Silicon, applied as calcium silicate slag (20% Si), was evaluated for its potential to suppress gray leaf spot (Magnaporthe grisea) and increase plant growth in newly planted St. Augustinegrass in the summers of 2000 and 2001. Calcium silicate was applied (1,000 kg Si/ha) to three sites that contained Si-deficient Histosols prior to sprigging St. Augustinegrass, cv. Floratam, in southern Florida. This treatment was compared with foliar sprays of chlorothalonil, calcium silicate plus chlorothalonil, and an untreated control. Immediately after planting, applications of chlorothalonil (720 g/liter) were made every 10 days for a total of seven sprays at a rate of 7.6 kg a.i./ha with a commercial sprayer. Based on area under the disease progress curve (AUDPC) values for the treatments calcium silicate alone, chlorothalonil, and calcium silicate plus chlorothalonil, gray leaf spot was reduced by 7, 65, and 68% at site one, 28, 34, and 59% at site two, and 41, 55, and 68% at site three, respectively when compared with the untreated control. The application of calcium silicate alone significantly reduced the final AUDPC of gray leaf spot when compared with the control at site two only. However, when disease severities were analyzed by week, the calcium silicate treatment significantly reduced the percentage of disease at weeks 2, 6, and 8 at site one and weeks 3 to 8 at site three when compared with the control. The final percent bare ground coverage for St. Augustinegrass was increased significantly using calcium silicate by 17 and 34% over the control at sites one and two, respectively (P ≤ 0.05). Silicon was the only element to significantly increase in the leaf tissue for treatments amended with calcium silicate. Levels of Si in leaves for treatments amended with calcium silicate were from 1.2 to 1.3%, while those not receiving calcium silicate had only 0.6 to 0.7%. Amendments with calcium silicate slag for St. Augustinegrass sod production on Si-deficient soils may be an option to reduce gray leaf spot development in newly sprigged fields and promote earlier ground coverage of grass when the environment is favorable for disease.
Southern chinch bug, Blissus insularis Barber (Hemiptera: Blissidae), is the most serious insect pest of St. Augustinegrass Stenotaphrum secundatum (Walter) Kuntze, a common lawngrass grown in southeastern U.S. states. Host plant resistance to southern chinch bug has been identified in the polyploid St. Augustinegrass 'FX-10' and the diploid 'Captiva'. The objective of this research was to identify possible physical mechanism(s) explaining chinch bug resistance in these cultivars. We studied the distribution of chinch bug salivary sheaths in the preferred tissue for feeding (the axillary shoot) of the two resistant cultivars and two susceptible cultivars, paired for ploidy ('Floratam', polyploid, and Palmetto, diploid). We also investigated the potential role of axillary shoot lignification and anatomy in chinch bug resistance. Salivary sheaths were more abundant on the outermost leaf sheath of axillary shoots of resistant cultivars compared with susceptible cultivars. In contrast, fewer salivary sheaths reached the innermost meristematic tissue in the axillary shoots of resistant St. Augustinegrass cultivars than in the two susceptible cultivars. The polyploid cultivars FX-10 and Floratam had higher total lignin in axillary shoots compared with the diploid cultivars Captiva and Palmetto. However, total lignin content was not correlated with resistance to southern chinch bug. Light microscopic studies found no differences in epidermal layer thickness among resistant and susceptible St. Augustinegrass cultivars. However, transmission electron microscopic studies revealed that the cell walls of the sclerenchyma cells around the vascular bundle of southern chinch bug-resistant FX-10 and Captiva were significantly thicker than the cell walls in susceptible Floratam and Palmetto. Our research suggests that the thick-walled sclerenchyma cells around the vascular bundle play a role in southern chinch bug resistance in St. Augustinegrass, possibly by reducing stylet penetration to the vascular tissue.
Over 400,000 ha of St. Augustinegrass, Stenotaphrum secundatum (Walt.) Kuntze, are managed as a turfgrass in the southern United States, and the southern chinch bug, Blissus insularis Barber, is its most important insect pest. New sources of host plant resistance to southern chinch bugs became necessary due to the development of virulent populations of chinch bugs which were able to feed on the only acceptable resistant cultivar, Floratam. Initial testing evaluated 14 lines for chinch bug resistance using insects collected from five locations from Palm Beach Co., FL. Host plant resistance was determined by mortality of adult chinch bugs held on a turfgrass for 14 d. A second study was conducted with five lines from the first test with southern chinch bugs collected from nine locations throughout Florida. Tests showed a high level of southern chinch bug resistance in NUF 76, NUF 216 and FX-10. Leaf blades of NUF-76 are significantly shorter and narrower than other tested St. Augustinegrass lines when evaluated 2 wks after mowing. NUF-76 is unique because for the first time, resistance to the southern chinch bug has been identified within a diploid line of St. Augustinegrass. Prior to this, southern chinch bug resistance was only associated with polyploid lines which generally have large leaves and reduced or no seed set due to sterility problems. This discovery will allow chinch bug resistance to be more easily bred into other St. Augustinegrass lines.
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