33 research outputs found
Alkaline stress and iron deficiency regulate iron uptake and riboflavin synthesis gene expression differently in root and leaf tissue: implications for iron deficiency chlorosis
Iron (Fe) is an essential mineral that has low solubility in alkaline soils, where its deficiency results in chlorosis. Whether low Fe supply and alkaline pH stress are equivalent is unclear, as they have not been treated as separate variables in molecular physiological studies. Additionally, molecular responses to these stresses have not been studied in leaf and root tissues simultaneously. We tested how plants with the Strategy I Fe uptake system respond to Fe deficiency at mildly acidic and alkaline pH by measuring root ferric chelate reductase (FCR) activity and expression of selected Fe uptake genes and riboflavin synthesis genes. Alkaline pH increased cucumber (Cucumis sativus L.) root FCR activity at full Fe supply, but alkaline stress abolished FCR response to low Fe supply. Alkaline pH or low Fe supply resulted in increased expression of Fe uptake genes, but riboflavin synthesis genes responded to Fe deficiency but not alkalinity. Iron deficiency increased expression of some common genes in roots and leaves, but alkaline stress blocked up-regulation of these genes in Fe-deficient leaves. In roots of the melon (Cucumis melo L.) fefe mutant, in which Fe uptake responses are blocked upstream of Fe uptake genes, alkaline stress or Fe deficiency up-regulation of certain Fe uptake and riboflavin synthesis genes was inhibited, indicating a central role for the FeFe protein. These results suggest a model implicating shoot-to-root signaling of Fe status to induce Fe uptake gene expression in roots
Identification of MOS9 as an interaction partner for chalcone synthase in the nucleus
Plant flavonoid metabolism has served as a platform for understanding a range of fundamental biological phenomena, including providing some of the early insights into the subcellular organization of metabolism. Evidence assembled over the past three decades points to the organization of the component enzymes as a membrane-associated complex centered on the entry-point enzyme, chalcone synthase (CHS), with flux into branch pathways controlled by competitive protein interactions. Flavonoid enzymes have also been found in the nucleus in a variety of plant species, raising the possibility of alternative, or moonlighting functions for these proteins in this compartment. Here, we present evidence that CHS interacts with MOS9, a nuclear-localized protein that has been linked to epigenetic control of R genes that mediate effector-triggered immunity. Overexpression of MOS9 results in a reduction of CHS transcript levels and a metabolite profile that substantially intersects with the effects of a null mutation in CHS. These results suggest that the MOS9–CHS interaction may point to a previously-unknown mechanism for controlling the expression of the highly dynamic flavonoid pathway
Crosstalk Between Cadmium, And Copper And Iron Homeostasis In Arabidopsis Thaliana
Copper and iron are essential minerals for plant growth, and human health and nutrition. Cadmium, on the other hand, is a highly toxic element that competes with essential elements for uptake and partitioning, and poses a threat to crop productivity and human health. While substantial progress has been made towards understanding how plants maintain homeostasis of copper and iron, how it is achieved in an environment that also contains cadmium is still poorly understood. Two separate studies have identified cross-talk between cadmium toxicity and copper and iron homeostasis in Arabidopsis thaliana. With respect to the effect of cadmium on copper homeostasis, we show that cadmium mimics transcriptional copper deficiency responses that result in increased copper uptake and likely intracellular copper reallocation in A. thaliana. These effects of cadmium are attributed to a transcription factor, SPL7, and its downstream targets, copper transporters COPT1, COPT2, and COPT6; and Cu/Zn superoxide dismutases, CSD1 and CSD2. With respect to the effect of cadmium on iron homeostasis, we found that cadmium increased expression of an oligopeptide transporter, OPT3. Studies of the biological relevance of this phenomenon revealed that OPT3 is a phloem-specific iron transporter that loads iron into the phloem, controls iron redistribution from mature to developing tissues and seeds, and is involved in systemic iron signaling. We also found that OPT3-dependent systemic iron signaling is important for controlling cadmium partitioning: loss of OPT3 function leads to increased accumulation of cadmium while decreasing accumulation of iron in seeds of A. thaliana. Together, these data suggest that manipulation of the components of essential mineral element homeostasis provide promising avenues for targeted biofortification strategies directed at increasing mineral nutrient density while preventing the entry of toxic elements such as cadmium into edible portions of crops
Plant responses to iron deficiency and toxicity and iron use efficiency in plants
Iron (Fe) is the fourth most abundant mineral in the Earth's crust essential for plant growth. However, if overloaded, Fe becomes toxic for plants as a highly reactive Fenton catalyst. Higher plants have developed two distinct adaptive strategies to cope with low Fe availability in soils, such as the reduction-based strategy (Strategy 1) in nongraminaceous plants, and the chelation-based strategy (Strategy 2) in graminaceous species. The ability of plants to improve Fe availability in the rhizosphere and its internal use efficiency will strongly affect both crop yield and quality in terms of Fe source for humans. Understanding the mechanisms involved in Fe uptake, transport, and storage is essential for breeding crops more tolerant to Fe-limited conditions. This review summarizes the current knowledge of root acquisition of Fe (deficiency), binding and detoxification of Fe (toxicity), long-distance root-to-shoot transport including loading of Fe into edible tissues, and molecular regulation of Fe use efficiency