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il ' ii - Northern Research Station - USDA Forest Service

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GENETIC AND ENVIRONMENTAL CONTRIBUTIONS TO VARIATION<br />

- IN THE RESISTANCE OF PICEAABIES TO THE GALL-FORMING<br />

ADELGID, ADELGES ABIETIS (HOMOPTERA: ADELGIDAE)<br />

..<br />

W<strong>il</strong>liam J. Mattsonl, Jean Levieux2,and Dominique Piou 3<br />

_North Central <strong>Forest</strong> Exper. <strong>Station</strong>, <strong>USDA</strong> <strong>Forest</strong> <strong>Service</strong>, Pesticide Res. Center, Michigan State University, East<br />

Lansing, Mi: 48824<br />

.2Department of Bietogy, University of Orleans, Orleans, France<br />

3 Barres National Arboretum, 45290 Nogent sur Vernisson, France<br />

Abstract.--Norway spruce, Picea abies, varies widely among individuals in its<br />

susceptib<strong>il</strong>ity to the common gall-forming aphid, Adelges abietis (Homoptera:<br />

Adelgidae), an Old World species which now has a circumtemperate, eircumboreal<br />

distribution. We estimated the genetic and environmental contributions to this variation ,<br />

in a polyclonal spruce plantation at the Barres National Aboretum in the southern Paris<br />

basin of France. Aphids infested 98 percent of the clones, but infestation levels were<br />

highly variable, ranging from an average of less than 1 to 95 galls/branch/ramet/clone.<br />

Neither altitude nor forest region of clonal origin made a significant contribution to<br />

. .variation in tree resistance. Instead, most of the variation was due to individual tree<br />

genetics because broad sense heritab<strong>il</strong>ity of resistance against A. abietis was estimated<br />

to be 0.86. There was no consistent relationship between tree infestation by A. abietis,<br />

and another common, co-occurring adelgid, A. laricis.<br />

INTRODUCTION affected by the genetics of the tree can be inferred from<br />

the fact that (a) progeny from different mother x father<br />

The spruce gall adelgid, Adelges abietis, is one of about crosses exhibit different levels of infestation (Eidmann<br />

52 species of primitive, aphid-like insects (Homoptera: and Eriksson 1978), (b) the distribution of insect galls<br />

Ade!gida e) which attack conifers in the fam<strong>il</strong>y Pinaceae per tree in plantations is not random and is highly<br />

• (Carter 1971, Ghosh 1983). A. abietis is probably the consistent from year to year (Ewert 1967, Tjia and<br />

• , best kn0wn and most widely distributed of these species. Houston 1975, Eidmann and Eriksson 1978, Mattson et<br />

It has a nearly circumboreal and circumtemperate al. 1994), (c) putative resistant and susceptible trees<br />

distribution on several species of spruce, Picea spp., on differ in their reactions to aphid stylets inserted into their<br />

. which it completes its entire life cycle and forms bud cortex tissues (Thalenhorst 1972; Rohfritsch 1981,<br />

characteristic pineapple-shaped galls (Rose and Lindquist 1988), and (d) and in their foliar phenolic prof<strong>il</strong>es (Tj<strong>il</strong>a<br />

. 1985). North American spruces are recent hosts of A. and Houston 1975).<br />

abietis (since thel 9th century); European and west Asian<br />

spruces i such as Norway spruce, Picea abies, are Because so very little is known about the genetic bases of<br />

believed to be its ancestral hosts '(Patch 1909). woody plant resistance to insects (Fritz and Simms<br />

• 1992), we proposed to quantify the extent to which such<br />

AS is typical for "intimate" plant-feeders such as aphids, tree-to-tree variation in aphid infestations is due to<br />

scales, and gall-forming insects (Fritz and Price 1988, genetic or environmental factors. To make such esti-<br />

Mattson etal. 1988), there is abundant, unequivocal mates we measured the broad sense heritab<strong>il</strong>ity of tree<br />

evidence showing that individual trees vary widely in resistance (H2), i.e., the proportion of the total phenotypic<br />

, their susceptib<strong>il</strong>ity to A. abietis (Ewert 1967, Thalenhorst variation (Vp) (where Vp = Vg + Ve) in a trait that can be<br />

1972, Tjia and Houston 1975, Eidmann and Eriksson attributed to total genetic variation (Vg) in the trait: H2=<br />

i978, Rohfritsch 1981). That this variation is strongly Vg/Vp (Falconer 1989). We hypothesized that broad<br />

304<br />

O<br />

A

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