Researchers have revealed a fundamental weakness in bacteria that may pave the way for the development of a new generation of antibiotics. Scientists have found that some viruses that infect bacteria can inactivate a vital protein known as MurJ, which is a protein necessary to build the cell wall of bacteria.
Antibiotic-resistant bacteria are one of the most serious health challenges in the world, as they develop rapidly and acquire the ability to resist available medications. This leads to the death of tens of thousands of people annually as a result of infections that no longer respond to traditional treatment. Therefore, scientists seek to discover new weak points that can be targeted with antibiotics different from current medications.
Many researchers focus on the process of building the cell wall of bacteria, because this solid structure made of a substance called peptidoglycan is found only in bacteria and is not found in human cells, which makes it an ideal target for treatment. Some antibiotics, such as penicillin and amoxicillin, actually work by disrupting certain stages of the manufacture of this wall.
The MurJ protein plays a pivotal role in this process, as it acts as a transporter that transports the components of building the cell wall from inside the bacterial cell across the membrane to the outside, where they are assembled to form the wall. If this protein is disrupted, the entire building process stops and the bacteria dies.
Researchers have discovered that viruses that infect bacteria, known as phages, have evolved small proteins capable of inactivating MurJ, and although these viruses are not related to each other, their different proteins inactivate MurJ in much the same way. High-resolution images showed that these viral proteins bind to a specific cleft in MurJ and hold it in one position, preventing it from changing its shape necessary to transport cell wall building materials.
When MurJ is held in this position, the wall-building process stops, which ultimately leads to the death of the bacterial cell. This discovery is important because the form in which the protein is fixed is relatively exposed to the outside, which may make it easier to target for drugs in the future.
The researchers believe that understanding how viruses use to inactivate this protein may help design new antibiotics that mimic this natural mechanism.
If successful, this could provide a new weapon against highly drug-resistant bacteria, a problem that is worsening globally as the effectiveness of current antibiotics declines.
