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Cycloheximide Treatments Implicate Papilla Formation in Resistance of Reed Canarygrass to Fungi. C. P. Vance, Research Associate, Department of Plant Pathology, The Pennsylvania State University, University Park, PA 16802; R. T. Sherwood, Research Plant Pathologist, U.S. Department of Agriculture, Agricultural Research Service, U.S. Regional Pasture Research Laboratory, University Park, PA 16802. Phytopathology 66:498-502. Accepted for publication 24 October 1975. DOI: 10.1094/Phyto-66-498.

Reed canarygrass leaf-disks were floated on water and inoculated with spore suspensions of Helminthosporium catenarium, H. avenae, Stemphylium botryosum, Leptosphaerulina trifolii, Botrytis cinerea, and an Ascochyta sp. Only H. catenarium was pathogenic on reed canarygrass. With the noninfecting species, a papilla (host cell wall thickening) formed in the epidermal wall beneath each fungal appressorium from which penetration was attempted, and no penetration occurred. With H. catenarium most appressoria induced papilla formation and did not initiate penetration, but about 1% of appressoria initiated direct penetration through a thin-walled, poorly-formed papillar swelling. When leaf-disks were floated on aqueous solutions of cycloheximide (10-25 µg/ml), protein synthesis was inhibited, papilla formation was prevented, and more than 80% of appressoria of all fungi gave rise to direct penetrations. Primary infection hyphae grew well and invaded adjacent epidermal cells. Transfer of leaf-disks from cycloheximide solutions to water prior to appressorium formation, restored protein synthesis, restored papilla formation, and prevented penetration. No inducible antifungal compounds could be detected by the drop-diffusate technique. Papilla formation appears to be a defense mechanism against fungal penetration that requires response-dependent protein synthesis.

Additional keywords: resistance, phytoalexin, protein synthesis, lignituber, Phalaris arundinacea.