New study reveals bacterial survival strategy

When bacteria enter the human body, the immune system reacts with a series of measures. For example, oxidizing conditions can be created locally, where so-called reactive oxygen radicals are formed in the cells. These oxygen radicals react chemically with the bacteria's proteins and DNA, and can damage them.

Bacteria's defense when faced with changes in the environment, such as oxidative stress, is the formation of multicellular structures called biofilms. In order for bacterial cells to stick together in a biofilm, they synthesize and secrete exopolysaccharides, which are large, sticky molecules that form a protective membrane around the cells. In this way, resistance to stress factors in the surrounding environment increases.

Modifies protein to meet environmental challenges

In bacteria, biofilm formation is controlled by several mechanisms, one of which involves tyrosine kinases, which are proteins that phosphorylate (attach a phosphate group to) key enzymes important in the synthesis and transport of exopolysaccharides.

My group has worked on protein phosphorylation in bacteria for more than two decades, and our interest lies in understanding how bacteria use protein modification to deal with challenges in the surrounding environment. In our study, we saw how the bacteria model, Bacillus subtilismodulates protein tyrosine phosphorylation in order to survive oxidative stress, says Ivan Mijakovic, professor of systems biology at Chalmers University, and the study's research leader.

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It all starts with the enzyme DefA, which is very sensitive to reactive oxygen radicals and is deactivated when oxidized. The inactive form of the enzyme interacts with an important tyrosine kinase, PtkA, i.e Bacillus subtilis This is prohibited. PtkA activity then decreases, which in turn leads to a change in the exopolysaccharides that are formed. This change makes biofilms physically stronger and more resistant to oxidative stress.

– It is important to have a detailed understanding of the molecular mechanism that leads to protein tyrosine kinase inhibition. Molecular mechanisms of this type are usually evolutionarily conserved, and this is what we discovered in our model bacteria B. Kind It is likely to apply to many other bacteria, including pathogens, that is, disease-causing bacteria, says Ivan Mijakovic.

Why is this area of ​​research important and how can the findings be taken forward?

We presented this result at an international conference on post-translational modifications in bacteria, and many researchers working in the field of pathogenic bacteria were interested in it. They will now investigate whether this mechanism exists in their pathogenic bacterial strains. Oxidative stress is critical to the pathogenesis of disease, and this may lead to new ways to fight infections. However, in my group, we will continue to push and increase scientific knowledge at the fundamental level with the help of our team B. KindModel, says Ivan Mijakovic.

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