It seems that all known chlamydiae are obligate intracellular symbionts -- they can only reproduce inside eukaryotic cells, and remain metabolically inactive outside of their hosts (a virus-like lifestyle). Chlamydiae can infect different kinds of animals (mammals, birds, fishes, arthropods, crustaceans) and unicellular eukaryotes (such as environmental amoebae). Remarkably, chlamydiae have never been found in plants or in other plastid-containing organisms (red and green algae, plants and glaucophytes, together known as Plantae or Archaeplastida).On the other hand, as I have explained in a previous post (A cell potpourri: eukaryotes and their organelles), an important number of Archaeplastida genes are derived from ancient chlamydiae, suggesting a long-term symbiosis between ancestors of chlamydiae and Archaeplastida. The bacterial endosymbiont was later lost, leaving some of its genes behind.
So, the question is: why don't present-day Archaeplastida have any chlamydial symbionts (parasitic, mutualistic, commensal)? Why can't they be infected, once more, by chlamydiae?
I may think of some possible answers:
(1) Actually, there are chlamyidial symbionts in Archaeplastida. We just haven't found them. (Have we looked for them?)
(2) Archaeplastida are not special: other eukaryotic lineages appear to lack chlamydial symbionts (just a hypothesis, I have no idea). In other words, chlamydiae are able to infect cells from only specific eukaryotic lineages. (How wide is chlamydial host-range? Has anybody tried to infect Archaeplastida cells with chlamydiae?)
(3) Archaeplastida are special: after being infected by chlamydia-like bacteria, the Archaeplastida lineage became resistant to over-infection by other chlamydiae. (If this is the case, it would be nice to know the molecular mechanisms responsible for the resistance. Can we make an Archaeplastida cell susceptible to infection by knocking-out specific genes? Are these genes derived from chlamyidiae? Or, the other way around, can we make an Archaeplastida cell susceptible to infection by adding specific genes from other eukaryotes? This knowledge could be useful to design new anti-chlamydial therapies.)
You can contribute to this discussion here (post a comment), or at the PLoS ONE site where a relevant article was published (Chlamydiae has contributed at least 55 genes to Plantae with predominantly plastid functions).
Related links:
- Chlamydiae, Wikipedia.
- Chlamydiae.com (a comprehensive reference and education site).
Image:
Electron micrograph of a cell infected by Chlamydia trachomatis. © American Society for Microbiology. Reference: Beatty WL, Morrison RP, Byrne GI. Persistent chlamydiae: from cell culture to a paradigm for chlamydial pathogenesis. Microbiol. Rev. (1994) 58, 686-699.
I would tend to suspect that it's because Chlamydia-type bacteria are substantially less environment-resistant that viruses.
ReplyDeleteAs far as I know, all plant viruses require physical damage to the plant cells to achieve an initial infection (though some or all of them can then pass viral material from cell to cell once infection is established). I suspect that due to the cell wall, the same would be true of endoparasitic bacteria like Chlamydia.
Since establishing an infection means hanging around on the surface of either a plant or something that will damage a plant (such as insects or animal claws) for extended periods, I'm guess few or none of these types of bacteria possess that kind of hardiness. I'd further guess that this might have something to do with their tiny size - don't they have an especially small genome? No room for extra "bonus" genes to provide some kind of adaptation like spore formation.
I guess I'm not so sure that chlamydia are tender. Psittacosis gets around from bird to bird (and occasionally bird to humans) in aerosols, which have to be tough environments especially as they dry out. Getting through plant cell walls is trickier. Has anybody ever tried to infect scratched Arabidopsis leaves with a lot of chlamydia?
ReplyDelete-- stan zahler