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"Tasmanian devil."
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Tasmanian devils
Learn all about these furry and ferocious little predators, marsupials from the island of Tasmania, south of Australia.
Book
A second transmissible cancer in Tasmanian devils
Clonally transmissible cancers are somatic cell lineages that are spread between individuals via the transfer of living cancer cells. There are only three known naturally occurring transmissible cancers, and these affect dogs, soft-shell clams, and Tasmanian devils, respectively. The Tasmanian devil transmissible facial cancer was first observed in 1996, and is threatening its host species with extinction. Until now, this disease has been consistently associated with a single aneuploid cancer cell lineage that we refer to as DFT1. Here we describe a second transmissible cancer, DFT2, in five devils located in southern Tasmania in 2014 and 2015. DFT2 causes facial tumors that are grossly indistinguishable but histologically distinct from those caused by DFT1. DFT2 bears no detectable cytogenetic similarity to DFT1 and carries a Y chromosome, which contrasts with the female origin of DFT1. DFT2 shows different alleles to both its hosts and DFT1 at microsatellite, structural variant, and major histocompatibility complex (MHC) loci, confirming that it is a second cancer that can be transmitted between devils as an allogeneic, MHC-discordant graft. These findings indicate that Tasmanian devils have spawned at least two distinct transmissible cancer lineages and suggest that transmissible cancers may arise more frequently in nature than previously considered. The discovery of DFT2 presents important challenges for the conservation of Tasmanian devils and raises the possibility that this species is particularly prone to the emergence of transmissible cancers. More generally, our findings highlight the potential for cancer cells to depart from their hosts and become dangerous transmissible pathogens.
Journal Article
Transmission dynamics of Tasmanian devil facial tumor disease may lead to disease-induced extinction
Most pathogens threatening to cause extinction of a host species are maintained on one or more reservoir hosts, in addition to the species that is threatened by disease. Further, most conventional host—pathogen theory assumes that transmission is related to host density, and therefore a pathogen should become extinct before its sole host. Tasmanian devil facial tumor disease is a recently emerged infectious cancer that has led to massive population declines and grave concerns for the future persistence of this largest surviving marsupial carnivore. Here we report the results of mark—recapture studies at six sites and use these data to estimate epidemiological parameters critical to both accurately assessing the risk of extinction from this disease and effectively managing this disease threat. Three sites were monitored from before or close to the time of disease arrival, and at three others disease was well established when trapping began, in one site for at least 10 years. We found no evidence for sex-specific differences in disease prevalence and little evidence of consistent seasonal variation in the force of infection. At all sites, the disease was maintained at high levels of prevalence (>50% in 2–3-year-old animals), despite causing major population declines. We also provide the first estimates of the basic reproductive rate R₀ for this disease. Using a simple age-structured deterministic model, we show that our results are not consistent with transmission being proportional to the density of infected hosts but are consistent with frequency-dependent transmission. This conclusion is further supported by the observation that local disease prevalence in 2–3-year-olds still exceeds 50% at a site where population density has been reduced by up to 90% in the past 12 years. These findings lend considerable weight to concerns that this host-specific pathogen will cause the extinction of the Tasmanian devil. Our study highlights the importance of rapidly implementing monitoring programs to determine how transmission depends on host density and emphasizes the need for ongoing management strategies involving a disease-free \"insurance population,\" along with ongoing field monitoring programs to confirm whether local population extinction occurs.
Journal Article
Meet a baby Tasmanian devil
\"Did you know that Tasmanian devils are only the size of a grain of rice when they are born? Or that baby Tasmanian devils can climb trees? Learn more fascinating facts all about baby Tasmanian devils in this book!\"-- Provided by publisher.
Book
Evolution of a contagious cancer: epigenetic variation in Devil Facial Tumour Disease
The emergence of Devil Facial Tumour Disease (DFTD), a highly contagious cancer, is driving Tasmanian devils (Sarcophilus harrisii) to extinction. The cancer is a genetically and chromosomally stable clonal cell line which is transmitted by biting during social interactions. In the present study, we explore the Devil Facial Tumour (DFT) epigenome and the genes involved in DNA methylation homeostasis. We show that tumour cells have similar levels of methylation to peripheral nerves, the tissue from which DFTD originated. We did not observe any strain or region-specific epimutations. However, we revealed a significant increase in hypomethylation in DFT samples over time (p < 0.0001). We propose that loss of methylation is not because of a maintenance deficiency, as an upregulation of DNA methyltransferase 1 gene was observed in tumours compared with nerves (p < 0.005). Instead, we believe that loss of methylation is owing to active demethylation, supported by the temporal increase in MBD2 and MBD4 (p < 0.001). The implications of these changes on disease phenotypes need to be explored. Our work shows that DFTD should not be treated as a static entity, but rather as an evolving parasite with epigenetic plasticity. Understanding the role of epimutations in the evolution of this parasitic cancer will provide unique insights into the role of epigenetic plasticity in cancer evolution and progression in traditional cancers that arise and die with their hosts.
