Explore the vast range of titles available.

Iron, as an essential micronutrient, is required by all living organisms. In plants, the deficiency and excess of iron will impair their growth and development. For maintaining a proper intracellular iron concentration, plants evolved different regulation mechanisms to tightly control iron uptake, translocation and storage. FIT, a bHLH transcription factor, is the master regulator of the iron deficiency responses and homeostasis in Arabidopsis. It interacts with different proteins, functioning in controlling the expression of various genes involved in iron uptake and homeostasis. In this review, we summarize the recent progress in the studies of FIT and FIT-binding proteins, and give an overview of FIT-regulated network in iron deficiency response and homeostasis.

The genome sequence and its analysis of the diploid wild wheat Triticum urartu (progenitor of the wheat A genome) represent a tool for studying the complex, polyploid wheat genomes and should be a valuable resource for the genetic improvement of wheat. An A to D of wheat genomes The hexaploid genome of bread wheat Triticum aestivum , designated AABBDD, evolved as a result of hybridization between three ancestral grasses. Two papers published in the issue of Nature present genome sequences and analysis of two of these wheat progenitors. First, the genome sequence of the diploid wild wheat T. urartu (ancestor of the A genome), which resembles cultivated wheat more strongly than either Aegilops speltoides (the B ancestor) or Ae. tauschii (the D donor). And second, the Ae. tauschii genome, together with an analysis of its transcriptome. These genomes and their analyses will be powerful tools for the study of complex, polyploid wheat genomes and a valuable resource for genetic improvement of wheat. Bread wheat ( Triticum aestivum, AABBDD) is one of the most widely cultivated and consumed food crops in the world. However, the complex polyploid nature of its genome makes genetic and functional analyses extremely challenging. The A genome, as a basic genome of bread wheat and other polyploid wheats, for example, T. turgidum (AABB), T. timopheevii (AAGG) and T. zhukovskyi (AAGGA m A m ), is central to wheat evolution, domestication and genetic improvement 1 . The progenitor species of the A genome is the diploid wild einkorn wheat T. urartu 2 , which resembles cultivated wheat more extensively than do Aegilops speltoides (the ancestor of the B genome 3 ) and Ae. tauschii (the donor of the D genome 4 ), especially in the morphology and development of spike and seed. Here we present the generation, assembly and analysis of a whole-genome shotgun draft sequence of the T. urartu genome. We identified protein-coding gene models, performed genome structure analyses and assessed its utility for analysing agronomically important genes and for developing molecular markers. Our T. urartu genome assembly provides a diploid reference for analysis of polyploid wheat genomes and is a valuable resource for the genetic improvement of wheat.

Iron is an essential element for plant growth and development. Iron homeostasis in plants is tightly regulated at both transcriptional and posttranscriptional level. Several bHLH transcription factors involved in iron homeostasis have been identified recently. However, their regulatory mechanisms remain unknown. In this work, we demonstrate that the transcription factor FIT interacted with AtbHLH38 and AtbHLH39 and directly conferred the expression regulation of iron uptake genes for iron homeostasis in Arabidopsis. Yeast two-hybrid analysis and transient expression in Arabidopsis protoplasts showed that AtbHLH38 or AtbHLH39 interacted with FIT, a central transcription factor involved in iron homeostasis in Arabidopsis. Expression of FIT/AtbHLH38 or FIT/AtbHLH39 in yeast cells activated GUS expression driven by ferric chelate reductase （FRO2） and ferrous transporter （IRT1） promoters. Overexpression of FITwith either AtbHLH38 or AtbHLH39 in plants converted the expression of the iron uptake genes FRO2 and IRT1 from induced to constitutive. Further analysis revealed that FRO2 and IRT1 were not regulated at the posttranscriptional level in these plants because IRT1 protein accumulation and high ferric chelate reductase activity were detected in the overexpression plants under both iron deficiency and iron sufficiency. The double overexpression plants accumulated more iron in their shoots than wild type or the plants overexpressing either AtbHLH38, AtbHLH39 or FIT. Our data support that ferric-chelate reductase FRO2 and ferrous-transporter IRT1 are the targets of the three transcription factors and the transcription of FRO2 and IRT1 is directly regulated by a complex of FIT/AtbHLH38 or FIT/AtbHLH39.

