Rose rosette disease (RRD) caused by the rose rosette emaravirus (RRV) and transmitted by the eriophyid mite Phyllocoptes fructiphilus (Pf), both native to North America, has caused significant damage to roses over the last several decades. As cultural and chemical control of this disease is difficult and expensive, a field trial was established to systematically screen rose germplasm for potential sources of resistance. One hundred and eight rose accessions representing the diversity of rose germplasm were planted in Tennessee and Delaware, managed to encourage disease development, and evaluated for symptom development and viral presence for three years. All major commercial rose cultivars were susceptible to this viral disease to varying levels. The rose accessions with no or few symptoms were species accessions from the sections Cinnamomeae, Carolinae, Bracteatae, and Systylae or hybrids with these. Among these, some were asymptomatic; they displayed no symptoms but were infected by the virus. Their potential depends on their ability to serve as a source of viruses. The next step is to understand the mechanism of resistance and genetic control of the various sources of resistance identified.

Thousand cankers disease (TCD), first documented in the western United States in the early 2000s, has spread into nine western and seven eastern states in the United States and northern Italy. TCD incidence and severity differ between eastern and western United States outbreak localities. Black walnut ( Juglans nigra ) trees, introduced into both urban and plantation settings in the western United States, have been severely impacted as evident by the documented high disease incidence and mortality. However, in eastern United States localities, where J. nigra is native, host-pathogen-vector interactions resulted in two different outcomes: trees either die or partly recover followed by infection. Recent genetic studies on the TCD causal agent, Geosmithia morbida , indicate the spatial genetic structure and high levels of genetic diversity among United States populations. Using detached branch inoculation assays, we reported differential virulence among 25 G. morbida isolates collected across the current distribution range of the disease. As a proxy for virulence, the canker area was measured to 7 days after inoculation. Varying degrees of virulence were observed among tested G. morbida isolates, which was partly explained by their genetic provenance (genetic clusters). Isolates that grouped within genetic cluster 2 ( n = 7 from the eastern United States and n = 6 from the western United States; mean = 210.34 mm 2 ) induced significantly larger cankers than isolates that grouped within genetic cluster 1 ( n = 12; all western United States isolates; mean = 153.76 mm 2 ). Canker sizes varied among isolates within each genetic cluster and were not correlated with a geographic region (eastern vs. western United States) but rather to the isolated state of origin. Mean canker size also differed in response to isolates that originated from different tree host species. G. morbida isolates collected from Juglans major induced statistically smaller cankers when compared to isolates recovered from undetermined Juglans species but not from J. nigra . In sum, the increased mortality reported for western United States walnut tree populations cannot be explained by a higher virulence of local G. morbida . Plausible explanations for the observed disparity include environmental conditions, such as prolonged drought, greater population densities of walnut twig beetle causing a higher number of inoculation events to individual trees, and multiple introductions of G. morbida originating from multiple locations. Future experimental evaluation should be undertaken to quantify the influence of these factors on the local epidemics.

Resistance to rose rosette disease (RRD), a fatal disease of roses (Rosa spp.), is a high priority for rose breeding. As RRD resistance is time-consuming to phenotype, the identification of genetic markers for resistance could expedite breeding efforts. However, little is known about the genetics of RRD resistance. Therefore, we performed a quantitative trait locus (QTL) analysis on a set of inter-related diploid rose populations phenotyped for RRD resistance and identified four QTLs. Two QTLs were found in multiple years. The most consistent QTL is qRRV_TX2WSE_ch5, which explains approximately 20% and 40% of the phenotypic variation in virus quantity and severity of RRD symptoms, respectively. The second, a QTL on chromosome 1, qRRD_TX2WSE_ch1, accounts for approximately 16% of the phenotypic variation for severity. Finally, a third QTL on chromosome 3 was identified only in the multiyear analysis, and a fourth on chromosome 6 was identified in data from one year only. In addition, haplotypes associated with significant changes in virus quantity and severity were identified for qRRV_TX2WSE_ch5 and qRRD_TX2WSE_ch1. This research represents the first report of genetic determinants of resistance to RRD. In addition, marker trait associations discovered here will enable better parental selection when breeding for RRD resistance and pave the way for marker-assisted selection for RRD resistance.

