Throwing new light on the hypersensitive response

The hypersensitive response (HR) is a pathogen-localised cell death believed to contribute towards suppression of disease development. Amongst the key initiators of the HR are reactive oxygen species (ROS). We observed the formation of HR elicited by Pseudomonas syringae pv. tomato (Pst) avrRpm1 in Arabidopsis to be influenced by light in a fluence-dependent manner. Higher fluence rates were required for rapid cell death, ROS generation, and the accumulation of the defence signals, salicylic and jasmonic acid, as well as expression of several defence-related genes. Conversely, lower light fluence rates (< 25 mmol m−1 s−1) initiated senescence-like symptoms around the infected area and expression of Senescence-Associated Gene 12. A defining feature of leaf senescence is chlorophyll catabolism, which proceeds via a series of intermediates including the breakdown of phaeophorbide (phaeide) to red chlorophyll catabolite (RCC) through the enzymatic action of phaeophorbide a oxygenase (PaO), which is encoded by ACD1 in Arabidopsis. Maize and Arabidopsis mutants deficient in PaO exhibit light-dependent cell death attributed to the accumulation of phototoxic phaeide. HPLC analysis of developing Pst avrRpm1 HR lesions in the Arabidopsis acd1 mutants showed accumulation of phaeide as early as 9 h following challenge. Mendel's I gene, mutations of which partially disable chlorophyll catabolism, has recently been identified. Crucially, Arabidopsis lines where I gene expression was suppressed by RNAi exhibited a delayed Pst avrRpm1 HR. We propose that certain chlorophyll catabolites are previously unsuspected components in the HR mechanism. These could contribute to ROS generation by virtue of being uncoupled from the photosynthetic reaction centres