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Plant Physiol, December 1999, Vol. 121, pp. 1299-1308
N-Acylethanolamines in Signal Transduction of
Elicitor Perception. Attenuation of Alkalinization Response and
Activation of Defense Gene Expression1
Swati
Tripathy,
Barney J.
Venables, and
Kent D.
Chapman*
University of North Texas, Department of Biological Sciences,
Division of Biochemistry and Molecular Biology, Denton, Texas
76203-5220 (S.T., K.D.C.); and TRAC Laboratories, 113 S. Cedar,
Denton, Texas 76201 (B.J.V.)
In a recent study of
N-acylphosphatidylethanolamine (NAPE) metabolism in
elicitor-treated tobacco (Nicotiana tabacum L.) cells, we identified a rapid release and accumulation of medium-chain N-acylethanolamines (NAEs) (e.g.
N-myristoylethanolamine or NAE 14:0) and a compensatory
decrease in cellular NAPE (K.D. Chapman, S. Tripathy, B. Venables, A.D.
Desouza [1998] Plant Physiol 116: 1163-1168). In the present study,
we extend this observation and report a 10- to 50-fold increase in NAE
14:0 content in leaves of tobacco (cv Xanthi) plants treated with
xylanase or cryptogein elicitors. Exogenously supplied synthetic NAE
species affected characteristic elicitor-induced and short- and
long-term defense responses in cell suspensions of tobacco and
long-term defense responses in leaves of intact tobacco plants. In
general, synthetic NAEs inhibited elicitor-induced medium
alkalinization by tobacco cells in a time- and concentration-dependent
manner. Exogenous NAE 14:0 induced expression of phenylalanine ammonia
lyase in a manner similar to fungal elicitors in both cell suspensions and leaves of tobacco. NAE 14:0, but not myristic acid, activated phenylalanine ammonia lyase expression at submicromolar concentrations, well within the range of NAE 14:0 levels measured in elicitor-treated plants. Collectively, these results suggest that NAPE metabolism, specifically, the accumulation of NAE 14:0, are part of a signal transduction pathway that modulates cellular defense responses following the perception of fungal elicitors.
1
This research was supported initially by U.S.
Department of Agriculture-National Research Initiative Competitive
Grants Program (agreement no. 96-35304-3862) and also by the Texas
Higher Education Coordinating Board (Advanced Research Program grant
no. 003594-028).
*
Corresponding author; e-mail chapman{at}unt.edu; fax 94-565-4136.
© 1999 American Society of Plant Physiologists
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