Rose rosette disease (RRD), caused by the Rose rosette emaravirus (RRV), is a major threat to the garden rose industry in the United States. There has been limited work on the genetics of host plant resistance to RRV. Two interconnected tetraploid garden rose F-1 biparental mapping populations were created to develop high-quality tetraploid rose linkage maps that allowed the discovery of RRD resistance quantitative trait loci (QTLs) on linkage groups (LGs) 5, 6, and 7. These QTLs individually accounted for around 18-40% of the phenotypic variance. The locus with the greatest effect on partial resistance was found in LG 5. Most individuals with the LG 5 QTL were in the simplex configuration; however, two individuals were duplex (likely due to double reduction). Identification of resistant individuals and regions of interest can help the development of diagnostic markers for marker-assisted selection in a breeding program.

The eriophyid mite, Phyllocoptes fructiphilus, vectors the causal agent, Rose rosette virus (RRV), that results in rose rosette disease. Parts of the southeastern United States have remained free of the disease, except for infected plant material introductions that were eradicated. A survey of sampling points through Alabama, Georgia, and Mississippi (n = 204) revealed the southeastern border of RRV. The presence of RRV in symptomatic plant tissue samples (n = 39) was confirmed by TaqMan-quantitative reverse transcription polymerase chain reaction (RT-qPCR). Samples were also collected at every plot for detection of eriophyid mites, specifically for P. fructiphilus. Three different species of eriophyid mites were found to be generally distributed throughout Alabama, Georgia, and Mississippi. Most of these sites (n = 60) contained P. fructiphilus, found further south than previously thought, but in low populations (<10 mites/gram of tissue) south of the RRV line of incidence. Latitude was found to be significantly correlated with the probability of detecting RRV-positive plants, but plant hardiness zones were not. Plot factors such as plant size, wind barriers, and sun exposure were found to have no effect on P. fructiphilus or the presence of RRV. The reason for the absence of RRV and low populations of P. fructiphilus in this southeast region of the United States are unclear.

Abstract Eleven switchgrass cultivars (eight ornamental and three agronomic) were inoculated with 40 switchgrass rust isolates collected from the southeastern U.S. to study host resistance, rust virulence and host/pathogen interactions by measuring urediniospore germination percentage, latent period, and the number of uredia and urediniospores produced per cm2 of leaf surface. In general, ornamental switchgrass cultivars had reduced number of uredia and urediniospores produced per cm2 than did agronomic cultivars. Rust isolates were variable for virulence in culture (on grass blades in petri dishes); however they could not be segregated into groups based on collection locations or years. The results of this study will provide information concerning durable horizontal resistance in switchgrass for the ornamental industry. Index words:, Switchgrass, leaf rust, resistance. Species used in the study: switchgrass (Panicum virgatum L., rust (Puccinia emaculata).

