the study along with Tracy Smith, New York Genome Center, NY, USA. To better treat and control tuberculosis, we need to understand the bacteria’s strengths and identify their weaknesses. We wanted to learn more about how they are able to form biofilms by revealing the genes and epigenetic regions involved in biofilm growth, as well as how bacteria evolve in response to changes in their environment. »

To do this, the team used the experimental evolution of Mr. tuberculosis A powerful tool to shed light on the strengths and weaknesses of bacteria that have led to important insights into the fundamental processes that guide their adaptation. They have developed six closely related Mr. tuberculosis Strains are under selective pressure to grow as a biofilm. At regular intervals, they photographed the biofilm and described its growth according to four criteria: the liquid surface covered by the biofilm, its fixation and growth on the sides of the plate, the biofilm thickness and growth continuity (compared to the discontinuous biofilm of growth plates).

Their work revealed that each strain was able to adapt quickly to environmental stress, with the biofilm growing thicker and therefore more robust. The genetic regions mutated during the experiment, which caused the growth of these biofilms, were regulators such as regX3, phoP, embR and Rv2488c. “These regulators control the activity of multiple genes, which means that one mutation can cause many changes simultaneously,” Youngblum says. “It is an efficient process that we observed when we looked at the different characteristics of bacteria, such as the size of their cells and their growth rate.”

In addition, the team found evidence to suggest that the genetic makeup of the parental strain Mr. tuberculosis It had an effect on increasing the growth of biofilms. This means that interactions between genetic factors can play an important role in adaptation to mr. tuberculosis to changing environments.

“Bacteria potentially grow as biofilms in many places, including infecting humans and other hosts, and when colonizing natural and built environments,” says lead author Caitlin Pepperell, principal investigator at the University of Wisconsin-Madison. “In the medical context, the insights gained from our work can be used to explore potential new antibiotics that are better able to attack bacteria that grow in this way. To help shorten and simplify current treatment strategies.”

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