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Hydrogen Peroxide from the Oxidative Burst Is Neither Necessary
Nor Sufficient for Hypersensitive Cell Death Induction, Phenylalanine
Ammonia Lyase Stimulation, Salicylic Acid Accumulation, or Scopoletin
Consumption in Cultured Tobacco Cells Treated with Elicitin
Stéphan Dorey1,
Marguerite Kopp,
Pierrette Geoffroy,
Bernard Fritig, and
Serge Kauffmann*
Institut de Biologie Moléculaire des Plantes du Centre
National de la Recherche Scientifique, Université Louis Pasteur,
12 rue du Général Zimmer, 67084 Strasbourg cedex, France
H2O2 from the
oxidative burst, cell death, and defense responses such as the
production of phenylalanine ammonia lyase (PAL), salicylic acid (SA),
and scopoletin were analyzed in cultured tobacco (Nicotiana
tabacum) cells treated with three proteinaceous elicitors: two
elicitins ( -megaspermin and -megaspermin) and one glycoprotein.
These three proteins have been isolated from Phytophthora
megasperma H20 and have been previously shown to be equally
efficient in inducing a hypersensitive response (HR) upon infiltration
into tobacco leaves. However, in cultured tobacco cells these elicitors
exhibited strikingly different biological activities. -Megaspermin
was the only elicitor that caused cell death and induced a strong,
biphasic H2O2 burst. Both elicitins stimulated
PAL activity similarly and strongly, while the glycoprotein caused only
a slight increase. Only elicitins induced SA accumulation and
scopoletin consumption, and -megaspermin was more efficient. To
assess the role of H2O2 in HR cell death and
defense response expression in elicitin-treated cells, a gain and loss
of function strategy was used. Our results indicated that
H2O2 was neither necessary nor sufficient for
HR cell death, PAL activation, or SA accumulation, and that
extracellular H2O2 was not a direct cause of
intracellular scopoletin consumption.
1
S.D. was supported by a doctoral fellowship of
the French Ministry of Research.
*
Corresponding author; e-mail
serge.kauffmann{at}ibmp-ulp.u-strasbg.fr; fax 33-388-61-4442.
Plant Physiol. (1999) 121: 163-172
Copyright Clearance Center: 0032-0889/99/121//10
© 1999 American Society of Plant Physiologists
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