Abstract Rose rosette disease, caused by rose rosette virus (RRV), is an epidemic affecting nearly every rose cultivar in the United States. The only hosts for Phyllocoptes fructiphilus, the eriophyid mite that vectors RRV, are Rosa species. Eighteen Rosa species were evaluated for mite resistance by collecting foliage samples from July to November in 2016 and 2017, from which mites were extracted. Mites were isolated through a series of sieves and counted using a stereomicroscope. The response variable was expressed as the number of mites per gram of optimal rose tissue. Mite data were evaluated to determine the peak week for mite populations for each year. The mite populations varied by rose species (α = 0.05) in 2016 but not 2017. Due to high variability in mite counts, the species were not as clearly distinguishable as expected. This high variability is likely due to factors such as differential growth rates of the roses, weather, presence of RRV in the rose, and the quality of the tissue collected throughout the season. Experimental design revisions are proposed for future studies looking at Rosa species resistance to eriophyid mite populations. Index words: rose rosette virus, rose rosette disease, Phyllocoptes fructiphilus Keifer, virus, vector. Species used in this study: Phyllocoptes fructiphilus (Keifer), Prairie Rose [Rosa arkansana (Porter), Forest Farm]; Carolina Rose [Rosa carolina (L.), Forest Farm]; Rosa clinophylla (Thory), Rogue Valley Rose; White Prairie Rose [Rosa foliolosa (Nutt.), Rogue Valley Rose]; White Prairie Rose [Rosa foliolosa (Nutt.) Antique Rose Emporium]; Father Hugo Rose [Rosa hugonis, Rogue Valley Rose]; Musk Rose [Rosa moschata (J. Herrm.), Antique Rose Emporium]; Multiflora Rose [Rosa multiflora (Thunb.)]; Shining Rose [Rosa nitida (Willd.), Rogue Valley Rose]; Shining Rose [Rosa nitida (Willd.), Antique Rose Emporium]; Nootka Rose [Rosa nutkana (C. Presl.), Rogue Valley Rose]; Tea Rose [Rosa odorata (Andrews), Foundation Plant Services, Davis, CA]; Swamp Rose [Rosa palustris (Marshall), Antique Rose Emporium]; Swamp Rose [Rosa palustris (Marshall), Ever Blooming Antique Rose Emporium]; Chestnut Rose [Rosa roxburghii (Tratt.), Antique Rose Emporium]; ‘Plena' Chestnut Rose [Rosa roxburghii (Tratt.), Rogue Valley Rose]; Rugosa Rose [Rosa rugosa (Thunb.), Bailey's Nursery]; ‘Alba' Rugosa Rose [Rosa rugosa (Thunb.), Bailey's Nursery]; Climbing Prairie Rose [Rosa setigera (Michx.), Antique Rose Emporium]; Rosa soulieana (Crép.), Ralph Moore; Virginia Rose [Rosa virginiana (Mill.), Forest Farm]; Porterfolia Memorial Rose [Rosa wichuraiana (Crép.), Antique Rose Emporium]; Mountain Woods' Rose [Rosa woodsii (Lindl.), Rogue Valley Rose].

Current eriophyid mite quantification techniques require transportation of the Rosa spp. cuttings to the laboratory. It is thought that the change in xylem hydraulic conductance within the cut cane could trigger the mites to abandon their host, owing to the changes to the microenvironments that these mites are inhabiting. An experiment was conducted to determine the necessity of floral cuts (reducing stem embolisms by an additional cut underwater) for the retention of eriophyid mites during transit. Four groups of plants (rose rosette virus (RRV)-free Knock Out roses, RRV-infected Knock Out roses, RRV-free multiflora roses, and RRV-infected multiflora roses) were evaluated at different time intervals (0.5, 2, 4, 8, 24, 48, 72, and 96 h postharvest) to assess mite populations on each plant (number of mites per gram of tissue). Cut type (floral or dry cut) and rose species were found not to have a significant effect on the number of mites per gram of tissue found, indicating that floral cuts are not needed for accurately estimating eriophyid mite populations. Rose cuttings infected with RRV were found to have an average of 46 times more mites per gram in comparison with RRV-free cuttings.

