| Project Detail |
Antimicrobial resistance is on the rise and it is predicted to become the first cause of death by 2050. One of the characteristic bacteria phenotypes of antibiotic resistance (and more generally of a stress response) is filamentation, which has been linked to survival strategies and virulence and is present in the most common form of bacteria in nature: biofilms. Thus, characterizing the filamentation phenotype opens the door to understanding the physiology and adaptation of bacterial cells under stress and during colonization processes.
Filamentation results from a coordination of growth and division which are driven by the assembly machinery of the Fts system, the Min oscillatory system, and the nuclear occlusion system. In particular, Fts participates in the septum assembly, a ring-forming cell wall that will separate the daughter cells, whereas the Min oscillatory system restricts the assembly of the division machinery at specific locations to avoid nucleoid cleavage. When bacteria grow regularly, a single septum forms by the middle (symmetric division) to separate the nucleoids of daughter cells. However, when bacteria grow anomalously longer (filamentation), multiple nucleoids continue to segregate along the cell at regular intervals and several putative septa are created. Yet, filamentous bacteria do not grow indefinitely, and division events occur “randomly” (in terms of their timing and the selected septum). This raises the unexplored question of how size is regulated during filamentation processes. In this context, we hypothesize that the interplay between mechanical cues (e.g. filament bending) and changes in the bacteria membrane potential play a key role to regulate bacterial filamentation. Thus, the main objective of this project is determining how mechanosensitive and electrical properties of the division/growth machinery in E. coli regulate its filamentation. |
