Marine phytoplankton are responsible for ~50 % of global primary production and encompass a wide range of microorganisms characterized by being phototrophs. Within this group are the marine picocyanobacteria encompassing the phylogenetically closely related genera Synechococcus and Prochlorococcus. Bacteriophage lysis, as well as grazing by eukaryotic protists, play central roles as the major biotic causes of Synechococcus mortality in pelagic systems. However, Synechococcus populations show no extinction, suggesting high rates of production counteract this mortality, or that specific bacteriophage resistance and prey-selectivity mechanisms exist. This thesis set out to determine the molecular basis of cyanophage resistance in marine Synechococcus, using previously isolated cyanophage resistant Synechococcus sp. WH7803 mutants. Whole genome sequencing (WGS) analysis revealed that these cyanophage-resistant Synechococcus sp. WH7803 mutants, as well as a re-sequenced wild type strain, possessed a distinctive mutation profile, with a high number of mutations present in each mutant and with mutations present at a variable frequency. Such a profile is in stark contrast to what was recently found in Prochlorococcus where specific mutations could be identified at 100 % frequency (Avrani et al., 2011). The mutation profile of Synechococcus sp. WH7803 prevented the precise identification of specific genes involved in cyanophage resistance in this strain. This profile was hypothesised to be related to Synechococcus sp. WH7803 being an oligoploid organism, i.e. possessing more than one chromosome copy. Indeed, a qPCR assay that was optimised showed this strain possesses on average four chromosome copies. Subsequent isolation and WGS characterisation of cyanophage resistant mutants from the monoploid strain Synechococcus sp. WH7805 revealed a completely different mutation profile, most similar to that previously described for Prochlorococcus. This identified mutations in a single gene, encoding a possible glycosyltransferase, that were confirmed by Sanger sequencing, as being potentially responsible for cyanophage resistance in this strain.