The theory of an ongoing evolutionary arms race that is taking
place in biological systems has long been established. This is the idea that
organisms develop defence mechanisms to out run, outwit or out perform their
predators, and subsequently predators evolving strategies to overcome this. A
similar dynamic can be observed in the relationship between organism and
pathogen in cases of infection. This association has been described as the Red
Queen dynamic due to the similarity with the Alice in Wonderland novel in which
Alice is constantly running, yet remaining in the same place. However in some
species this trend is questionable, for example in Emiliania
Huxleyi there are no
geographical subpopulations of host or virus; if local viruses only infected
local hosts, geographical speciation would soon occur. This trend is not seen
in E. huxleyi and its relationship with a giant phycodnaviruses called Emiliania
huxleyi Virus (EhVs), as a virus strain isolated from the North Atlantic
has been shown to be capable of easily infecting host cells originating from
the Mediterranean Sea.
The
coccolithophore E. huxleyi is one of the most successful eukaryotes in
modern oceans and its blooms can be seen from space. This success can be
attributed to a stage in its life-cycle which has exceptionally high phosphate uptake
and very low photoinhibition of photosynthesis. At the end of its life-cycle these
blooms are eradicated by a virus specific to E. huxleyi. This begs the
question of why has little to no ‘evolutionary investment’ gone into a defence
mechanism against this virus?
This paper
shows that E. huxleyi occurs as a haplodiploid organism in which its
lifecycle alternates between the two ploidies. The massive blooms occur as a
calcified, coccolith-bearing diploid phase which can profoundly impact global biochemical equilibria,
and a non-calcified flagellated haploid phase. This sexual cycling is
temporarily separated by an as of yet unknown cause, however this paper
hypothesises that viral infection may trigger meiosis and induces a shift from
diploid to haploid. This viral escape mechanism has been described as a
“Cheshire Cat” method of survival, due to a continuation of the Alice in
Wonderland theme in which the Cheshire cat makes its body invisible in order to
escape beheading. The susceptibility of diploid-stage and haploid-stage cells
to EhVs was tested over a 50 day period and it was found that none of the
haploid strains were sensitive, compared to a 100% infection rate of the
diploid cells. From this it has been hypothesised that even if a diploid stage
bloom is virally eradicated, the motile haploid stage is invisible to the virus
and can therefore enable the continuity of the species.
As eukaryotic
marine protists are responsible for nearly half of global primary productivity
and carbonate production, further research in this area is essential to
understand the genomic control and method of action of this escape strategy as
this significantly advance assessment of marine eukaryotes on biogeochemical
cycles and further reveal details of the control of the flux of matter between
the atmosphere and the lithosphere.
Hi Harri, this is a very interesting strategy to outsmart the virus and I haven’t heard of ploidy change in phytoplankton before. Do the viruses manage to replicate to some extent before the coccolithophores become “invisible” to them? If the Cheshire Cat escape strategy worked perfectly every time (as suggested by their experiment), then the virus would on the long term fail to replicate, so what enables the continuity of the virus?
ReplyDeleteI like how the authors took the allegory of Alice in Wonderland even further.
Hi Anna. Glad you liked it. :)
ReplyDeleteYes, the virus infects the diploid cell which forms massive blooms. Then, only when the bloom is wiped out completely, the haploid cells emerge and these are invisible to the virus and ensure the continuity of the species. The author does state that with the current level of research it is unknown whether the haploid cells are present in the bloom or whether the diploid cells change into haploid cells though.
The second question you state is an interesting point and one which is not mentioned in the paper. The authors offer no explanation on the life cycle of the virus and I would bve interested in finding out the answer to this myself! By purely speculation I would suggest that the virus is present in a dormant state in very low concentrations in oceans where a bloom has previously developed, then becomes active when a bloom occurs (this is purely a speculation though, please don't quote me on that!)
Hi Anna and Harri,
ReplyDeleteWhilst I can't offer any real answers on the point you've brought up on viral life cycles and how they can continue to replicate in the long term, I can offer a few pointers. Firstly about E.huxleyi; ploidy change, or Chesire cat stragegy to avoid the virus, can surely only be short term, as to complete the life cycle and produce gametes it has to return to the diploid phase. And secondly about the virus and it potential dormancy; it is known that different viruses have different viabilities which often depend on environmental factor such as U.V., it may simply be that this virus is viable for longer than the coccolithophore can stay in Chesire cat, haploid mode and still sustain a population.
(Hope that makes sense)
Do you mean that the virus possibly replicates by the lysogenic cycle, so while E. huxleyi thinks it got rid of the virus by passing on to the haploid stage, the virus's nucleic acid is integrated into the genome of its host? So once the coccolithophore "feels safe" and returns to the diploid stage, the virus can attack straight away and replicate. I might have wondered off in the world of speculations.. would be an interesting strategy though and would mean that the virus has its very own version of Chesire cat ;)
ReplyDelete