PARASITIC MELOIDOGYNE AND MUTUALISTIC ACREMONIUM INCREASE CHITINASE IN TALL FESCUE

被引:24
作者
ROBERTS, CA [1 ]
MAREK, SM [1 ]
NIBLACK, TL [1 ]
KARR, AL [1 ]
机构
[1] UNIV MISSOURI,DEPT PLANT PATHOL,COLUMBIA,MO 65211
关键词
FESTUCA-ARUNDINACEA; ACREMONIUM-COENOPHIALUM; EPICHLOE-TYPHINA; MELOIDOGYNE-MARYLANDI; PATHOGENESIS-RELATED PROTEINS; ELICITOR; PLANT DEFENSE; FESCUE TOXICOSIS; NEMATODES;
D O I
10.1007/BF00980066
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Tall fescue (Festuca arundinacea Schreb.) is a C-3 perennial grass noted for its persistence in harsh environments. Tall fescue persistence is enhanced by Acremonium coenophialum, a mutualistic fungal endophyte that increases resistance to drought, pathogens, and insects. This research was conducted to identify and elicit biochemical mechanism(s) that could account for tall fescue persistence. In initial studies, two cultivars known to differ in persistence were analyzed for chitinase, an antifungal hydrolase associated with disease resistance in other plants. Acremonium-infected Kentucky 31 (KY31), a persistent cultivar, and Johnstone, a nonpersistent cultivar, were inoculated with the parasitic nematode, Meloidogyne marylandi, grown for 50 days, and analyzed at 10-day intervals. Chitinase fluctuated throughout the 50-day period of seedling development, and activity was highest in the persistent Acremonium-infected KY31. In addition, chitinase was elicited by parasitic M. marylandi and expressed systemically. Subsequent studies were conducted to determine whether or not mutualistic Acremonium could increase chitinase activity. Genetically identical KY31, with and without Acremonium, were grown for 25 days and analyzed for chitinase at 5-day intervals. After 20 days, Acremonium-infected KY31 expressed more chitinase than Acremonium-free KY31. We concluded that chitinase is related to tall fescue persistence; it was highest in the most persistent cultivar, increased under pathogen attack, and increased in the presence of Acremonium, a symbiont known to enhance disease resistance.
引用
收藏
页码:1107 / 1116
页数:10
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