LAUSR

Filamentation is an important biological mechanism that aids in the survival, pathogenesis, and antibiotic resistance of bacteria within different environments, including pathogenic bacteria such as uropathogenic Escherichia coli. Here, we have identified a bacteriophage-encoded cell division inhibitor which contributes to the filamentation that occurs during the SOS response. ABSTRACT Rod-shaped bacteria such as Escherichia coli can regulate cell division in response to stress, leading to filamentation, a process where cell growth and DNA replication continue in the absence of division, resulting in elongated cells. The classic example of stress is DNA damage, which results in the activation of the SOS response. While the inhibition of cell division during SOS has traditionally been attributed to SulA in E. coli, a previous report suggests that the e14 prophage may also encode an SOS-inducible cell division inhibitor, previously named SfiC. However, the exact gene responsible for this division inhibition has remained unknown for over 35 years. A recent high-throughput overexpression screen in E. coli identified the e14 prophage gene, ymfM, as a potential cell division inhibitor. In this study, we show that the inducible expression of ymfM from a plasmid causes filamentation. We show that this expression of ymfM results in the inhibition of Z ring formation and is independent of the well-characterized inhibitors of FtsZ ring assembly in E. coli, SulA, SlmA, and MinC. We confirm that ymfM is the gene responsible for the SfiC phenotype, as it contributes to the filamentation observed during the SOS response. This function is independent of SulA, highlighting that multiple alternative division inhibition pathways exist during the SOS response. Our data also highlight that our current understanding of cell division regulation during the SOS response is incomplete and raises many questions regarding how many inhibitors there actually are and their purpose for the survival of the organism. IMPORTANCE Filamentation is an important biological mechanism that aids in the survival, pathogenesis, and antibiotic resistance of bacteria within different environments, including pathogenic bacteria such as uropathogenic Escherichia coli. Here, we have identified a bacteriophage-encoded cell division inhibitor which contributes to the filamentation that occurs during the SOS response. Our work highlights that there are multiple pathways that inhibit cell division during stress. Identifying and characterizing these pathways are critical steps in understanding survival tactics of bacteria, which become important when combating the development of bacterial resistance to antibiotics and their pathogenicity.