Plants, unlike other higher eukaryotes, possess all the necessary enzymatic equipment for de novo synthesis of methionine, an amino acid that supports additional roles than simply serving as a building block for protein synthesis. This is because methionine is the immediate precursor of S -adenosylmethionine (AdoMet), which plays numerous roles of being the major methyl-group donor in transmethylation reactions and an intermediate in the biosynthesis of polyamines and of the phytohormone ethylene. In addition, AdoMet has regulatory function in plants behaving as an allosteric activator of threonine synthase. Among the AdoMet-dependent reactions occurring in plants, methylation of cytosine residues in DNA has raised recent interest because impediment of this function alters plant morphology and induces homeotic alterations in flower organs. Also, AdoMet metabolism seems somehow implicated in plant growth via an as yet fully understood link with plant-growth hormones such as cytokinins and auxin and in plant pathogen interactions. Because of this central role in cellular metabolism, a precise knowledge of the biosynthetic pathways that are responsible for homeostatic regulation of methionine and AdoMet in plants has practical implications, particularly in herbicide design.

Summary: Photorespiration is a light‐dependent source of H₂O₂ in the peroxisomes, where concentrations of this signalling molecule are regulated by catalase. Growth of Arabidopsis knock‐out mutants for CATALASE2 (cat2) in ambient air caused severely decreased rosette biomass, intracellular redox perturbation and activation of oxidative signalling pathways. These effects were absent when cat2 was grown at high CO₂ levels to inhibit photorespiration, but were re‐established following a subsequent transfer to air. Growth of cat2 in air at different daylengths revealed that photoperiod is a critical determinant of the oxidative stress response. Decreased growth was observed in 8‐h, 12‐h and 16‐h photoperiods, but lesion development was dependent on long days. Experiments at different light fluence rates showed that cell death in cat2 was linked to long days and not to total light exposure or the severity of oxidative stress. Perturbed intracellular redox state and oxidative signalling pathway induction were more prominent in short days than in long days, as evidenced by glutathione status and induction of defence genes and oxidative stress‐responsive transcripts. Similar daylength‐dependent effects were observed in the response of mature plants transferred from short days in high CO₂ conditions to ambient air conditions. Prior growth of plants with short days in air alleviated the cat2 cell‐death phenotype in long days. Together, the data reveal the influence of photoperiodic events on redox signalling, and define distinct photoperiod‐dependent strategies in the acclimation versus cell‐death decision in stress conditions.

Pyridine nucleotides are key redox carriers in the soluble phase of all living cells, and both NAD and NADP play crucial roles in pro-oxidant and antioxidant metabolism. Recent data also suggest a number of non-redox mechanisms by which these nucleotides could influence cell function. In cases where these mechanisms involve NAD(P) consumption, resynthesis must occur to maintain nucleotide pools. Important information on the pathways involved in NAD synthesis in plants is beginning to appear, but many outstanding questions remain. This work provides an overview of the current state of knowledge on NAD synthesis pathways in plants and other organisms, analyses plant sequences for the first two enzymes of the de novo synthesis of NAD, proposes a preliminary model for the intracellular distribution of NAD synthesis, presents plant homologues of recently identified yeast mitochondrial NAD transporters, and discusses factors likely to be important in the regulation of NAD synthesis and contents in plants, with particular reference to stress conditions.

Since cysteine is the first committed molecule in plant metabolism containing both sulphur and nitrogen, the regulation of its biosynthesis is critically important. Cysteine itself is required for the production of an abundance of key metabolites in diverse pathways. Plants alter their metabolism to compensate for sulphur and nitrogen deficiencies as best as they can, but limitations in either nutrient not only curb a plant’s ability to synthesize cysteine, but also restrict protein synthesis. Nutrients such as nitrate and sulphate (and carbon) act as signals; they trigger molecular mechanisms that modify biosynthetic pathways and thereby have a profound impact on metabolite fluxes. Cysteine biosynthesis is modified by regulators acting at the site of uptake and throughout the plant system. Recent data point to the existence of nutrient‐specific signal transduction pathways that relay information about external and internal nutrient concentrations, resulting in alterations to cysteine biosynthesis. Progress in this field has led to the cloning of genes that play pivotal roles in nutrient‐induced changes in cysteine formation.

Leaf metabolism produces H₂O₂ at high rates, but current concepts suggest that the potent signalling effects of this oxidant require that concentrations be controlled by a battery of antioxidative enzymes. The extent to which H₂O₂ is allowed to accumulate remains unclear. There is little consensus on leaf H₂O₂ values in the literature and measured concentrations in unstressed conditions range from 50–5000 nmol g⁻¹ fresh weight, a difference that probably reflects technical inaccuracies as much as biological variability. This article uses new experimental and literature data to examine some of the difficulties in accurately measuring H₂O₂ in leaf extracts. Potential problems relate to sensitivity, interference from other redox-active compounds, and H₂O₂ stability during sample preparation. Particular attention is drawn to the influence of tissue mass/extraction volume in the quantitative estimation of H₂O₂ contents, and the possibility that this factor could contribute to the variability of literature data.