SummaryLeaf senescence is a complex process that is controlled by multiple developmental and environmental signals and is manifested by induced expression of a large number of different genes. In this paper we describe experiments that show, for the ®rst time, that the salicylic acid (SA)-signalling pathway has a role in the control of gene expression during developmental senescence. Arabidopsis plants defective in the SA-signalling pathway (npr1 and pad4 mutants and NahG transgenic plants) were used to investigate senescence-enhanced gene expression, and a number of genes showed altered expression patterns. Senescence-induced expression of the cysteine protease gene SAG12, for example, was conditional on the presence of SA, together with another unidenti®ed senescence-speci®c factor. Changes in gene expression patterns were accompanied by a delayed yellowing and reduced necrosis in the mutant plants defective in SA-signalling, suggesting a role for SA in the cell death that occurs at the ®nal stage of senescence. We propose the presence of a minimum of three senescence-enhanced signalling factors in senescing leaves, one of which is SA. We also suggest that a combination of signalling factors is required for the optimum expression of many genes during senescence.

The nature and origin of the reactive oxygen species (ROS) involved in the early part of Ultraviolet-B (UV-B)-induced signaling pathways were investigated in Arabidopsis thaliana using a range of enzyme inhibitors and free radical scavengers. The increase in PR-1 transcript and decrease in Lhcb transcript in response to UV-B exposure was shown to be mediated through pathways involving hydrogen peroxide (H(2)O(2)) derived from superoxide (O(2)(&z.rad;-)). In contrast, the up-regulation of PDF1.2 transcript was mediated through a pathway involving O(2)(&z.rad;-) directly. The origins of the ROS were also shown to be distinct and to involve NADPH oxidase and peroxidase(s). The up-regulation of Chs by UV-B was not affected by ROS scavengers, but was reduced by inhibitors of nitric oxide synthase (NOS) or NO scavengers. Together these results suggest that UV-B exposure leads to the generation of ROS, from multiple sources, and NO, through increased NOS activity, giving rise to parallel signaling pathways mediating responses of specific genes to UV-B radiation.

Treatment with supplementary UV‐B resulted in decreases in transcripts of the photosynthetic genes Lhcb and psbA and concomitant increase in transcripts of two pathogen‐related genes, PR‐1 and PDF1·2, in Arabidopsis thaliana. UV‐B exposure caused increases in jasmonic acid (JA) levels and ethylene production. UV‐B treatment of jar1 and etr1‐1 mutants, which are insensitive to JA and ethylene, respectively, showed that the increase in PR‐1 transcripts was dependent on ethylene and PDF1·2 transcripts on both JA and ethylene. In contrast, the down‐regulation of photosynthetic transcripts was independent of both compounds. Previous studies have indicated a role for reactive oxygen species (ROS) in the UV‐B‐induced down‐regulation of the photosynthetic genes and up‐regulation of PR‐1 genes. Here we have shown that ROS are also required for the UV‐B‐induced up‐regulation of PDF1·2 genes. The results indicate that the effects of UV‐B on the three sets of genes are mediated through three distinct signal transduction pathways which are similar, but not identical, to pathways initiated in response to pathogen infection. In addition, the increased sensitivity of both jar1 and etr1‐1 mutants to UV‐B radiation, as compared with wild‐type plants, indicated that intact JA and ethylene signal pathways are required for defence against UV‐B damage.

Exposure to UV-B radiation resulted in a loss of chlorophyll and an increase in lipid damage in a similar manner to that induced during natural senescence. In addition, exposure to UV-B led to the induction of a number of genes associated with senescence (SAG12, 13, 14, and 17). These results show, for the first time, that exposure to UV-B can lead to cellular decline through active and regulated processes involving many genes also associated with natural senescence.

Exposure to UV-B radiation resulted in a loss of chlorophyll and an increase in lipid damage in a similar manner to that induced during natural senescence. In addition, exposure to UV-B led to the induction of a number of genes associated with senescence (SAG12, 13, 14, and 17). These results show, for the first time, that exposure to UV-B can lead to cellular decline through active and regulated processes involving many genes also associated with natural senescence.