The StPti5 ethylene response factor acts as a susceptibility factor by negatively regulating the potato immune response to pathogens.

Ethylene response factors (ERFs) have been associated with biotic stress in Arabidopsis, while their function in non-model plants is still poorly understood. Here we investigated the role of potato ERF StPti5 in plant immunity. We show that StPti5 acts as a susceptibility factor. It negatively regulates potato immunity against potato virus Y and Ralstonia solanacearum, pathogens with completely different modes of action, and thereby has a different role than its orthologue in tomato. Remarkably, StPti5 is destabilised in healthy plants via the autophagy pathway and accumulates exclusively in the nucleus upon infection. We demonstrate that StEIN3 and StEIL1 directly bind the StPti5 promoter and activate its expression, while synergistic activity of the ethylene and salicylic acid pathways is required for regulated StPti expression. To gain further insight into the mode of StPti5 action in attenuating potato defence responses, we investigated transcriptional changes in salicylic acid deficient potato lines with silenced StPti5 expression. We show that StPti5 regulates the expression of other ERFs and downregulates the ubiquitin-proteasome pathway as well as several proteases involved in directed proteolysis. This study adds a novel element to the complex puzzle of immune regulation, by deciphering a two-level regulation of ERF transcription factor activity in response to pathogens.

Cryptochrome-1-dependent execution of programmed cell death induced by singlet oxygen in Arabidopsis thaliana.

Programmed cell death (PCD) plays an important role during the life cycle of higher organisms. Although several regulatory mechanisms governing PCD are thought to be conserved in animals and plants, light-dependent cell death represents a form of PCD that is unique to plants. The light requirement of PCD has often been associated with the production of reactive oxygen species during photosynthesis. In support of this hypothesis, hydrogen peroxide and superoxide have been shown to be involved in triggering a PCD response. In the present work, we have used the conditional flu mutant of Arabidopsis to analyze the impact of another reactive oxygen species, singlet oxygen, on cell death. Unexpectedly, the light-dependent release of singlet oxygen alone is not sufficient to induce PCD of flu seedlings but has to act together with a second concurrent blue light reaction. This blue-light-specific trigger of PCD could not be attributed to a photosynthetic reaction or redox change within the chloroplast but to the activation of the blue light/UVA-specific photoreceptor cryptochrome. The singlet oxygen-mediated and cryptochrome-dependent cell death response differs in several ways from PCD triggered by hydrogen peroxide/superoxide.