|Ph.D Student||Avrani Sarit|
|Subject||Resistance of Marine Cyanobacteria to Cyanophage Infection:|
An Experimental Evolution Approach
|Department||Department of Biology||Supervisor||Professor Debbie Lindell|
|Full Thesis text|
Up to 50% of the photosynthesis on earth is carried out in the oceans. A significant part of this photosynthesis is carried out by cyanobacteria belonging to the genus Prochlorococcus, which are extremely abundant in the oceans as are the viruses that infect them. How hosts and viruses coexist in nature remains unclear, although the presence of both susceptible and resistant cells may enable this coexistence. Investigating this hypothesis is the topic of my PhD thesis. Genome analysis of 78 Prochlorococcus substrains selected for resistance to 11 viruses, revealed mutations primarily in non-conserved, horizontally transferred genes that localized to a single hypervariable genomic island. Homology-based annotation of the mutant genes in this susceptibility region suggests that these genes are cell-surface related and include potential cell-wall biosynthesis and modification enzymes (e.g. sugar isomerases and methyl-, carbamoyl- and aminotransferases), a transporter, and proteins of unknown function with predicted membrane domains. These mutations impacted viral attachment to the cell surface and imposed a fitness cost to the host. This cost was manifested by significantly slower growth rates or more rapid infection by other viruses. The latter ‘enhanced infection’ cost was described for the first time in this study. The mutant genes are generally uncommon in nature yet some carry polymorphisms matching those found experimentally. These data indicate that viral attachment genes are preferentially located in genomic islands and that viruses are a selective pressure enhancing their diversity. The result of this diversity of ‘susceptibility genes’ in the oceans is a mix of various Prochlorococcus subpopulations, each being susceptible to a different set of viruses. In this way, the effective size of the host population for infection by a given virus is reduced and no virus can cause the collapse of the entire Prochlorococcus population. Moreover, the adaptive cost of resistance prevents a single resistant bacterial strain from taking over the population. In addition, the novel ‘enhanced infection’ cost of resistance constantly supplies the phage population with novel hosts that replace the hosts that are lost to resistance. Together, this dynamic system enables the coexistence of phage and their hosts in the ocean.