Bacteria without their phages are just not competitive.

Abstract

As a veterinarian by training, José Penadés never thought he would stick with a scientific career. For his PhD, he already switched gears and worked on the human autoimmune disease Goodpasture syndrome. However, he quickly realised that studying autoantigens gave him quite a hard time and ‘immunology was just not [my] his thing’. Afterwards he decided to stay in Valencia, Spain, and get some teaching experience at a private school. Yet, here, he recognised that indeed he was missing research. So, José chose to go back to a previous lab where he could apply his newly acquired molecular biology toolbox to their project on bacterial biofilms. He focused on the Gram-positive Staphylococcus aureus and studied how this pathogen forms biofilms to persist in the host. He and his team found a new cell-wall associated protein that they called Bap for biofilm-associated protein showing that proteins are integral parts of bacterial biofilms (Cucarella et al. 2001). They discovered that S. aureus produces Bap and attaches it to its outer membrane as a sensor. Upon contact with a surface or another cell, for example during infection, Bap is cleaved off the bacterial membrane and released to the surrounding. During an inflammatory response in the human body, the pH of the local environment drops. This triggers the N-terminal amyloid-like regions of Bap to form aggregates that further become functional scaffolds of the biofilm matrix (Taglialegna et al. 2016). With this dip into the microbiology world, José was more determined and started to enjoy the scientific process. In comparison with immunological studies, he found microbiological experiments more rewarding, since ‘it is easier to see a phenotype. You can complement and move genes between bacteria as you like and you are pretty confident about the results that you see.’