Greg Hannon

They want to know how the tumors spread—not just in individual animals, but throughout the species. Says Hannon: “The tumor is treating the entire population almost as if it were a single organism.” An outward feature of the tumors gives a clue to their mode of transmission. The growths are scaly, and cells can detach readily when, for instance, devils fight over food or mates. Scientists are now convinced that DFTD spreads when an unaffected devil bites an infected one and dislodged tumor cells are absorbed into the bloodstream from saliva.

Researchers in Australia have discovered that tumors from different Tasmanian devils are genetically identical—clones of one another. The secret of their seemingly unfettered journey through the population was the question addressed last year by an HHMI-supported summer intern working in Hannon's lab.

Karla Claudio, from Puerto Rico, examined mitochondria—organelles in the cell best known for their role in generating energy for biochemical processes. Mitochondria have their own genomes, distinct from the genetic material compressed in the cell nucleus, that are inherited exclusively from the mother. Hence, mitochondrial genomes can be used to trace matrilineal descent. Claudio's study of mitochondria sampled from devil tissues revealed almost no genetic diversity in the animals.

At some point in recent history, the devil population evidently came under severe threat and was nearly extinguished. While the species recovered, the surviving population is dangerously inbred. It is widely suspected that a lack of genetic diversity has left the devil's immune system wide open to an insidious invader like DFTD.

Hannon's group is using advanced technologies to learn more about the tumors' characteristic “transcriptome”—the readout of all the genes expressed in any given tissue type. In particular, Murchison and Bender have been using techniques developed by Hannon and colleagues to characterize the population of small RNAs—a class of gene-regulating molecules characterized through Hannon's pioneering efforts—in tumor-laden devil tissue samples. This method “can give us a signature of cell-type identity,” Hannon explains.

The tumor transcriptome will position the team to find genes that contribute to tumor formation. The key, says Hannon, is in “making comparisons to known networks of oncogenes and suppressor genes in tumors that have been carefully characterized in previous work.” More broadly, he notes, understanding something of devil genomics might support selective breeding of captive animals; this would enable wildlife biologists to maintain maximum diversity in an “insurance population” raised against the possibility of eradication.

There is hope, however, that work in Hannon's lab and elsewhere will contribute to an effective treatment strategy in the 20- to 30-year window before the wild devil population is consumed by DFTD. “We lost the thylacine, or Tasmanian tiger—a striped, dog-sized marsupial carnivore—in the 1930s,” says Murchison. “The devils occupy an ecological niche that's absolutely critical because of the tiger's extinction. To lose them as well would be a devastating loss of species diversity, not only for Tasmania but for all of us.”

FOR MORE INFORMATION: To view the Tasmanian devil on video and hear its vocalizations, visit www1.parks.tas.gov.au/wildlife/mammals/devil.html.

Photo: Zack Seckler / AP, ©HHMI

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