No abstract

Selenium (Se) at very low doses has crucial functions in humans and animals. Since plants represent the main dietary source of this element, Se-containing crops may be used as a means to deliver Se to consumers (biofortification). Several strategies have been exploited to increase plant Se content. Selenium assimilation in plants affects both sulfur (S) and nitrogen (N) metabolic pathways, which is why recent research has also focused on the effect of Se fertilization on the production of S- and N- secondary metabolites with putative health benefits. In this review we discuss the function of Se in plant and human nutrition and the progress in the genetic engineering of Se metabolism to increase the levels and bioavailability of this element in food crops. Particular attention is paid to Se biofortification and the synthesis of compounds with beneficial effects on health.

Although selenium (Se) is a known anticarcinogen, little is known regarding how Se affects other nutritional qualities in crops. Tomato ( Solanum lycopersicon ) was supplied with 0-50 μM selenate and analyzed for elemental composition and antioxidant compounds. When supplied at low doses (5 and 10 μM) via the roots, Se stimulated the synthesis of phenolic compounds in leaves and reduced the levels of Mo, Fe, Mn, and Cu in roots. At higher doses (25 and 50 μM Se) leaf glutathione levels were 3-5-fold enhanced. Supply of selenate via foliar spray (0, 2, or 20 mg Se plant(-1)) resulted in Se-biofortified tomato fruits, with Se levels low enough not to pose a health risk. The Se-biofortified fruits showed enhanced levels of the antioxidant flavonoids naringenin chalcone and kaempferol and a concomitant decrease of cinnamic acid derivatives. Thus, tomato fruits can be safely enriched with Se, and Se biofortification may enhance levels of other neutraceutical compounds.

Deprivation of mineral nutrients causes significant retardation of plant growth. This retardation is associated with nutrient-specific and general stress-induced transcriptional responses. In this study, we adjusted the external supply of iron, potassium and sulfur to cause the same retardation of shoot growth. Nevertheless, limitation by individual nutrients resulted in specific morphological adaptations and distinct shifts within the root metabolite fingerprint. The metabolic shifts affected key metabolites of primary metabolism and the stress-related phytohormones, jasmonic, salicylic and abscisic acid. These phytohormone signatures contributed to specific nutrient deficiency-induced transcriptional regulation. Limitation by the micronutrient iron caused the strongest regulation and affected 18% of the root transcriptome. Only 130 genes were regulated by all nutrients. Specific co-regulation between the iron and sulfur metabolic routes upon iron or sulfur deficiency was observed. Interestingly, iron deficiency caused regulation of a different set of genes of the sulfur assimilation pathway compared with sulfur deficiency itself, which demonstrates the presence of specific signal-transduction systems for the cross-regulation of the pathways. Combined iron and sulfur starvation experiments demonstrated that a requirement for a specific nutrient can overrule this cross-regulation. The comparative metabolomics and transcriptomics approach used dissected general stress from nutrient-specific regulation in roots of Arabidopsis.

Two selenium (Se) fertilization methods were tested for their effects on levels of anticarcinogenic selenocompounds in radish (Raphanus sativus), as well as other nutraceuticals. First, radish was grown on soil and foliar selenate applied 7 days before harvest at 0, 5, 10, and 20 mg Se per plant. Selenium levels were up to 1200 mg Se/kg DW in leaves and 120 mg Se/kg DW in roots. The thiols cysteine and glutathione were present at 2–3-fold higher levels in roots of Se treated plants, and total glucosinolate levels were 35% higher, due to increases in glucoraphanin. The only seleno-aminoacid detected in Se treated plants was Se-methyl-SeCys (100 mg/kg FW in leaves, 33 mg/kg FW in roots). The levels of phenolic aminoacids increased with selenate treatment, as did root total nitrogen and protein content, while the level of several polyphenols decreased. Second, radish was grown in hydroponics and supplied with 0, 5, 10, 20, or 40 μM selenate for 1 week. Selenate treatment led to a 20–30% increase in biomass. Selenium concentration was 242 mg Se/kg DW in leaves and 85 mg Se/kg DW in roots. Cysteine levels decreased with Se in leaves but increased in roots; glutatione levels decreased in both. Total glucosinolate levels in leaves decreased with Se treatment due to repression of genes involved in glucosinolates metabolism. Se-methyl-SeCys concentration ranged from 7–15 mg/kg FW. Aminoacid concentration increased with Se treatment in leaves but decreased in roots. Roots of Se treated plants contained elevated transcript levels of sulfate transporters (Sultr) and ATP sulfurylase, a key enzyme of S/Se assimilation. No effects on polyphenols were observed. In conclusion, Se biofortification of radish roots may be achieved via foliar spray or hydroponic supply. One to ten radishes could fulfill the daily human requirement (70 μg) after a single foliar spray of 5 mg selenate per plant or 1 week of 5–10 μM selenate supply in hydroponics. The radishes metabolized selenate to the anticarcinogenic compound Se-methyl-selenocysteine. Selenate treatment enhanced levels of other nutraceuticals in radish roots, including glucoraphanin. Therefore, Se biofortification can produce plants with superior health benefits.

