Project description:<p><strong>INTRODUCTION:</strong> Larvae of the invasive emerald ash borer [EAB, <em>Agrilus planipennis</em> Fairmaire (Coleoptera: Buprestidae)], kill over 99% of green ash (<em>Fraxinus pennsylvanica</em> Marshall) trees they infest, yet a small percentage of green ash (“lingering ash”) survive years of heavy EAB attack. In the face of an ongoing invasion that threatens multiple North American <em>Fraxinus</em> species with extinction, any evidence for reproducible defensive responses in the native species merits investigation.</p><p><strong>METHODS: </strong>We evaluated the capacity of 3 families of green ash F1 progeny to kill EAB larvae when challenged in greenhouse studies by infestation with a uniform density of EAB eggs followed by dissection 8 weeks post-infestation and comparison of the host metabolomic profiles.</p><p><strong>RESULTS:</strong> The mean proportions of host-killed larvae in the 2 families of F1 progeny from lingering ash parents were significantly higher than that of host-killed larvae in the family of F1 progeny from susceptible ash parents (<em>p</em> < 0.001). Untargeted metabolomics comparing F1 progeny in the quartile with the highest percent host-killed larvae (HHK) to F1 progeny in the quartile with the lowest percent host-killed larvae (LHK) and to the uninfested F1 progeny within each family revealed evidence for induced biochemical responses to EAB. Infested trees produced significantly higher levels of select secoiridoids than uninfested trees, and LHK progeny produced significantly higher levels of select secoiridoids than the HHK progeny. HHK progeny produced significantly higher abundances of 3 metabolites annotated as aromatic alkaloids than the LHK and uninfested individuals.</p><p><strong>DISCUSSION: </strong>Based on these results, we hypothesize that green ash responds to EAB infestation. However, only certain trees have the genetic capacity to tailor a response that kills enough EAB larvae to prevent lethal damage to the vascular system. Rigorous tests of this hypothesis will require 15–20 years of additional crossing, phenotyping, and omics analyses. The results of this investigation will encourage the establishment and continuation of breeding programs that, in concert with biocontrol and management, could provide trees that slow, if not halt, the decimation of the <em>Fraxinus</em> gene pool. At the same time, ongoing work on host-insect interaction will contribute to our understanding of how forest trees recognize and defend themselves against phloem-feeding insects.</p>
Project description:European common ash, Fraxinus excelsior L., is currently threatened by Ash dieback (ADB) caused by the fungus, Hymenoscyphus fraxineus. To detect and identify metabolites that may be products of pathways important in contributing to resistance against H. fraxineus we performed untargeted metabolomic profiling on leaves from selected F. excelsior individuals showing strong tolerance or susceptibility to H. fraxineus. We identified sets of "features" [small molecules] that enabled strong discrimination between tolerant or susceptible genotypes of F. excelsior. Strikingly, tolerant F. excelsior lines exhibited low levels of iridoid glycosides, known anti-feeding deterrents. As Europe is threatened by Emerald Ash Borer (Agrilus planipennis), an invasive wood boring beetle native to East Asia that has devastated North American ash, our study raises the question whether selection for resistance to H. fraxineus leads to ecological trade-offs that result in susceptibility to emerging pests such as emerald ash borer.
Project description:We performed RNA-seq and proteomics on naturally infested green ash (F. pennsylvanica) trees at low, medium and high levels of increasing emerald ash borer (A. planipennis) infestation. Our integrative analysis of the RNA-Seq and proteomics data identified 14 proteins and 4 transcripts that contribute most to the difference between highly infested and low infested trees.
Project description:ASH-1 orthologs are H3K36-specific methyltransferases that are conserved from fungi to humans but are poorly understood, in part because they are typically essential for viability. Here we examine the H3K36 methylation pathway of Neurospora crassa, which we find has just two H3K36 methyltransferases, ASH-1 and RNA polymerase II-associated SET-2. Our investigation of the interplay between SET-2 and ASH-1 uncovered a regulatory mechanism connecting ASH-1-catalyzed H3K36 methylation to repression of poorly transcribed genes. Our findings provide new insight into ASH-1 function, H3K27me2/3 establishment, and repression at facultative heterochromatin.