The key step in bacterial cell division is the assembly of the tubulin-like protein FtsZ in a ring structure, the Z ring. The Z ring then acts as a scaffold onto which at least ten more proteins will assemble, creating a large complex known as the divisome and whose activity will build the new division septum. Despite the extensive studies carried out so far, a detailed molecular description of bacterial division is still missing. One of the remaining challenges is to identify the full complement of division proteins in a given organism. Thus, the goal of this project was to use in silico methods to identify novel FtsZ-interacting proteins among the conserved hypothetical proteins whose function has not been established experimentally in B. subtilis.  To do that, we have used the comparative genomics tools available at the STRING (Search Tool for the Retrieval of Interacting Genes) database (http://string.embl.de/), as well as targeted searches of domain functional annotation in the Pfam database (http://www.sanger.ac.uk/Software/Pfam/). Using both methods we identified thirteen new candidates potentially involved with division in B. subtilis. Among these candidates, we focused our efforts initially in the characterization of the hypothetical protein YpbR, which possesses significant similarity to dynamin, a motor protein capable to associate with microtubules and to promote organelle fission in eukaryotes. To test whether YpbR plays a role in division in B. subtilis we constructed a strain bearing a YpbR-GFP fusion and used it in fluorescence microscopy experiments to determine the subcellular localization of YpbR. These experiments revealed an accumulation of YpbR-GFP in midcell membrane structures suggesting that it localizes to the nascent division septum. We have also knocked out ypbR and characterized the ypbR null mutants by microscopy. These experiments revealed that inactivation of YpbR had no apparent phenotype, indicating that YpbR is not essential for division. One possible explanation for the absence of a division phenotype is that YpbR plays a redundant role in septum formation. We are currently combining the ypbR deletion with mutations in other genes to try to identify synthetic phenotypes.