Thousand cankers disease (TCD) results from the combined activity of the fungal pathogen, Geosmithia morbida Kolařík, Freeland, Utley, and Tisserat and its principle vector, Pityophthorus juglandis (Blackman) (Coleoptera: Curculionidae: Scolytinae) in Juglans L. spp. and Pterocarya Kunth spp. host plants. TCD has been reported from the eastern and western United States. To evaluate potential for other beetle species to vector the fungus in east Tennessee, specimens were collected using ethanol-baited traps that were suspended beneath crowns of TCD-symptomatic trees. Associations of G. morbida with insect species collected in traps were assessed in an unsuccessful, preliminary culture-based fungal assay, and then with a molecular-based detection method. For culture-based assays, rinsate from washed, individual insects was plated on nutrient media and growing colonies were subcultured to obtain axenic G. morbida cultures for identification. For the molecular-based method, G. morbida presence was detected by amplifying the previously developed, species-specific microsatellite locus GS004. Capillary electrophoresis was used to detect the amplified amplicons and representative reactions were validated using Sanger sequencing. Eleven beetle species were found to carry G. morbida, including Cnestus mutilatus (Blandford), Dryoxylon onoharaensum (Murayama), Hylocurus rudis (LeConte), Monarthrum fasciatum (Say), Monarthrum mali (Fitch), Xyleborinus saxesenii (Ratzeburg), Xylosandrus crassiusculus (Motschulsky), Xylosandrus germanus (Blandford) (all Coleoptera: Curculionidae: Scolytinae), Stenomimus pallidus (Boheman) (Coleoptera: Curculionidae: Cossoninae), Oxoplatypus quadridentatus (Olivier) (Coleoptera: Curculionidae: Platypodinae), and Xylops basilaris (Say) (Coleoptera: Bostrichidae). These findings raise concerns that alternative subcortical insect species that already occur within quarantined habitats can sustain incidence of introduced G. morbida and contribute to spread within the native range of black walnut, Juglans nigra L., in the eastern United States.

Rose rosette disease (RRD) is incited by a negative-sense RNA virus (genus Emaravirus), which is vectored by a wind-transported eriophyid mite (Phyllocoptes fructiphilus). Symptoms include witches broom/rosette-type growth, excessive prickles (thorns), discolored and distorted growth, and, unlike most other rose diseases, usually results in plant death. RRD is endemic to North America and was first described in Manitoba, Wyoming, and California in the 1940s. It has spread east with the aid of a naturalized rose species host and has become epidemic from the Great Plains to the East Coast of North America on garden roses in home and commercial landscapes where losses have been high. The disease was suggested to be incited by a virus from the beginning, but only recently has this been confirmed and the virus identified. The presence of the vector mite on roses has been associated with RRD since the first symptoms were described. However, more recently, the mite was demonstrated to be the vector of the disease and confirmed to transmit the virus itself. As a result of the RRD epidemic in North America and its effects on the national production and consumer markets for roses, a research team comprising five major universities (Texas, Florida, Tennessee, Oklahoma, and Delaware), a dozen growers and nurseries (all regions), six rose breeding programs (California, Wisconsin, Texas, and Pennsylvania), the major rose testing programs (Earth-Kind and AGRS), the major rose organization (American Rose Society), and the major trade organization AmericanHort has formed. This research project has been funded by the Specialty Crops Research Initiative through the U.S. Department of Agriculture (USDA) with the short-term objective of improving and disseminating best management practices (BMPs) and the long-term goal of identifying additional sources of resistance and developing the genetic tools to quickly transfer resistance into the elite commercial rose germplasm.

Rose rosette disease (RRD) whose causal agent, the Emaravirus Rose rosette virus (RRV), was only recently identified has caused widespread death of roses in the midwestern and eastern sections of the United States. A national research team is working on the detection and best management practices for this highly damaging disease. Unfortunately, little is known about the host plant resistance to either the causal viral agent or its vector, the eriophyid mite Phyllocoptes fructiphilus . Thus far, the only confirmed resistance is among Rosa species. Of the over 600 rose cultivars observed, only 7% have not exhibited symptoms of RRD. Replicated trials are in progress to confirm resistance and/or susceptibility of ≈300 rose accessions in Tennessee and Delaware. Rose is a multispecies cultivated complex that consists of diploid, triploid, and tetraploid cultivars. The basic breeding cycle is 4 years with a 3-year commercial trial coupled with mass propagation before release. Thus, if only one breeding cycle is needed, a new cultivar could be produced in 7 years. Unfortunately, for the introgression of a new trait such as disease resistance from a related species into the commercial rose germplasm, multiple generations are required which can easily take two decades from the first cross to cultivar release. Research is ongoing to develop a rapid selection procedure for resistance to RRD with the aid of molecular markers associated with the resistance. Such an approach has the potential of reducing the breeding cycle time by 50% and increasing the efficiency of seedling and parental selection manifold, leading to commercially acceptable rose cultivars with high RRD resistance in less time and with less expense.