Search for: All records

Tef Eragrostis tef(Zucc.) Trotter] is the major staple crop for millions of people in Ethiopia and Eritrea and is believed to have been domesticated several thousand years ago. Tef has the smallest grains of all the cereals, which directly impacts its productivity and presents numerous challenges to its cultivation. In this study, we assessed the natural variation in seed size of 189 tef and 11 accessions of its wild progenitor Indian lovegrass (Eragrostis pilosa (L.) P. Beauv.) and explored the mineral distribution of representative accessions. Our findings revealed significant natural variation in seed size and mineral concentration among both the tef and E. pilosa accessions. We observed significant variation in seed length, seed width, and seed area among the accessions of both Eragrostis spp. we analyzed. Using representative accessions of both species, we also found significant variation in 1000-grain weight. The observed variation in seed size attributes prompted us to use comparative genomics to identify seed size regulating genes based on the well-studied and closely related monocot cereal rice (Oryza sativa L.]. Using this approach, we identified putative orthologous genes in the tef genome that belong to a number of key pathways known to regulate seed size in rice. Phylogenetic analysis of putative tef orthologs of ubiquitin-proteasome, G-protein, MAPK, and brassinosteroid (BR)-family genes indicate significant similarity to seed size regulating genes in rice and other cereals. Because tef is known to be more nutrient-dense than other more common cereals such as rice, wheat, and maize, we also studied the mineral concentration of selected accessions using ICP-OES and explored their distribution within the seeds using synchrotron-based X-ray fluorescence (SXRF) microscopy. The findings showed significant variation in seed mineral concentration and mineral distribution among the selected accessions of both Eragrostis spp. This study highlights the natural variation in seed size attributes, mineral concentration, and distribution, while establishing the basis for understanding the genetic mechanisms regulating these traits. We hope our findings will lead to a better understanding of the evolution of tef at the genetic level and for the development of elite tef cultivars to improve seed size, yield, and quality of the grains. 

This article is a Commentary onCaiet al. (2024),242: 1206–1217. 

Abstract Copper (Cu) and iron (Fe) are essential micronutrients that are toxic when accumulating in excess in cells. Thus, their uptake by roots is tightly regulated. While plants sense and respond to local Cu availability, the systemic regulation of Cu uptake has not been documented in contrast to local and systemic control of Fe uptake. Fe abundance in the phloem has been suggested to act systemically, regulating the expression of Fe uptake genes in roots. Consistently, shoot-to-root Fe signaling is disrupted in Arabidopsis thaliana mutants lacking the phloem companion cell-localized Fe transporter, OLIGOPEPTIDE TRANSPORTER 3 (AtOPT3). We report that AtOPT3 also transports Cu in heterologous systems and contributes to its delivery from sources to sinks in planta. The opt3 mutant contained less Cu in the phloem, was sensitive to Cu deficiency and mounted a transcriptional Cu deficiency response in roots and young leaves. Feeding the opt3 mutant and Cu- or Fe-deficient wild-type seedlings with Cu or Fe via the phloem in leaves downregulated the expression of both Cu- and Fe-deficiency marker genes in roots. These data suggest the existence of shoot-to-root Cu signaling, highlight the complexity of Cu/Fe interactions, and the role of AtOPT3 in fine-tuning root transcriptional responses to the plant Cu and Fe needs. 

Abstract Iron (Fe) uptake and translocation in plants are fine-tuned by complex mechanisms that are not yet fully understood. In Arabidopsis thaliana, local regulation of Fe homeostasis at the root level has been extensively studied and is better understood than the systemic shoot-to-root regulation. While the root system is solely a sink tissue that depends on photosynthates translocated from source tissues, the shoot system is a more complex tissue, where sink and source tissues occur synchronously. In this study, and to gain better insight into the Fe deficiency responses in leaves, we overexpressed Zinc/Iron-regulated transporter-like Protein (ZIP5), an Fe/Zn transporter, in phloem-loading cells (proSUC2::AtZIP5) and determined the timing of Fe deficiency responses in sink (young leaves and roots) and source tissues (leaves). Transgenic lines overexpressing ZIP5 in companion cells displayed increased sensitivity to Fe deficiency in root growth assays. Moreover, young leaves and roots (sink tissues) displayed either delayed or dampened transcriptional responses to Fe deficiency compared to wild-type (WT) plants. We also took advantage of the Arabidopsis mutant nas4x-1 to explore Fe transcriptional responses in the opposite scenario, where Fe is retained in the vasculature but in an unavailable and precipitated form. In contrast to proSUC2::AtZIP5 plants, nas4x-1 young leaves and roots displayed a robust and constitutive Fe deficiency response, while mature leaves showed a delayed and dampened Fe deficiency response compared to WT plants. Altogether, our data provide evidence suggesting that Fe sensing within leaves can also occur locally in a leaf-specific manner. 

Abstract Age-dependent changes in reactive oxygen species (ROS) levels are critical in leaf senescence. While H2O2-reducing enzymes such as catalases and cytosolic ASCORBATE PEROXIDASE1 (APX1) tightly control the oxidative load during senescence, their regulation and function are not specific to senescence. Previously, we identified the role of ASCORBATE PEROXIDASE6 (APX6) during seed maturation in Arabidopsis (Arabidopsis thaliana). Here, we show that APX6 is a bona fide senescence-associated gene. APX6 expression is specifically induced in aging leaves and in response to senescence-promoting stimuli such as abscisic acid (ABA), extended darkness, and osmotic stress. apx6 mutants showed early developmental senescence and increased sensitivity to dark stress. Reduced APX activity, increased H2O2 level, and altered redox state of the ascorbate pool in mature pre-senescing green leaves of the apx6 mutants correlated with the early onset of senescence. Using transient expression assays in Nicotiana benthamiana leaves, we unraveled the age-dependent post-transcriptional regulation of APX6. We then identified the coding sequence of APX6 as a potential target of miR398, which is a key regulator of copper redistribution. Furthermore, we showed that mutants of SQUAMOSA PROMOTER BINDING PROTEIN-LIKE7 (SPL7), the master regulator of copper homeostasis and miR398 expression, have a higher APX6 level compared with the wild type, which further increased under copper deficiency. Our study suggests that APX6 is a modulator of ROS/redox homeostasis and signaling in aging leaves that plays an important role in developmental- and stress-induced senescence programs. 

Summary Mitochondria and chloroplasts are organelles with high iron demand that are particularly susceptible to iron‐induced oxidative stress. Despite the necessity of strict iron regulation in these organelles, much remains unknown about mitochondrial and chloroplast iron transport in plants. Here, we propose that Arabidopsis ferroportin 3 (FPN3) is an iron exporter that is dual‐targeted to mitochondria and chloroplasts.FPN3is expressed in shoots, regardless of iron conditions, but its transcripts accumulate under iron deficiency in roots.fpn3mutants cannot grow as well as the wild type under iron‐deficient conditions and their shoot iron levels are lower compared with the wild type. Analyses of iron homeostasis gene expression infpn3mutants and inductively coupled plasma mass spectrometry (ICP‐MS) measurements show that iron levels in the mitochondria and chloroplasts are increased relative to the wild type, consistent with the proposed role of FPN3 as a mitochondrial/plastid iron exporter. In iron‐deficientfpn3mutants, abnormal mitochondrial ultrastructure was observed, whereas chloroplast ultrastructure was not affected, implying that FPN3 plays a critical role in the mitochondria. Overall, our study suggests that FPN3 is essential for optimal iron homeostasis.