An international research team at European Molecular Biology Laboratory (EMBL) in Hamburg found the genome of bacteria that performs the toxin-antitoxin system to stop the disease.
The researchers provided a detail analysis of the activity of bacteria that causes tuberculosis. They demonstrated that the bacterium mycobacterium tuberculosis holds 80 so-called toxin-antitoxin (TA) systems inn its genome, which means that the same gene is capable of producing a toxic protein and anti-toxin. When the nutrients are not sufficient for the bacterium to grow, or under stress conditions, dedicated enzymes rapidly degrade the antitoxin molecules.
Annabel Parret, EMBL staff scientist in the Wilmanns group and lead author of the study, said: “Our goal was to see the TA system’s structure, so we could try to understand and even manipulate it. It was as if we were working blindly before. Suicide system in tuberculosis bacteria might hold key to treatment.”
The researchers used a high-resolution structure of mycobacterium tuberculosis bacteria, which revealed a large and compact system with a double-doughnut shape. The structures were similar to the toxins of cholera and diphtheria. “If we find molecules that can disrupt the TA system—and thus trigger cell death—in TB patients, that would be the perfect drug,” explained Parret.
The findings were published in the journal Molecular Cell in February 2019. The researchers studied the toxin-antitoxin system in detail to find a therapeutic targets and allow survival of the antitoxin elements to keep a check on the growth of mycobacterium tuberculosis. Now the scientists are involved in activating the toxin cells in a controlled way in order to increase the lifetime of mice infected with TB.