There are lots of parasites in this world, but I know of only two cases in which the parasite actually evolved from its host. Both of these are cancers. One is the canine transmissible venereal tumor (CTVT), and the other a transmissible cancer affecting the Tasmanian devil. A paper in this week’s Science (see also this report at the BBC) traces the origin of this cancer to a mutant cell in the nervous system. More interesting — at least for our purposes — are the evolutionary implications.
The Tasmanian devil (Sacrophilis harrisii; see photo below) is the largest marsupial carnivore, with a range limited to Tasmania. In 1996, researchers noticed that some devils were afflicted with “devil tumor facial disease”(DTFD). This is a nasty disease (see photo below), with facial and throat metastases that usually kill the animal. And DTFD is transmitted by biting, so tumor cells must be in the saliva or gums. (This leads me to suspect that the tumor has actually evolved to make itself more transmissible, since tumors that spread less easily would die off with their carrier.)
Murchison et al. looked at the DNA of 25 infected devils (both the individuals and their tumors) and of 10 “control” uninfected individuals. The results were intriguing. First, all of the 14 genes examined showed that all the tumors had a similar genotype — a genotype palpably different from (and less diverse than) the devil hosts themselves. DFTD is a clone, which means it had a single origin, almost certainly a mutant cell in a single unlucky devil.
What kind of cell was it? The authors answered that question by looking at the “transcriptome,” the set of RNA molecules produced by DNA, which gives you an idea which genes are actually expressed. The transcriptome of individual devils differed from that of the tumors, with the tumors showing much higher expression of those genes involved in the “myelinization pathway”: genes that build the myelin sheaths of nerves and fight off agents that attack nerves.
From this observation, the researchers conclude that the parasitic tumor originated from Schwann cells, a particular group of cell in the peripheral nevous systems that act as a neuron “tenders,” wrapping themselves around nerve axons to maintain myelin sheaths and helping those axons grow.
The differential expression of the tumor cells, and the identification of where they came from, gives scientists a marker for identifying the disease, and holds promise for eradicating it. I have my doubts, though, for research is slow and the disease is spreading so rapidly that it could drive the devils to extinction within 25 years.
The evolutionary twist is that the tumor is now an independent parasite, derived from devil cells but no longer part of the devil body itself. It can be thought of as a separate organism, genetically free to undergo independent evolution. And its evolutionary interests are in conflict with that of the host from whence it came. (The authors don’t dwell on this aspect of the problem.)
It’s not clear where that evolution will go, though. It’s possible that because transmission depends on virulence, or at least on the parasite’s ability to quickly get into the mouth, the tumor could become more and more virulent, speeding up the extinction of not only the Tasmanian devil, but of the tumor itself. (Here’s an example where evolution has no foresight!)
Increased virulence is not a certainty, though, for those tumors that kill the devils too quickly won’t get a chance to spread. DFTD is like a cold: its spread requires its carrier to be active, and so extreme lethality is a detriment. It may eventually evolve to become less lethal, but that may be too late, for evolution is slow and the tumor is already virulent enough to exterminate itself and its host.
One devil, named Cedric, appears to be naturally immune to the cancer, so perhaps some captive breeding may be in order.
Fig. 1. A Tasmanian devil
Fig. 2. A devil afflicted with DFTD
h/t: Greg Mayer
Murchison, E. P. et al. 2010. The Tasmanian Devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer. Science 327:84-87.