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Article << Previous     |     Next >>   Contents Vol 61(1)

Towards an understanding of the genetic basis behind 1080 (sodium fluoroacetate) tolerance and an investigation of the candidate gene ACO2

Janine E. Deakin A G , Desmond W. Cooper B , Jennifer J. Sinclair B , Catherine A. Herbert C , Marilyn B. Renfree D and Matthew Wakefield E F

A Divison of Evolution, Ecology and Genetics, Research School of Biology, The Australian National University, Canberra, ACT 0200, Australia.
B School of Biological, Earth and Environmental Sciences, University of New South Wales, Sydney, NSW 2052, Australia.
C Faculty of Veterinary Science, The University of Sydney, NSW 2006, Australia.
D Department of Zoology, The University of Melbourne, Melbourne, Vic. 3010, Australia.
E Bioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Vic. 3052, Australia.
F Department of Genetics, The University of Melbourne, Melbourne, Vic. 3010, Australia.
G Corresponding author. Email: janine.deakin@anu.edu.au

Australian Journal of Zoology 61(1) 69-77 http://dx.doi.org/10.1071/ZO12108
Submitted: 22 October 2012  Accepted: 3 May 2013   Published: 23 May 2013


 
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Abstract

Sodium fluoroacetate, commonly referred to as 1080, is a pesticide heavily used to control vertebrate pests. The development of tolerance to this poison by target species is a critical concern raised by its intensive use. Tolerance to 1080 is common amongst many native vertebrates in south-west Western Australia and is thought to be the result of a long period of coevolution with plant species that produce 1080 in their seeds and flowers. Among those vertebrate species tolerant to 1080 exposure is a subspecies of the tammar wallaby (Macropus eugenii). Tammars from Western Australia are tolerant while the subspecies present on Kangaroo Island is susceptible to 1080 exposure. The availability of genetic and genomic information, combined with a distinct difference in tolerance to 1080 between subspecies, makes the tammar wallaby an ideal species in which to study the genetic basis behind 1080 resistance. To date, research in this area has focussed on a candidate gene approach. Since 1080 inhibits the action of the mitochondrial aconitase enzyme, the aconitase gene ACO2 was considered a prime candidate for involvement in 1080 tolerance. However, sequencing of the full-length ACO2 transcript failed to identify a sequence variant between the two subspecies that would result in an amino acid change in the active site of the enzyme. Future studies will need to take a genome-wide approach to identify the gene(s) responsible for 1080 tolerance.





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