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2012 APS Annual Meeting Abstract

 

Poster Session: Systematics/Evolution/Ecology-Fungi

28-P

Infection and colonization of bermudagrass by Ophiosphaerella korrae, a causal fungus of spring dead spot of bermudagrass.
F. FLORES (1), N. Walker (1), T. Mitchell (2), S. Marek (1), J. Anderson (1)
(1) Oklahoma State University, Stillwater, OK, U.S.A.; (2) The Ohio State University, Department of Plant Pathology, Columbus, OH, U.S.A.

Bermudagrass (Cynodon dactylon and C. dactylon x C. transvaalensis) is a commonly used turfgrass in the Southern United States where it is severely affected by spring dead spot (SDS). SDS is caused by one of three fungi in the genus Ophiosphaerella, namely O. herpotricha, O. korrae, or O. narmari. Despite the importance of SDS, the biology and ecology of the causal agents and the etiology of the disease remain poorly understood. In this study, the infection and colonization of bermudagrass tissues by O. korrae were characterized using fluorescence microscopy. Agrobacterium mediated transformation was used to transform O. korrae to express the red fluorescent protein tdTomato (tdTom). Roots and stolons of the interspecific hybrid cultivars Midlawn and Tifway, and C. transvaalensis accessions Uganda and 3200 were inoculated with tdTom expressing O. korrae and observed from 2 to 22 days post infection (DPI). O. korrae colonized roots and stolons of all cultivars at a similar rate with necrosis evident as early as 2 DPI on Tifway and Midlawn, while on 3200 and Uganda necrosis appeared at 8 DPI. Root epidermal and cortical cells were colonized rapidly in all bermudagrasses. However, vascular colonization did not occur until 4 DPI in Uganda, 8 DPI in 3200 and Midlawn, and 14 DPI in Tifway. For stolons, necrotic lesions were evident on Midlawn and Tifway at 4 DPI while 3200 and Uganda stolons showed discoloration but not necrosis up to 22 DPI. For all cultivars, the fungus did not penetrate beyond the epidermis of the stolons. These differences in infection and colonization of bermudagrasses suggest the underlying host genetics can be exploited for effective management of SDS.

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