Evolution of devil facial tumour disease chromosomes — ASN Events

Evolution of devil facial tumour disease chromosomes (#80)

Janine E Deakin 1 , Yiru Zhang 2 , Gayitha Sakthivel 2 , Jennifer Schoning 2 , Robyn Taylor 3 , Anne-Maree Pearse 3
  1. Institute for Applied Ecology, University of Canberra, Canberra, ACT, Australia
  2. Research School of Biology, The Australian National University, Canberra, ACT, Australia
  3. Animal Health Laboratory , Department of Primary Industries, Parks and Water and Environment, Launceston, Tasmania, Australia

An usual transmissible cancer, known as devil facial tumour (DFT) disease, is threatening the Tasmanian devil with extinction in the wild. DFT disease appears to have arisen in a female devil toward the end of last century. It is the tumour itself that is the infectious agent, having since spread through much of the population when devils bite each other.  DFT disease has caused a dramatic drop in devil numbers across much of Tasmania. The only other example of a transmissible tumour in the wild is canine transmissible venereal tumour (CTVT), which has been spreading through dogs for over 1000 years. The most important difference between DFT and CTVT is that CTVT in most cases does not kill its host the tumour and host are able to co-exist in the population. Is there a chance that DFT could evolve to reach this more desirable scenario? 

 The initial tumour appears to have resulted from a shattering and rejoining of two chromosomes, followed by the accumulation of other structural mutations, which resulted in the formation of several distinctive DFT marker chromosomes. Interestingly, these genomic regions are not only extensively rearranged in DFT but are also highly rearranged between different marsupial species, suggesting a potential link between tumour and evolutionary breakpoints. By cytogenetically mapping genes to DFT chromosomes isolated from individuals from different geographical locations, it has been possible to trace the evolution of this tumour as it is passes through the population. Until recently, structural mutations in DFTs were seemingly restricted to particular genomic regions, predominantly regions consisting of chromosome 4, 5 and X material but a more recent karyotypic strain of the DFT has been detected in a population where DFT disease prevalence is reduced and there has been a limited effect on population structure compared to other areas affected by DFT disease. This DFT strain has an additional large marker chromosome. The possible implications of this relatively major chromosomal change on the impact of DFT disease will be discussed.