226 ing as protocols to thwart Ophiostoma are devel- oped. Clearly, fungi have the ability to evolve more quickly, and adapt to challenges, than do trees. While several genetic loci implicated in fungal disease have been identified (e.g., Et-Touil et al. 1999), only three genes of Ophiostoma have been functionally analyzed. The first, cu, encodes a hydrophobin (a surface protein) known as cerato- ulmin. Early studies implied that this was a wilt toxin, and the pathogenic factor for DED had therefore been discovered (Stevenson et al. 1979). The amino acid sequence for this protein was elu- cidated (Yaguchi et al. 1993). However, in 1995, it was reported that isolated Ophiostoma mutants that failed to produce CU were as pathogenic as the CU-producing strains (Brasier et al. 1995). When a mutant of the less aggressive Ophiostoma ulmi was created by inserting a single copy of the cu gene taken from the aggressive O. novo-ulmi, an increase in the CU protein was detected. Nev- ertheless, the transformant was not more virulent. However, the overexpressor had an altered pheno- type and more hydrophobic and adherent yeast-like cells. It appears that the CU protein plays a role in making the fungus more fit by protecting infectious propagules of Ophiostoma from desiccation and increasing their adherence to bark beetles (Temple et al. 1997). When cu is expressed in O. quercus, a nonpathogen of Ulmus, it influences the virulence of this normally nonaggressive species of Ophiostoma (Del Sorbo et al. 2000). Any gene that increases the load of yeast-like cells carried on the vector or provides an advantage during environmental stress provides an advantage for a pathogen (Temple and Horgen 2000). It has been suggested that one form of biological control would be to create a competi- tor for the highly pathogenic strains of Ophiostoma novo-ulmi by introducing strains that overproduce CU (Temple and Horgen 2000). To date, this con- cept has not resulted in any promising reports. The second gene, now known as epg1, is thought to play a role in the fungal colonization of xylem (Svaldi and Elgersma 1982). It codes for endopoly- galacturonase, which dissolves vessel cell walls. While it was reported that aggressive isolates of Ophiostoma caused the release of more arabinose and xylose from cell walls of elm wood than non- aggressive strains (Svaldi and Elgersma 1982), another study using a genetically altered form of ©2017 International Society of Arboriculture Marcotrigiano: Elms Revisited Ophiostoma with a targeted disruption of the epg1 gene suggests that epg1 is only partially responsible for cell wall breakdown and likely acts in concert with yet unidentified genes (Temple et al. 2009). The third functionally analyzed gene is one related to fungal mating. With Ophiostoma, mating must occur between sexually compatible individuals— i.e., those having different alleles at the mating locus (Bernier et al. 2015). This mating locus (MAT1) has been used to show that interspecific gene transfer has occurred between the less viru- lent O. ulmi and O. novo-ulmi and to demonstrate that rapid adaptation of an invasive pathogen to new environments can occur (Paoletti et al. 2006). Genome projects (e.g., the human genome proj- ect), while laborious and expensive, provide the most valuable genetic information for isolating functional genes of an organism. The genome of Ophiostoma novo-ulmi was sequenced (Forgetta et al. 2013), as was the genome of O. ulmi (Khoshraſtar et al. 2013). Metabolic pathways were reconstructed and specific enzymes that may play a role in virulence were iden- tified. Information such as this will be very useful if a genetic attack on DED is to be mounted. This has now begun with functional annotation research— i.e., looking at the functional characteristics of gene products, assessing the physical characteristics of genes and associated proteins, and elucidating a metabolic profile of the organism (Comeau et al. 2015). It is predicted that studies like this will allow for a better understanding of the entire pathosystem. ELM YELLOWS: AN OLD NEW PROBLEM Most research on elm disease has focused on DED even though elm yellows (also known as elm phlo- em necrosis) is more deadly. First thought to be caused by a virus and noted in the U.S. as far back as the late 1800s (Baker 1948), elm yellows is now known to be caused by a single-celled organism that belongs to a large group called phytoplasma. Phy- toplasmas are bacteria-like organisms that have no cell wall, are too small to be seen with a compound microscope, and cannot be cultured ex situ (Pataky 1998). Although first noticed in North America, it has been proposed that the pathogen has a Eurasian origin (Sinclair 2000). The elm yellows group of pathogens is associated with disease in elm, grape- vine, blackberry, cherry, peach, and others, making
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