|Ph.D Student||Kirzner Shay|
|Subject||Different Infection Properties of Two Distinct T7-like|
Podoviruses Infecting the Marine Synechococcus
|Department||Department of Biology||Supervisor||Professor Debbie Lindell|
|Full Thesis text|
Recent years have marked a new era in the research of viruses with a growing realization of the importance of marine bacteriophages. They play a central role in gene exchange and are a selective force influencing the genomes of their hosts. Cyanobacterial phages (cyanophages) in particular have received rapidly escalating attention by the scientific community, owing to their high abundance and diversity, the importance of their marine hosts, and novel findings that challenge previously accepted concepts. Despite their importance, little is known about the interactions between cyanophages and their hosts. One of the most abundant cyanophage groups is the T7-like cyanopodoviruses. They are highly host specific and belong to two discrete phylogenetic clades: A and B. The aim of this work was to investigate and compare infection properties of representative viruses from these two clades. The Syn5 virus from clade A infects Synechococcus WH8109 and was already available. Here I isolated a clade B virus, S-TIP37, from the Red Sea that infects the same Synechococcus host and found it to be morphologically and genomically similar to T7. These two cyanopodoviruses resemble T7 in genome content of replication and structural genes. However, they both differ from T7 in carrying other host-like genes and in replicating much more slowly than T7. Syn5 also differs to T7 in transcription of two genes out of their order on the genome and in its impact on host gene expression. In addition, Syn5 and S-TIP37 each carry genes not found in the other. For instance, only Syn5 carries the thioredoxin gene while only S-TIP37 carries photosynthesis-related genes. Both also carry unique genes of unknown function. We found dramatic physiological differences between these two cyanopodoviruses. The attachment to the cells by the clade A virus is much faster than that of the clade B virus. The clade A virus also replicates and transcribes its genome much more rapidly and produces new progeny three times faster than the clade B virus. The clade A virus is more virulent as it kills more cells and also produces a much greater number of viruses per burst cell than the clade B virus. These multiple differences in infection properties suggest involvement of a number of genes that are different between the two viruses. Future research will enable better understanding of the influence of such genes on the observed phenomenon of distinctly different infection strategies of the two viruses.