The oceans play a major role in determining world climate. In part, this is due to the production of oxygen and the consumption of carbon dioxide by very small, single celled organisms, the photosynthetic picoplankton. Marine cyanobacteria of the closely-related genera Prochlorococcus and Synechococcus form the prokaryotic components of this picophytoplankton assemblage. These organisms can together be responsible for up to 70% of CO2 fixation in some oceanic regions.

Cyanophage, viruses that specifically infect cyanobacteria, shape the structure of picophytoplankton populations and by lysing host cells dramatically affect nutrient cycling by releasing large amounts of cellular material containing carbon and other nutrients back into the system. Moreover, cyanophage have recently been shown to directly inhibit host CO2 fixation capacity likely through their possession of auxiliary metabolic genes (AMGs). These AMGs include core components of photosystem II e.g. psbA, encoding the rapidly turned over D1 protein, which is thought to be vital for maintenance of photosynthesis during the infection process, whilst other AMGs likely subvert host metabolism in a manner yet to be determined.

Elucidation of the functional role of cyanophage AMGs is hampered by the lack of a cyanophage genetic system. Here, we present a random mutagenesis approach using a chemical mutagen that we intend to be generally applicable for assessing the function of such genes during the infection process. The use of next generation sequencing will allow the identification of phage mutants through variant calling using heuristic methods.