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A microbe's surprising defense
Posted by Jennifer Evans
[Entry posted at 29th September 2008 11:49 PM GMT]
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A single-celled phytoplankton has a wily way of resisting viral attack, according to a study out this week in the Proceedings of the National Academy of Science. The organism makes itself invisible to its viral predator by shifting from the diploid to haploid life cycle stage.

The findings are the first to show a eukaryote is capable of switching stages in its life cycle to avoid viral attack, and to point to a previously unrecognized role of sexual reproduction in the phytoplankton, Emiliania huxleyi (E. huxleyi), as an alternative to classical evolutionary host-predator dynamic, where hosts and predator co-evolve.

"In this paper, we show how a species can escape from [environmental] pressure by switching to a life-cycle phase or form that's not recognizable by a predator," said Miguel Frada, a marine microbiologist at Equipe Evolution du Plancton et PaleoOceans in France and first author on the study. "By avoiding the [evolutionary] arms race, [E. huxleyi] can keep its highly metabolic way of life" through bloom formation, he said.

E. huxleyi is one of the most abundant microbes in the ocean and forms the basis for most marine food webs. E. huxleyi is characterized by two phenotypically disparate life cycle stages. In the diploid stage, E. huxleyi dons a calcium carbonate coat called a coccolith, and forms extensive blooms that help regulate the chemical equilibrium in the ocean and atmosphere by cycling carbon dioxide. In the haploid stage, the phytoplankton sheds its calcium carbonate outer layer and becomes mobile, using its flagella to navigate.

E. huxleyi blooms undergo rapid cycles, shifting from covering thousands of kilometers to largely disappearing within a matter of weeks, said Kay Bidle, a marine microbiologist at Rutgers University who studies how the organism responds to physiological stress. The blooms' crashes are typically caused by lack of nutrients or the presence of E. huxleyi viruses (EhV), he said.

Frada, who studies the E. huxleyi life cycle, noticed in cell culture experiments that after the virus wiped out the diploid population, flagellated cells that looked like the phytoplankton in their haploid phase remained. These findings, Frada explained, suggested the phytoplankton could be entering a different phase of its life-cycle in order to gain immunity from the virus.

By exposing cultures of diploid and haploid E. huxleyi to EhV Frada's team confirmed that haploid populations of E. huxleyi were resistant to virus. Further tests using transmission electron microscopy and PCR verified that the gene coding for EhV's major capsid protein (MCP) was not absorbed or produced by the haploid populations.

The team also found that exposing mixed haploid-diploid populations of E. huxleyi to EhV over three weeks caused a spike in the numbers of cells in the haploid stage, while diploid populations crashed.

Although the researchers were unable to discern whether the viral infection caused meiosis, or spurred the growth of previously unrecognized haploid cells, the findings suggest a new way to consider sexual reproduction as part of a viral resistance mechanism, Bidle said.

"Even though a bloom collapses after viral attack, the shift to haploid state allows the genetic strain of the host to be conserved so that it can go on to produce subsequent blooms," he explained.

Frada now hopes to move his E. huxleyi observations from the lab to the ocean to begin to understand the concentration of haploid populations of E. huxleyi in nature and how haploid populations contribute to blooms.

"One might argue if haploid phase is really important [to maintain survival], you'd find abundant haploid populations, maybe even as abundant as the diploid populations [observed in nature]," Bidle said. Alternatively, he said, if the concentrations of haploid populations are low, it may suggest haploid populations don't have to be abundant in order to feed populations for future blooms.

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