Leaf senescence is an essential developmental process that impacts dramatically on crop yields and involves altered regulation of thousands of genes and many metabolic and signaling pathways, resulting in major changes in the leaf. The regulation of senescence is complex, and although senescence regulatory genes have been characterized, there is little information on how these function in the global control of the process. We used microarray analysis to obtain a high-resolution time-course profile of gene expression during development of a single leaf over a 3-week period to senescence. A complex experimental design approach and a combination of methods were used to extract high-quality replicated data and to identify differentially expressed genes. The multiple time points enable the use of highly informative clustering to reveal distinct time points at which signaling and metabolic pathways change. Analysis of motif enrichment, as well as comparison of transcription factor (TF) families showing altered expression over the time course, identify clear groups of TFs active at different stages of leaf development and senescence. These data enable connection of metabolic processes, signaling pathways, and specific TF activity, which will underpin the development of network models to elucidate the process of senescence.

Selenium (Se) is an essential plant micronutrient, but is toxic at high tissue concentrations. It is chemically similar to sulphur (S), an essential plant macronutrient. The interactions between Se and S nutrition were investigated in the model plant Arabidopsis thaliana (L.) Heynh. Arabidopsis plants were grown on agar containing a complete mineral complement and various concentrations of selenate and sulphate. The Se/S concentration ratio in the shoot ([Se]_shoot/[S]_shoot) showed a complex dependence on the ratio of selenate to sulphate concentration in the agar ([Se]_agar/[S]_agar). Increasing [S]_agar increased shoot fresh weight (FW) and [S]_shoot, but decreased [Se]_shoot. Increasing [Se]_agar increased both [Se]_shoot and [S]_shoot, but reduced shoot FW. The reduction in shoot FW in the presence of Se was linearly related to the shoot Se/S concentration ratio. These data suggest (i) that Se and S enter Arabidopsis through multiple transport pathways with contrasting sulphate/selenate selectivities, whose activities vary between plants of contrasting nutritional status, (ii) that rhizosphere sulphate inhibits selenate uptake, (iii) that rhizosphere selenate promotes sulphate uptake, possibly by preventing the reduction in the abundance and/or activity of sulphate transporters by sulphate and/or its metabolites, and (iv) that Se toxicity occurs because Se and S compete for a biochemical process, such as assimilation into amino acids of essential proteins.

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.