The original aim of this thesis was to utilise Vibrio harveyi luciferase as a reporter of the expression of cell division genes during the cell cycle. Several plasmids expressing luxAB genes from ftsZ promoters were constructed. To achieve maximal luciferase expression, the ribosome binding site in front of the luxA gene was improved, which led to increased expression of luciferase. The level of expression of the improved luciferase reporter from plasmids was sufficiently high to be detected in single cells, although not high enough to be used in lower copy number constructs. However, luciferase activity showed significant fluctuations that did not appear to be linked to cell cycle events. These fluctuations made the detection of any cell cycle related changes in luciferase expression impossible. Another direction of this thesis is represented by the studies on the topology of the cell shape determining RodA protein. The ampicillin resistance levels were measured in 52 fusions with the topology probe BlaM made to different parts of the RodA protein. The combination of the BlaM fusion data and computer modelling argue for a topological structure of this protein consisting of ten transmembrane segments with both ends of the protein located in the cytoplasm. An important feature of the protein appears to be a large periplasmic loop - a highly conserved part of the protein possibly interacting with other members of the shape controlling system. The topology of the protein as well as the location of conserved regions suggests a possible function as a transporter of peptidoglycan precursors. During the course of RodA characterisation a mutation was isolated that permits stable growth of a rodA null strain in rich media. The cause of this stabilisation appears to be a simultaneous increase in the amounts of FtsZ and FtsA proteins.