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Genetic diversity of an introduced pest, the green spruce aphid Elatobium abietinum (Hemiptera: Aphididae) in New Zealand and the United Kingdom

Published online by Cambridge University Press:  10 July 2009

D. Nicol*
Affiliation:
Soil, Plant and Ecological Sciences Division, PO Box 84, Lincoln University, Canterbury, New Zealand
K.F. Armstrong
Affiliation:
Soil, Plant and Ecological Sciences Division, PO Box 84, Lincoln University, Canterbury, New Zealand
S.D. Wratten
Affiliation:
Soil, Plant and Ecological Sciences Division, PO Box 84, Lincoln University, Canterbury, New Zealand
P.J. Walsh
Affiliation:
Forest Research Associates Ltd, PO Box 1031, Rotorua, New Zealand
N.A. Straw
Affiliation:
Forestry Research, Alice Holt Lodge, Wrecclesham, Farnham, Surrey, GL10 4LH, UK
C.M. Cameron
Affiliation:
Soil, Plant and Ecological Sciences Division, PO Box 84, Lincoln University, Canterbury, New Zealand
C. Lahmann
Affiliation:
Soil, Plant and Ecological Sciences Division, PO Box 84, Lincoln University, Canterbury, New Zealand
C.M. Frampton
Affiliation:
Applied Management and Computing Division, PO Box 84, Lincoln University, Canterbury, New Zealand
*
*+64 3 325 3844nicold@lincoln.ac.nz

Abstract

The green spruce aphid Elatobium abietinum (Walker) is an introduced pest in the United Kingdom and more recently in New Zealand. In outbreak years this aphid can cause severe defoliation and sometimes death of spruce trees (Picea spp.). As chemical control is not financially viable, other options including host-plant resistance and biological control are currently being investigated. An understanding of the genetic variation of this pest is imperative in fully utilizing these control strategies. To examine this, E. abietinum was collected from Sitka spruce Picea sitchensis from four locations in the UK that were up to 240 km apart. Of these, 40 aphids were analysed via two alternative polymerase chain reaction (PCR) analyses using primer pairs. The first analysis used 10-mer random primers, whilst the second analysis used primers designed to amplify across the intergenic spacer region of rDNA. Combining results from the two analyses allowed the 40 UK aphids to be separated into 28 different genotypes. The genetic variation was also high within each UK site, with 77 to 89% of the aphids sampled being of a different genotype. The two PCR analyses were subsequently used to examine 40 aphids across six sites in New Zealand up to 1200 km apart. No genetic variation was identified. Further analysis of several of these New Zealand aphids with 87 individual 10-mer primers and two polymerase enzymes, still did not detect any genetic variation. The high degree of genotypic diversity in the UK populations was presumably due to a longer period of establishment, multiple introductions and/or sexual reproduction. The contrasting lack of genetic variation in New Zealand populations was probably due to a very limited founder population, continued isolation and lack of sexual reproduction. Reduced genetic diversity can seriously decrease the ability of a population to adapt to control strategies. Therefore the durability of certain control methods may be more readily maintained in such an isolated population in New Zealand.

Type
Review Article
Copyright
Copyright © Cambridge University Press 1998

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