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dc.contributor.authorRay, Jessica L.  Concept link
dc.contributor.authorHaramaty, Liti  Concept link
dc.contributor.authorThyrhaug, Runar  Concept link
dc.contributor.authorFredricks, Helen F.  Concept link
dc.contributor.authorVan Mooy, Benjamin A. S.  Concept link
dc.contributor.authorLarsen, Aud  Concept link
dc.contributor.authorBidle, Kay D.  Concept link
dc.contributor.authorSandaa, Ruth-Anne  Concept link
dc.identifier.citationJournal of Plankton Research 36 (2014): 943-955en_US
dc.description© The Author(s), 2014. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Journal of Plankton Research 36 (2014): 943-955, doi:10.1093/plankt/fbu029.en_US
dc.description.abstractThe mechanisms by which phytoplankton cope with stressors in the marine environment are neither fully characterized nor understood. As viruses are the most abundant entities in the global ocean and represent a strong top-down regulator of phytoplankton abundance and diversity, we sought to characterize the cellular response of two marine haptophytes to virus infection in order to gain more knowledge about the nature and diversity of microalgal responses to this chronic biotic stressor. We infected laboratory cultures of the haptophytes Haptolina ericina and Phaeocystis pouchetii with CeV-01B or PpV-01B dsDNA viruses, respectively, and assessed the extent to which host cellular responses resemble programmed cell death (PCD) through the activation of diagnostic molecular and biochemical markers. Pronounced DNA fragmentation and activation of cysteine aspartate-specific proteases (caspases) were only detected in virus-infected cultures of these phytoplankton. Inhibition of host caspase activity by addition of the pan-caspase inhibitor z-VAD-fmk did not impair virus production in either host–virus system, differentiating it from the Emiliania huxleyi-Coccolithovirus model of haptophyte–virus interactions. Nonetheless, our findings point to a general conservation of PCD-like activation during virus infection in ecologically diverse haptophytes, with the subtle heterogeneity of cell death biochemical responses possibly exerting differential regulation on phytoplankton abundance and diversity.en_US
dc.description.sponsorshipFunding to J.L.R, R.-A.S. and A.L. was provided by the Norwegian Research Council for the “VIPMAP” (nr. 186142) and “HAPTODIV” (nr. 190307) projects, and by the European Research Council Advanced Grant ERC-AG-LS8 “Microbial Network Organisation” (MINOS, project number 250254). J.L.R. received a FRIBIO overseas research fellowship from the Norwegian Research Council. K.D.B. and B.V.M. were supported by funding from the United States National Science Foundation (OCE-1061883).en_US
dc.publisherOxford University Pressen_US
dc.rightsAttribution 3.0 Unported*
dc.subjectDNA fragmentationen_US
dc.titleVirus infection of Haptolina ericina and Phaeocystis pouchetii implicates evolutionary conservation of programmed cell death induction in marine haptophyte–virus interactionsen_US

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Attribution 3.0 Unported
Except where otherwise noted, this item's license is described as Attribution 3.0 Unported