Genetic diversity and population structure of the endangered marsupial
            <i>Sarcophilus harrisii</i>
            (Tasmanian devil)

Miller, Webb; Hayes, Vanessa M.; Ratan, Aakrosh; Petersen, Desiree C.; Wittekindt, Nicola E.; Miller, Jason R.; Walenz, Brian P.; Knight, James; Qi, Ji; Zhao, Fangqing; Wang, Qingyu; Bedoya-Reina, Oscar C.; Katiyar, Neerja; Tomsho, Lynn P.; Kasson, Lindsay Mc Clellan; Hardie, Rae-Anne; Woodbridge, Paula; Tindall, Elizabeth A.; Bertelsen, Mads F.; Dixon, Dale J.; Pyecroft, Stephen; Helgen, Kristofer M.; Lesk, Arthur M.; Pringle, Thomas H.; Patterson, Nick; Yu, Zhongxin; Kreiss, Alexandre; Woods, Gregory M.; Jones, Menna Lloyd; Schuster, Stephan C.

doi:10.1073/pnas.1102838108

Cited by 188 publications

(201 citation statements)

References 30 publications

(24 reference statements)

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“…This could perhaps be mediated by this this species' apparent elevated susceptibility to neoplasia (21,22), low genetic diversity (10,(23)(24)(25), and/or biting behavior (26). However, if this is the case, it is surprising that tumors comparable with DFTD were not reported before 1996 (4,5).…”

Section: Discussionmentioning

confidence: 88%

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A second transmissible cancer in Tasmanian devils

Pye

Pemberton²,

Tovar

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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201

328

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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.

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Section: Discussionmentioning

confidence: 88%

“…Tasmanian devils have low levels of genetic diversity (10,(23)(24)(25), possibly caused by historical population declines driven by past climate change (27). Remaining genetic diversity was possibly further eroded by persecution following European settlement of Tasmania, and, more recently, by the DFTD epidemic (23,27).…”

Section: Discussionmentioning

confidence: 99%

A second transmissible cancer in Tasmanian devils

Pye

Pemberton²,

Tovar

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

201

328

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“…CABOG has now been used to assemble the Tasmanian devil genome using a combination of Illumina and 454 reads [39]. The CABOG pipeline will also attempt to construct multiple alelles for regions of sequence variation after contig assembly [40].…”

Section: Next-generation Assemblersmentioning

confidence: 99%

“…SGA was run with only trivial parallelization and could be run serially. No maximum memory requirement was reported for ALLPATHS-LG and so the total memory of the cluster used is given here [31,[36][37][38][39]45]. …”

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confidence: 99%

Next-Generation Sequencing and Large Genome Assemblies

2012

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The next-generation sequencing (NGS) revolution has drastically reduced time and cost requirements for sequencing of large genomes, and also qualitatively changed the problem of assembly. This article reviews the state of the art in de novo genome assembly, paying particular attention to mammalian-sized genomes. The strengths and weaknesses of the main sequencing platforms are highlighted, leading to a discussion of assembly and the new challenges associated with NGS data. Current approaches to assembly are outlined and the various software packages available are introduced and compared. The question of whether quality assemblies can be produced using short-read NGS data alone, or whether it must be combined with more expensive sequencing techniques, is considered. Prospects for future assemblers and tests of assembly performance are also discussed. Keywordsde novo assembly; genomics; next-generation sequencing; whole-genome shotgun Genome assembly continues to be one of the central problems of bioinformatics. This is owing, in large part, to the continuing development of the sequencing technology that provides 'reads' of short sequences of DNA, from which the genome is inferred. Larger sets of data, and changes in the properties of reads such as length and errors, bring with them new challenges for assembly. For the earliest sequencing efforts using the whole-genome shotgun (WGS) approach, in which reads are generated from random locations across the entire genome, assembly could be dealt with by arranging print-outs of the reads by hand. Through the next three decades, Sanger capillary sequencing gained substantially in throughput, and WGS became practical for increasingly large and complex genomes, from tens of kilobases in the early 1980s to gigabases by 2001 [1]. In line with this, assembly went on to use not only increasingly powerful computational means, but also increasingly time and memory-efficient assemblers.A further revolution in sequencing began around 2005, when second-generation sequencing (SGS) technologies began to produce massive throughput at far lower costs than Sanger sequencing, enabling a mammalian genome to be sequenced in a matter of days [2]. De novo assemblies of the Panda [3] and Turkey [4] genomes have now been made using SGS data alone, and several human resequencing projects have been completed [5][6][7]. The © The Wellcome Trust Sanger Institute * Author for correspondence: Tel.: +44 1223 494705, Fax: +44 1223 494919, zn1@sanger.ac.uk. Financial & competing interests disclosureThe authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript. Assembly is not at all a trivial task. Repeated sequences of DNA make it difficult to infer the relative positions in the genome corresponding to reads, and they occur far more often...

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“…It has been suggested that the cells monitor and regulate the length of individual telomeres to favor their genomic stability and possibly increased proliferation. 78 Finally, whole genome analysis 44,49 further substantiated the tumor's clonal origin and allograft theory of transmission by demonstrating that DFTs share structural variants and copy number changes distinct from their hosts.…”

Section: Allograft Theory Of Dftd Transmissionmentioning

confidence: 99%

Devil Facial Tumor Disease

2015

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Devil facial tumor disease (DFTD) is an emergent transmissible cancer exclusive to Tasmanian devils (Sarcophilus harrisii) and threatening the species with extinction in the wild. Research on DFTD began 10 years ago, when nothing was known about the tumor and little about the devils. The depth of knowledge gained since then is impressive, with research having addressed significant aspects of the disease and the devils' responses to it. These include the cause and pathogenesis of DFTD, the immune response of the devils and the immune evasion mechanisms of the tumor, the transmission patterns of DFTD, and the impacts of DFTD on the ecosystem. This review aims to collate this information and put it into the context of conservation strategies designed to mitigate the impacts of DFTD on the devil and the Tasmanian ecosystem.

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Genetic diversity and population structure of the endangered marsupial Sarcophilus harrisii (Tasmanian devil)

Cited by 188 publications

References 30 publications

A second transmissible cancer in Tasmanian devils

A second transmissible cancer in Tasmanian devils

Next-Generation Sequencing and Large Genome Assemblies

Devil Facial Tumor Disease

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