Journal Article
Tasmanian devils in danger
Tasmanian devils are found only on an island south of Australia. Though they are grouchy and feisty, they'd rather make a lot of noise than fight. Unfortunately, after being hunted almost to extinction, this rare marsupial has been decimated by disease. Readers will learn about the Tasmanian devils and what is being done to save them.
Book
Density trends and demographic signals uncover the long-term impact of transmissible cancer in Tasmanian devils
1. Monitoring the response of wild mammal populations to threatening processes is fundamental to effective conservation management. This is especially true for infectious diseases, which may have dynamic and therefore unpredictable interactions with their host. 2. We investigate the long-term impact of a transmissible cancer, devil facial tumour disease (DFTD), on the endemic Tasmanian devil. We analyse trends in devil spotlight counts and density across the area impacted by the disease. We investigate the demographic parameters which might be driving these trends, and use spatial capture-recapture models to examine whether DFTD has affected home range size. 3. We found that devils have declined by an average of 77% in areas affected by DFTD, and that there is a congruent trend of ongoing small decline in spotlight counts and density estimates. Despite this, devils have persisted to date within each of nine monitoring sites. One site is showing as yet unexplained small increases in density 8-10 years after the emergence of DFTD. 4. We also found the prevalence of DFTD has not abated despite large declines in density and that diseased sites continue to be dominated by young devils. The long-term impact of the disease has been partially offset by increased fecundity in the form of precocial breeding in 1-year-old females, and more pouch young per female in diseased sites. The lower densities resulting from DFTD did not affect home range size. 5. Synthesis and applications. Transmission of devil facial tumour disease continues despite large declines in devil density over multiple generations. Plasticity in life history traits has ameliorated the impact of devil facial tumour disease, however broad-scale trends in density show ongoing decline. In light of this, devil facial tumour disease and the impact of stochastic events on the reduced densities wrought by the disease, continue to threaten devils. In the absence of methods to manage disease in wild populations, we advocate managing the low population densities resulting from disease rather than disease per se.
Journal Article
Saving the Tasmanian devil : how science is helping the world's argest marsupial carnivore survive
\"In this addition to the critically acclaimed Scientist in the Field series, Dorothy Patent follows the scientists trying to put a stop to a gruesome disease before it's too late. Tasmanian devils are dying at an alarming rate from a type of tumor that appears to be contagious. What scientists are learning while researching the Tasmanian devil has potential to affect all animals, and even humans, as they learn more about how to prevent and hopefully eradicate certain genetic diseases.\"-- Provided by publisher.
Book
Contemporary Demographic Reconstruction Methods Are Robust to Genome Assembly Quality: A Case Study in Tasmanian Devils
Reconstructing species’ demographic histories is a central focus of molecular ecology and evolution. Recently, an expanding suite of methods leveraging either the sequentially Markovian coalescent (SMC) or the site-frequency spectrum has been developed to reconstruct population size histories from genomic sequence data. However, few studies have investigated the robustness of these methods to genome assemblies of varying quality. In this study, we first present an improved genome assembly for the Tasmanian devil using the Chicago library method. Compared with the original reference genome, our new assembly reduces the number of scaffolds (from 35,975 to 10,010) and increases the scaffold N90 (from 0.101 to 2.164 Mb). Second, we assess the performance of four contemporary genomic methods for inferring population size history (PSMC, MSMC, SMC++, Stairway Plot), using the two devil genome assemblies as well as simulated, artificially fragmented genomes that approximate the hypothesized demographic history of Tasmanian devils. We demonstrate that each method is robust to assembly quality, producing similar estimates of Ne when simulated genomes were fragmented into up to 5,000 scaffolds. Overall, methods reliant on the SMC are most reliable between ∼300 generations before present (gbp) and 100 kgbp, whereas methods exclusively reliant on the site-frequency spectrum are most reliable between the present and 30 gbp. Our results suggest that when used in concert, genomic methods for reconstructing species’ effective population size histories 1) can be applied to nonmodel organisms without highly contiguous reference genomes, and 2) are capable of detecting independently documented effects of historical geological events.
Journal Article