The professor at the CEU Cardenal Herrera University (CEU UCH) Nuria Quiles Puchalt, principal researcher of the MoBiLab research group, has participated in the last findings of characterization of the communication system called ‘arbitrium’which coordinates the decision between the two life cycles that bacterial viruses can follow after the infection process.
These viruses, called phages, once they have infected the bacterial cell, are capable of choosing between continuing with the lytic cycle that will cause the destruction or lysis of the bacteria they infect or integrating into the bacterial genomewhere they will remain in an inactive state, as reported by the academic institution in a statement.
These results, published in the prestigious scientific journal ‘Nature Microbiology’, provide “important” knowledge to advance the use of phages as an alternative to antibiotics in the treatment of multidrug-resistant bacterial infections.
Professor Nuria Quiles has collaborated with the research group led by Dr. Alberto Marina, research professor at the Institute of Biomedicine of Valencia (IBV-CSIC), and with the research group of the Center for Bacterial Resistance Biology (CBRB). , led by José Rafael Penadés, professor at CEU UCH and Imperial College London, where he has directed this British Research Center in recent years.
According to the CEU UCH researcher, “within the molecular study on the life cycle of phages, in which we work from the MoBiLab laboratory, Our most recent results advance our understanding of the small molecule communication system. called arbitrium, which coordinates the decision of which life cycle the phages follow after infecting the bacteria.”
Although the underlying mechanism is still “unknown”, the study published by ‘Nature Microbiology’ reveals “the evolutionary strategy used by this arbitrium system to control the lysis-lysogeny cycle, that is, the selection between the two possible pathways that a phage can continue after infecting a bacterial cell.
Dr. Nuria Quiles has led the characterization of a unique repression system, characteristic of phages with the arbitrium system of the SPbeta family, which has been published in the journal ‘Cell Host & Microbe’, with the participation of Valencian researchers from the CEU UCH, the IBV-CSIC and the CIBER for Rare Diseases (CIBERER), the Imperial College research team and scientists from the Universities of Glasgow and Tel-Aviv.
According to Dr. Quiles, “unlike how other phages repress their lytic genes through a single repressor, the phages that encode the arbitrium system encode at least three repressor proteins, forming a complex that binds to multiple binding sites in the genome. of the phage”.
Recently, Dr. Quiles has also published results from her postdoctoral work carried out at the Center for Bacterial Resistance Biology (CBRB) at Imperial College London.. These discoveries are part of a line of research of “growing interest” in recent years regarding the study of the “immense arsenal” of defense systems that bacteria have to confront viral infections, such as, for example, the defense system CRISPR-Cas.
In these studies it has been characterized how several phages that infect the multidrug-resistant bacteria Staphylococcus aureus They avoid being the target of their own defense systems by encoding an antagonistic system that allows them to block them from developing their life cycle when they are activated. This work also published in ‘Nature Microbiology’ has been led by Dr. Penadés at the CBRB of Imperial College London, and researchers from the Public University of Navarra have participated.
For Nuria Quiles, “advances to understand the behavior of phages at a molecular level are essential if we want to promote alternative strategies to the use of antibiotics to stop the increase in resistance of bacteria, such as Staphylococcus aureus, for which known treatments are leaving to be effective. This is the line of work that we have begun to develop this year from the MoBiLab laboratory of the CEU UCH, dedicated to the study of the Molecular Biology of mobile elements and host bacteria”.
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