Nitric oxide (NO) is a double-edged sword - it can be either beneficial and activate defence responses in plants and animals or, together with reactive oxygen species, it can kill not only the pathogen but also the host. A prime target of NO is the cytochrome c-dependent respiration. Only plants possess alternative-pathway respiration with alternative oxidase (AOX) as a terminal electron acceptor. AOX has been suggested to be barely affected by NO. Here we show that NO affects cytochrome-dependent respiration in Arabidopsis thaliana (L.) Heynh. At the same time, treatment of Arabidopsis cell cultures with NO actually strongly induced AOX1a transcription, as determined by using a cDNA microarray and by Northern analysis. In accordance with transcript accumulation, NO treatment of suspension cells resulted in increased respiration through the alternative pathway. Addition of an AOX inhibitor to Arabidopsis cell cultures resulted in dramatically increased NO-sensitivity and cell death. In all, our data suggest that NO induces the AOX1a gene and that AOX may participate to counteract the toxicity of NO. Electronic supplementary material to this paper can be obtained by using the Springer Link server located at http://dx.doi.org/10.1007/s00425-002-0828-z.

The bacterial quorum sensing signals N-acyl-L: -homoserine lactones enable bacterial cells to regulate gene expression depending on population density, in order to undertake collective actions such as the infection of host cells. Only little is known about the molecular ways of plants reacting to these bacterial signals. In this study we show that the contact of Arabidopsis thaliana roots with N-hexanoyl-DL: -homoserine-lactone (C6-HSL) resulted in distinct transcriptional changes in roots and shoots, respectively. Interestingly, unlike most other bacterial signals, C6-HSL influenced only a few defense-related transcripts. Instead, several genes associated with cell growth as well as genes regulated by growth hormones showed changes in their expression after C6-HSL treatment. C6-HSL did not induce plant systemic resistance against Pseudomonas syringae. The inoculation of roots with different types of AHLs led predominantly for short chain N-butyryl-DL: -homoserine lactone and C6-HSL to root elongation. Determination of plant hormone concentrations in root and shoot tissues supported alterations of auxin to cytokinin ratio. Finally, we provide evidence that Arabidopsis takes up bacterial C6-HSL and allows systemic distribution throughout the plant. In sum, the bacterial quorum sensing signal C6-HSL does induce transcriptional changes in Arabidopsis and may contribute to tuning plant growth to the microbial composition of the rhizosphere.

Arabidopsis (Arabidopsis thaliana) NADPH oxidases have been reported to suppress the spread of pathogen- and salicylic acid-induced cell death. Here, we present dual roles of RBOHD (for respiratory burst oxidase homolog D) in an Arabidopsis-Alternaria pathosystem, suggesting either initiation or prevention of cell death dependent on the distance from pathogen attack. Our data demonstrate that a rbohD knockout mutant exhibits increased spread of cell death at the macroscopic level upon inoculation with the fungus Alternaria brassicicola. However, the cellular patterns of reactive oxygen species accumulation and cell death are fundamentally different in the AtrbohD mutant compared with the wild type. Functional RBOHD causes marked extracellular hydrogen peroxide accumulation as well as cell death in distinct, single cells of A. brassicicola-infected wild-type plants. This single cell response is missing in the AtrbohD mutant, where infection triggers spreading-type necrosis preceded by less distinct chloroplastic hydrogen peroxide accumulation in large clusters of cells. While the salicylic acid analog benzothiadiazole induces the action of RBOHD and the development of cell death in infected tissues, the ethylene inhibitor aminoethoxyvinylglycine inhibits cell death, indicating that both salicylic acid and ethylene positively regulate RBOHD and cell death. Moreover, A. brassicicola-infected AtrbohD plants hyperaccumulate ethylene and free salicylic acid compared with the wild type, suggesting negative feedback regulation of salicylic acid and ethylene by RBOHD. We propose that functional RBOHD triggers death in cells that are damaged by fungal infection but simultaneously inhibits death in neighboring cells through the suppression of free salicylic acid and ethylene levels.