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

Abstract

H 2 O 2 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 H 2 O 2 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 H 2 O 2 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 H 2 O 2 was neither necessary nor sufficient for HR cell death, PAL activation, or SA accumulation, and that extracellular H 2 O 2 was not a direct cause of intracellular scopoletin consumption.

Alpha-picolinic acid, a fungal toxin and mammal apoptosis-inducing agent, elicits hypersensitive-like response and enhances disease resistance in rice

“…The transcriptional pattern of OsRboha implied that the PA-stimulated ROS generation of NADPH-oxidase dependence probably resulted from the PA modification of the enzyme rather than de novo protein synthesis (Fig 4B, C), and high PA might caused cell disruption leading to the decrease of OsRboha transcription. We did not find much influence of H 2 O 2 on cell death induced by PA (Fig 3C), indicating that the H 2 O 2 generation was not a key determinant of the cell death process as observed in tobacco cells [37]. The result implied that the relation between the hypersensitive cell death and the oxidative burst is very complicated [36].…”

Proteomics-based analysis reveals that Verticillium dahliae toxin induces cell death by modifying the synthesis of host proteins

“…supernatant). This finding suggests that the ROS burst was likely a plant defense response from V. dahliae, not the cause of cell death (Dorey et al 1999).…”

Programmed cell death in the plant immune system

“…If HR is not adaptive in restricting pathogen growth, it may be adaptive for the generation of long range signals, mediated by ROS and SA, that induce the systemic acquired resistance that primes a plant for secondary infection. [126][127][128] …”