I have been a big fan of Looney Tunes’ Tasmanian Devil since I was very young—probably because of the way Taz enters a scene and always demonstrates excellent communication skills! Needless to say, I was extremely sad a few years ago to hear that the real Tasmanian devils were being devastated by a transmissible form of cancer. Recent research hints that genetic variations may be the Tasmanian devils’ saving grace—as it may be the hallmark of a robust adaptive capacity allowing a species to survive even when threatened beyond the ability to thrive.
What’s Bedeviling the Devils?
A Nature Communications article published last week heralds a rapid evolutionary response to cancer that may save Tasmanian devils from all-but-certain extinction.1 The research is relatively vague in regard to what may actually be providing some Tasmanian devils with resistance to a transmissible form of cancer known as DFTD (devil facial tumor disease), but data points to changes in allele frequencies in two regions of chromosomes 2 and 3. The researchers speculate that genes in these regions may end up being key in providing Tasmanian devils with resistance to the aggressive and easily transmitted form of cancer that has wiped out 80 percent of the population in just two decades.
DFTD is a cancer spread by transmission of cells from an infected Tasmanian devil to another during typical social interactions that involve aggressive behavior and frequent biting. The cancer is almost universally lethal within six months and prevalence among animals of reproductive age is more than 50 percent. Historically, Tasmanian devils have experienced population bottlenecks and display overall low genetic variability with two genetic clusters occurring on the island. However, even with limited genetic variability, researchers believe they have found indications that existing genetic variability may be enough to save the species.
Signs for Hope
Researchers sequenced DNA extracted from 360 Tasmanian devils sampled between 1999 and 2014 from 39 localities. After genotyping and applying various filters, researchers focused on three focal populations, pooling samples according to date (prior to DFTD or after DFTD introduction) in an attempt to identify single nucleotide polymorphisms (SNPs) and associated genes that had extreme allele frequency changes in response to DFTD. SNPs were further pruned based on linkage disequilibrium considerations. This resulted in 64,124 SNPs from three locality populations. Candidate genomic loci were restricted to those indicated in all three populations. Two candidate regions—one on chromosome 2 and one on chromosome 3—were identified and contained nine unique SNPs that had allele frequency changes at or greater than the 97.5 percentile for the population harboring that specific SNP.
The candidate regions identified in chromosomes 2 and 3 correspond to regions harboring five genes (one on chromosome 2 and four on chromosome 3) associated with immune function or cancer in other mammals. The researchers speculate that the cereblon gene on chromosome 2 (a myeloma treatment target in humans) and two genes on chromosome 3, CD146 and THY1 (immune system regulators involved in cell-to-cell communication and cellular adhesion in humans), are likely to be of greatest interest. Based on characteristics of DFTD, the allele frequency changes in these regions, and localized genes and the homologous gene product function in other mammals, the researchers suggest that these allele changes are indicative of an adaptive immune response to DFTD cells.
Rapid Genetic Responses Indicate Standing Genetic Variation
The researchers conclude that a rapid genetic response has occurred in very few generations (four to six generations) due to the strong selective pressure imposed by DFTD. Such an extremely quick response indicates, as the researchers observe, that the selection most likely acts on standing genetic variation rather than new mutations. This indicates that genomic variability must harbor significant capacities for species adaptation under grave threats, especially so in regard to this example, as extremely low levels of genetic diversity occur among Tasmanian devils. (All of these focal populations come from a single genetic cluster, of which there are only two.) This strongly suggests that animals like Tasmanian devils have great inherent capacity already built into their genomes for species survival, and that the Tasmanian devils’ resistance and potential survival is no act of evolution but merely selective natural pressures weeding out a susceptible population.
The researchers admit that further investigation is absolutely necessary to identify which genetic changes and which genes may play a functional role in resistance to DFTD, as their findings point merely to disease-responsive SNPs. An ability to identify specific resistant genotypes may facilitate better stewardship of creation and allow conservationists to assist crossbreeding of off-island captive assurance populations with cancer-resistant Tasmanian devils to enhance genetic diversity and ensure larger populations and the survivability of Tasmanian devils in the future.
Does God Delight in Devils, Too?
These observations of rapid, allelic frequency changes in Tasmanian devils strongly suggests that creation is highly dynamic and adaptive, allowing persistence of species under a variety of stresses and threats. Such rapid adaptation demonstrates great complexity and brilliant adaptive potential built into the genetic variation of the Tasmanian devils’ genomes. And through additional research, God may provide us with the knowledge to better steward and care for the Tasmanian devil population as it fights to recover from this devastating disease. What an ongoing testimony to God’s goodness and greatness! I am delighted to think that God’s providence in the genetic variation of Tasmanian devils reflects his fondness for them, too.
- Brendan Epstein et al., “Rapid Evolutionary Response to a Transmissible Cancer in Tasmanian Devils,” Nature Communications 7 (August 2016): id. 12684, doi:10.1038/ncomms12684.