In the Molecular Ecology module I sat in the third year of my degree studies, we were given a mini project assignment where we wouldwrite a paper detailing a known issue and proposing applicable methodologies and hypotheses. I, along with my partner and another student, investigated Devil Facial Tumour Disease (DFTD); a facial cancer which has spread rapidly across Tasmania and is decimating the devil population. In a new report published in Proceedings of the Royal Society B, Siddle et al. (2010) comment on the genetic distinctiveness of animals in the north-west of the island and the possibility that they may be resistant.
The methodology and formative hypotheses employed were similar to those I described in my report and the results enhance some of my suggestions. Of course I’m not implying anything at all, nor am I mentioning this for the sake of ego. Rather, I find it encouraging that my reasoning and lines of enquiry were logical. Reading the new report has rekindled my interest; I’ve got some catching up to do.
As it’s worth elucidating on the topic, I’ve pasted an edited version of my previous introduction followed by the abstract from Siddle et al. (2010) below. For the full text of the recent report, follow this link – http://rspb.royalsocietypublishing.org/content/early/2010/03/01/rspb.2009.2362.full . Obviously, reports in the intervening months (and year) are not detailed:
(from Tasmanian Devil (Sarcophilus harrisii) Facial Tumour Disease (DFTD): Identifying Populations for Conservation, 2008-2009)
The Tasmanian devil (Sarcophilius harrisii) is the world’s largest extant marsupial carnivore, endemic to the island of Tasmania where they inhabit coastal scrub and sclerophyll forest (Guiler, 1970; Loh et al., 2006). Devils are primarily nocturnal scavengers with a solitary lifestyle, though they are known to aggregate when feeding and/or mating where biting and ‘jaw wrestling’ is common. Ubiquitous to eastern, northern and north-west Tasmania, devils are found at much lower densities in the less suitable habitats of the south-west (Jones et al., 2004).
The species is under threat from Devil Facial Tumour Disease (DFTD; Pearse and Swift, 2006); a cancer which manifests in facial tumours which spread to lymph nodes and other organs inevitably leading to death. All tumours have an identical genotype (Siddle et al., 2007a). It has been hypothesised that the disease is spread by allograft during jaw wrestling (Pearse and Swift, 2006, Loh et al., 2006). DFTD is host-specific and has never been found in any other member of the Dasyuridae family (McCallum, 2008).
Prior to the initial outbreak of DFTD in 1996, the total population size was estimated to be around 150,000. Between 1996 and 2005, devil numbers dropped by as much as 90%. Though populations in the western third of the state currently appear healthy, new cases continue to occur in areas where no incidence was previously recorded (Tasmanian Department of Primary Industries and Water, 2008).
Devils are thought to have undergone several population crashes in the last 150 years which has resulted in an extremely low level of genetic diversity at microsatellite loci (Jones et al., 2004, Siddle et al., 2007a). While diversity is known to be low in eastern devils (Siddle, et al., 2007b), the north-western population is yet to be studied. The construction of a spleen cDNA library by Siddle et al. (2007a) will allow further characterisation of MHC genes and in turn, a greater understanding of the devil immune system. In 2007, an animal from the western third of the island was found to exhibit an immune response following injection with live tumour cells. Despite initial optimism, it now appears that the cancer has developed in this individual (News.com.au, 2008).
Characterising the immune response of the devil at a genetic level is vital in ensuring the long-term survival of the species. This report detail[ed] an extensive study which compares evaluate levels of heterozygosity in microsatellite and MHC loci across the species range and which also utilises expressed sequence tags (EST) cloned from the spleen cDNA library as a basis for identifying novel genes.
(from Siddle et al., 2010)
Tasmanian devils face extinction owing to the emergence of a contagious cancer. Devil facial tumour disease (DFTD) is a clonal cancer spread owing to a lack of major histocompatibility complex (MHC) barriers in Tasmanian devil populations. We present a comprehensive screen of MHC diversity in devils and identify 25 MHC types and 53 novel sequences, but conclude that overall levels of MHC diversity at the sequence level are low. The majority of MHC Class I variation can be explained by allelic copy number variation with two to seven sequence variants identified per individual. MHC sequences are divided into two distinct groups based on sequence similarity. DFTD cells and most devils have sequences from both groups. Twenty per cent of individuals have a restricted MHC repertoire and contain only group I or only group II sequences. Counterintuitively, we postulate that the immune system of individuals with a restricted MHC repertoire may recognize foreign MHC antigens on the surface of the DFTD cell. The implication of these results for management of DFTD and this endangered species are discussed.
Guiler, E.R. (1970). Tasmanian devils and agriculture. Tasmanian Journal of Agriculture. 41:134–137
Jones, M.E., Paetkau, D., Geffen, E., Moritz, C. (2004). Genetic diversity and population structure of Tasmanian devils, the largest marsupial carnivore. Molecular Ecology. 13:2197–2209
Loh, R., Bergfeld, J., Hayes, D., O’Hara, A., Pyecroft, S., Raidal, S., Sharpe, R. (2006).The Pathology of Devil Facial Tumor Disease (DFTD) in Tasmanian devils (Sarcophilus harrisii). Veterinary Pathology. 43:890–895
Moseman, A. (2010). Hope for Taz? A Colony of Tasmanian Devils Resists the Species Deadly Disease. Available at: http://blogs.discovermagazine.com/80beats/2010/03/11/hope-for-taz-a-colony-of-tasmanian-devils-resists-the-species-deadly-disease/
McCallum, H. (2008). Tasmanian devil facial tumour disease: lessons for conservation biology. Trends in Ecology and Evolution. 23(11) 1008
News.com.au (2008). ‘Immune’ Tassie devil has cancer [online]. Available at: http://www.news.com.au/story/0,27574,24813926-421,00.html. Accessed January 3rd, 2009
Pearse, A.M., Swift, K. (2006). Allograft theory: transmission of devil facial-tumour disease. Nature. 439:549.
Siddle, H.V., Sanderson, C., Belov, K. (2007a). Characterization of major histocompatibility complex class I and class II genes from the Tasmanian devil (Sarcophilus harrisii). Immunogenetics. 59:753–760
Siddle, H.V., Kreiss, A., Eldridge, M.D.B., Noonan, E., Clarke, C.J., Pyecroft, S. (2007b) Transmission of a fatal clonal tumor by biting occurs due to depleted MHC diversity in a threatened carnivorous marsupial. PNAS. 104(41):16221–16226
Siddle, H.V., Marzec, J., Cheng, Y., Jones, M. and Belov, K. (2010). MHC gene copy number variation in Tasmanian devils: implications for the spread of a contagious cancer. Proceedings of the Royal Society B. Published online before print March 10, 2010.
Tasmanian Department of Primary Industries and Water (2008). Tasmanian devil facial tumour disease [online]. Available at: http://www.dpiw.tas.gov.au/inter.nsf/WebPages/LBUN-5QF86G?open Accessed December 10, 2008.