Virus induced cell death, evasion and resistance in the harmful bloom-forming alga, Heterosigma akashiwo

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Date

2015

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University of New Brunswick

Abstract

Phytoplankton make up a minute proportion of the Earth’s total biomass yet they contribute almost half of global primary productivity, the discrepancy being a result of the rapid turnover of phytoplankton due to grazing and environmentally-induced mortality. Marine viruses also contribute to this high mortality and often outnumber their hosts by at least an order of magnitude. With an estimated 1023 infections per second, viruses can be responsible for the death of 20% of the ocean’s biomass per day. The magnitude of the threat implies that phytoplankton employ strategies to avoid and limit the extent of viral lysis. However, for most phytoplankton groups, there is little knowledge regarding specific defensive strategies. This thesis investigated specific responses activated in the bloom-forming alga Heterosigma akashiwo in response to heat-stress and three viruses (HaV, HaNIV and HaRNAV) and provides evidence that this alga is capable of an active form of cell death known as programmed cell death (PCD). This cell death has classic hallmarks consistent with apoptosis-like cell death in response to heat-stress, HaV and HaNIV infection, and paraptosis during HaRNAV infection. In addition to PCD, Heterosigma is capable of forming resting cells in response to high-heat (40 and 50°C) and to viral infection with HaV, a DNA virus (Phycodnaviridae), which represents a successful but short-term evasion mechanism against cell death in this alga. The various responses, multiple PCD programs and the formation of resting cells, represent cell and population level survival strategies under stress conditions. The resting-cell phase of Heterosigma's life cycle is essential for population survival during viral infection, in addition to the previously reported overwintering survival strategies. This avoidance strategy would contribute to bloom termination by allowing a proportion of the cells to settle out on the ocean floor and would presumably contribute to a “seed stock” for future blooms when the viral load has decreased. Understanding the triggers and mechanisms underlying the virus induced resting-cell formation could also lead to an approach for the control of toxic algae, like Heterosigma, that are known to kill fish and harm coastal environments.

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