No abstract

Plants close stomata when root water availability becomes limiting. Recent studies have demonstrated that soil-drying induces root-to-shoot sulfate transport via the xylem and that sulfate closes stomata. Here we provide evidence for a physiologically relevant signaling pathway that underlies sulfate-induced stomatal closure in Arabidopsis (Arabidopsis thaliana). We uncovered that, in the guard cells, sulfate activates NADPH oxidases to produce reactive oxygen species (ROS) and that this ROS induction is essential for sulfate-induced stomata closure. In line with the function of ROS as the secondmessenger of abscisic acid (ABA) signaling, sulfate does not induce ROS in the ABA-synthesis mutant, aba3-1, and sulfateinduced ROS were ineffective at closing stomata in the ABA-insensitive mutant abi2-1 and a SLOW ANION CHANNEL1 loss-of-function mutant. We provided direct evidence for sulfate-induced accumulation of ABA in the cytosol of guard cells by application of the ABAleon2.1 ABA sensor, the ABA signaling reporter ProRAB18:GFP, and quantification of endogenous ABA marker genes. In concordance with previous studies, showing that ABA DEFICIENT3 uses Cys as the substrate for activation of the ABSCISIC ALDEHYDE OXIDASE3 (AAO3) enzyme catalyzing the last step of ABA production, we demonstrated that assimilation of sulfate into Cys is necessary for sulfate-induced stomatal closure and that sulfate-feeding or Cys-feeding induces transcription of NINE-CIS-EPOXYCAROTENOID DIOXYGENASE3, limiting the synthesis of the AAO3 substrate. Consequently, Cys synthesis-depleted mutants are sensitive to soil-drying due to enhanced water loss. Our data demonstrate that sulfate is incorporated into Cys and tunes ABA biosynthesis in leaves, promoting stomatal closure, and that this mechanism contributes to the physiological water limitation response.

Two maize genotypes differently responsive to nitrogen availability were characterized for their efficiency in nitrate accumulation via both the LATS (Low-Affinity Transport System) and HATS (High-Affinity Transport System) nitrate uptake systems. In addition, a full-length cDNA encoding a putative high-affinity nitrate transporter (ZmNrt2.1) was isolated and its expression evaluated in both the roots and leaves of the two maize genotypes, together with the expression of a maize H(+)-ATPase isoform (Mha1). The data showed the importance of the iHATS (Inducible High-Affinity System) system efficiency as a physiological marker of adaptation to low input and suggested that the transcript accumulation of ZmNrt2.1 might be a key step for the regulation of iHATS. However, ZmNrt2.1 transcription cannot account for the differences found between the two hybrids in terms of the activity of their respective iHATS and, as a consequence, of their adaptation to low input. Therefore, the involvement of some other transporter(s) or of some post-transcriptional/post-translational mechanism of regulation affecting the efficiency of iHATS may be hypothesized. In addition, the data suggest that the transcription of the Mha1 gene may also be involved in the global efficiency of the iHATS system.