Quantitative Trait Loci Associated with Gray Leaf Spot Resistance in St. Augustinegrass.

Gray leaf spot (GLS), caused by Magnaporthe grisea, is a major fungal disease of St. Augustinegrass (Stenotaphrum secundatum), causing widespread blighting of the foliage under warm, humid conditions. To identify quantitative trait loci (QTL) controlling GLS resistance, an F1 mapping population consisting of 153 hybrids was developed from crosses between cultivar Raleigh (susceptible parent) and plant introduction PI 410353 (resistant parent). Single-nucleotide polymorphism (SNP) markers generated from genotyping-by-sequencing constituted nine linkage groups for each parental linkage map. The Raleigh map consisted of 2,257 SNP markers and spanned 916.63 centimorgans (cM), while the PI 410353 map comprised 511 SNP markers and covered 804.27 cM. GLS resistance was evaluated under controlled environmental conditions with measurements of final disease incidence and lesion length. Additionally, two derived traits, area under the disease progress curve and area under the lesion expansion curve, were calculated for QTL analysis. Twenty QTL were identified as being associated with these GLS resistance traits, which explained 7.6 to 37.2% of the total phenotypic variation. Three potential GLS QTL "hotspots" were identified on two linkage groups: P2 (106.26 to 110.36 cM and 113.15 to 116.67 cM) and P5 (17.74 to 19.28 cM). The two major effect QTL glsp2.3 and glsp5.2 together reduced 20.2% of disease incidence in this study. Sequence analysis showed that two candidate genes encoding ß-1,3-glucanases were found in the intervals of two QTL, which might function in GLS resistance response. These QTL and linked markers can be potentially used to assist the transfer of GLS resistance genes to elite St. Augustinegrass breeding lines.

Identification and Pathogenicity of Bacteria Associated with Etiolation and Decline of Creeping Bentgrass Golf Course Putting Greens.

Bacterial etiolation and decline has developed into a widespread issue with creeping bentgrass (CBG) (Agrostis stolonifera) putting green turf. The condition is characterized by an abnormal elongation of turfgrass stems and leaves that in rare cases progresses into a rapid and widespread necrosis and decline. Recent reports have cited bacteria, Acidovorax avenae and Xanthomonas translucens, as causal agents; however, few cases exist where either bacterium were isolated in conjunction with turf exhibiting bacterial disease symptoms. From 2010 to 2014, turfgrass from 62 locations submitted to the NC State Turf Diagnostic Clinic exhibiting bacterial etiolation and/or decline symptoms were sampled for the presence of bacterial pathogens. Isolated bacteria were identified using rRNA sequencing of the 16S subunit and internal transcribed spacer region (16S-23S or ITS). Results showed diverse bacteria isolated from symptomatic turf and A. avenae and X. translucens were only isolated in 26% of samples. Frequently isolated bacterial species were examined for pathogenicity to 4-week-old 'G2' CBG seedlings and 8-week-old 'A-1' CBG turfgrass stands in the greenhouse. While results confirmed pathogenicity of A. avenae and X. translucens, Pantoea ananatis was also shown to infect CBG turf; although pathogenicity varied among isolated strains. These results illustrate that multiple bacteria are associated with bacterial disease and shed new light on culturable bacteria living in CBG turfgrass putting greens. Future research to evaluate additional microorganisms (i.e., bacteria and fungi) could provide new information on host-microbe interactions and possibly develop ideas for management tactics to reduce turfgrass pests.

Induced overexpression of cytochrome P450 sterol 14α-demethylase gene (CYP51) correlates with sensitivity to demethylation inhibitors (DMIs) in Sclerotinia homoeocarpa.

BACKGROUND: The fungus Sclerotinia homoeocarpa causes dollar spot, the most important turfgrass disease worldwide. Demethylation inhibitor (DMI) fungicides have been relied upon heavily to manage this disease. Presently, populations of S. homoeocarpa with reduced sensitivity or resistance to DMIs are widespread in the United States. RESULTS: Cytochrome P450 sterol 14α-demethylase (ShCYP51) and its flanking regions were identified and sequenced in 29 isolates of S. homoeocarpa with a range of DMI sensitivities. No modifications were found in the gene coding and upstream regions that were consistently related to DMI sensitivity. In the absence of propiconazole, ShCYP51 was expressed at a similar low level among DMI baseline and resistant isolates. In the presence of propiconazole, DMI-resistant isolates were induced to express ShCYP51 at significantly higher levels than baseline isolates by propiconazole at 5 mg L(-1) for 5 h or at 0.5 mg L(-1) for 72 h. The ShCYP51 expression level after 72 h exposure to 0.5 mg L(-1) of propiconazole was linearly related to EC50 values and ΔRG (the change in relative growth rate over time), with R(2) values equal to 83.7 and 90.0% respectively. CONCLUSION: Induced overexpression of ShCYP51 in resistant isolates following DMI exposure is an important factor determining DMI sensitivity in S. homoeocarpa.