Dataset Information

Tracing the rise of malignant cell lines: Distribution, epidemiology and evolutionary interactions of two transmissible cancers in Tasmanian devils.

ABSTRACT: Emerging infectious diseases are rising globally and understanding host-pathogen interactions during the initial stages of disease emergence is essential for assessing potential evolutionary dynamics and designing novel management strategies. Tasmanian devils (Sarcophilus harrisii) are endangered due to a transmissible cancer-devil facial tumour disease (DFTD)-that since its emergence in the 1990s, has affected most populations throughout Tasmania. Recent studies suggest that devils are adapting to the DFTD epidemic and that disease-induced extinction is unlikely. However, in 2014, a second and independently evolved transmissible cancer-devil facial tumour 2 (DFT2)-was discovered at the d'Entrecasteaux peninsula, in south-east Tasmania, suggesting that the species is prone to transmissible cancers. To date, there is little information about the distribution, epidemiology and effects of DFT2 and its interaction with DFTD. Here, we use data from monitoring surveys and roadkills found within and adjacent to the d'Entrecasteaux peninsula to determine the distribution of both cancers and to compare their epidemiological patterns. Since 2012, a total of 51 DFTD tumours have been confirmed among 26 individuals inside the peninsula and its surroundings, while 40 DFT2 tumours have been confirmed among 23 individuals, and two individuals co-infected with both tumours. All devils with DFT2 were found within the d'Entrecasteaux peninsula, suggesting that this new transmissible cancer is geographically confined to this area. We found significant differences in tumour bodily location in DFTD and DFT2, with non-facial tumours more commonly found in DFT2. There was a significant sex bias in DFT2, with most cases reported in males, suggesting that since DFT2 originated from a male host, females might be less susceptible to this cancer. We discuss the implications of our results for understanding the epidemiological and evolutionary interactions of these two contemporary transmissible cancers and evaluating the effectiveness of potential management strategies.

SUBMITTER: James S

PROVIDER: S-EPMC6752152 | biostudies-other | 2019 Oct

REPOSITORIES: biostudies-other

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Publications

Tracing the rise of malignant cell lines: Distribution, epidemiology and evolutionary interactions of two transmissible cancers in Tasmanian devils.

James Samantha S Jennings Geordie G Kwon Young Mi YM Stammnitz Maximilian M Fraik Alexandra A Storfer Andrew A Comte Sebastien S Pemberton David D Fox Samantha S Brown Bill B Pye Ruth R Woods Gregory G Lyons Bruce B Hohenlohe Paul A PA McCallum Hamish H Siddle Hannah H Thomas Frédéric F Ujvari Beata B Murchison Elizabeth P EP Jones Menna M Hamede Rodrigo R

Evolutionary applications 20190628 9

Emerging infectious diseases are rising globally and understanding host-pathogen interactions during the initial stages of disease emergence is essential for assessing potential evolutionary dynamics and designing novel management strategies. Tasmanian devils (<i>Sarcophilus harrisii</i>) are endangered due to a transmissible cancer-devil facial tumour disease (DFTD)-that since its emergence in the 1990s, has affected most populations throughout Tasmania. Recent studies suggest that devils are a ...[more]

PMID: 31548856

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Project description:BACKGROUND: The arrangement of the amino acids in the genetic code is such that neighbouring codons are assigned to amino acids with similar physical properties. Hence, the effects of translational error are minimized with respect to randomly reshuffled codes. Further inspection reveals that it is amino acids in the same column of the code (i.e. same second base) that are similar, whereas those in the same row show no particular similarity. We propose a 'four-column' theory for the origin of the code that explains how the action of selection during the build-up of the code leads to a final code that has the observed properties. RESULTS: The theory makes the following propositions. (i) The earliest amino acids in the code were those that are easiest to synthesize non-biologically, namely Gly, Ala, Asp, Glu and Val. (ii) These amino acids are assigned to codons with G at first position. Therefore the first code may have used only these codons. (iii) The code rapidly developed into a four-column code where all codons in the same column coded for the same amino acid: NUN = Val, NCN = Ala, NAN = Asp and/or Glu, and NGN = Gly. (iv) Later amino acids were added sequentially to the code by a process of subdivision of codon blocks in which a subset of the codons assigned to an early amino acid were reassigned to a later amino acid. (v) Later amino acids were added into positions formerly occupied by amino acids with similar properties because this can occur with minimal disruption to the proteins already encoded by the earlier code. As a result, the properties of the amino acids in the final code retain a four-column pattern that is a relic of the earliest stages of code evolution. CONCLUSION: The driving force during this process is not the minimization of translational error, but positive selection for the increased diversity and functionality of the proteins that can be made with a larger amino acid alphabet. Nevertheless, the code that results is one in which translational error is minimized. We define a cost function with which we can compare the fitness of codes with varying numbers of amino acids, and a barrier function, which measures the change in cost immediately after addition of a new amino acid. We show that the barrier is positive if an amino acid is added into a column with dissimilar properties, but negative if an amino acid is added into a column with similar physical properties. Thus, natural selection favours the assignment of amino acids to the positions that they occupy in the final code.

Dataset Information

Tracing the rise of malignant cell lines: Distribution, epidemiology and evolutionary interactions of two transmissible cancers in Tasmanian devils.

Publications

Tracing the rise of malignant cell lines: Distribution, epidemiology and evolutionary interactions of two transmissible cancers in Tasmanian devils.

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