Bacteria have developed extensive response systems to survive and prevail with the ever changing environment they are in. In particular, cells are able to carefully regulate cell division to allow time to deal with stressful situations, the canonical example being DNA damage. This regulation leads to the inhibition of cell division, resulting in filamentation, a process in which cell growth continues in the absence division, resulting in elongated cells. This is an important biological mechanism which aids in the survival, pathogenesis and antibiotic resistance of bacteria within different environments, including pathogenic bacteria such as uropathogenic Escherichia coli. However, regulators that enable filamentation remain largely unknown. To identify potential regulators, a novel E. coli expression library was created which allowed for the selection of genes that, when expressed induced filamentation. Filamentous cells were then isolated using flow cytometry based cell sorting. This screen identified several potential division regulators, including ymfM, an SOS (stress response) inducible gene of the e14 prophage. Inhibition of cell division following DNA damage has traditionally been attributed solely to SulA, which inhibits FtsZ polymerization and is activated by the RecA pathway. However,we have identified that ymfM is able to inhibit division independent of SulA, suggesting activation of an alternative pathway during stress. Furthermore, immunofluorescence microscopy of cells induced to express ymfM reveal that inhibition of division occurs at the level of FtsZ ring assembly (early stages of division). These results suggest that there are multiple pathways which regulate cell division during stress. Further work is currently underway to fully elucidate the role of ymfM and to understand the diverse pathways utilised by E. coli during stress. This will not only enable us to understand the intricacies of cell regulation, but also how bacteria are able to cope with stress under various conditions including pathogenesis.