Cadmium (Cd) is toxic to plant cells. Under Cd exposure, the plant displayed leaf chlorosis, which is a typical symptom of iron (Fe) deficiency. Interactions of Cd with Fe have been reported. However, the molecular mechanisms of Cd-Fe interactions are not well understood. Here, we showed that FER-like Deficiency Induced Transcripition Factor (FIT), AtbHLH38, and AtbHLH39, three basic helix-loop-helix transcription factors involved in Fe homeostasis in plants, also play important roles in Cd tolerance. The gene expression analysis showed that the expression of FIT, AtbHLH38, and AtbHLH39 was up-regulated in the roots of plants treated with Cd. The plants overexpressing AtbHLH39 and double-overexpressing FIT/AtbHEH38 and FIT/AtbHLH39 exhibited more tolerance to Cd exposure than wild type, whereas no Cd tolerance was observed in plants overexpressing either AtbHLH38 or FIT. Further analysis revealed that co-overexpression of FIT with AtbHLH38 or AtbHLH39 constitutively activated the expression of Heavy Metal Associated3 (HMA3), Metal Tolerance Protein3 (MTP3), Iron Regulated Transporter2 (IRT2), and Iron Regulated Gene2 (IREG2), which are involved in the heavy metal detoxification in (Arabidopis thaliana). Moreover, co-overexpression of FIT with AtbHLH38 or AtbHLH39 also enhanced the expression NICOTIANAMINE SYNTHETASE1 (NAS1) and NAS2, resulting in the accumulation of nicotiananamine, a crucial chelator Fe transportation and homeostasis. Finally, we showed that maintaining high Fe content in shoots under Cd exposure could alleviate the Cd toxicity. Our results provide new insight to understand the molecular mechanisms of Cd tolerance in plants.

Wheat tillering is an important agronomic trait influencing grain yield. Here, we identify an NHL repeat-containing protein, TaNHLP1, which positively regulates tiller number in wheat. We discovered that the core components of the abscisic acid (ABA) signaling pathway, type 2C protein phosphatase TaPP2C and SNF1-related protein kinase TaSnRK2, interact with TaNHLP1 to regulate its abundance. Furthermore, TaNHLP1 interacts with the Receptor for Activated C Kinase 1 (TaRACK1A), an ABA pathway negative regulator, and influences its subcellular localization. Importantly, both the TaNHLP1 and TaRACK1A mutations promote ABA accumulation in the shoot bases and tiller buds. Notably, the NHLP1-RACK1 module is conserved across monocots and eudicots, and natural variations in the promoter of TaNHLP1-A enhance its transcriptional activity, leading to increased tiller number and yield. Collectively, these findings elucidate the genetic mechanism of NHLP1-mediated tillering regulation and highlight its potential as a target for improving crop plant architecture. Si et al. demonstrated that wheat TaNHLP1 interacts with ABA regulators and RACK1A to increase tiller number, and that promoter variants that elevate TaNHLP1 expression enhance yield. This regulatory module is conserved across plants.

Parasitic plants are a special group deriving their nutrients from another plant, some of which such as witchweeds ( spp.) and broomrapes ( and spp.) are referred as weeds responsible for severe crop losses in agriculture. The parasite attaches to and feeds off its host using a haustorium, which also facilitates the transport of various molecules between the parasite and its host. These translocation molecules have received extensive attention from researchers. In this review, we summarize the existing knowledge on the transfer of molecules such as pathogens, herbicides, RNAs, and proteins between parasitic plants and their hosts, and discuss their potential implications. Additionally, we provide an overview of horizontal gene transfer (HGT) between species, which is particularly evident in the mitochondrial and nuclear genomes, with some transgenes assumed to have functional roles in their recipient species, offering new insights into the evolution of parasitic plants. Finally, we discuss the significance of parasitic plant research and the development of future research technologies to advance our understanding of plant parasitism.

Hybrid necrosis, a century-old mystery in wheat, is caused by complementary genes Ne1 and Ne2 . Ne2 , encoding a nucleotide-binding leucine-rich repeat (NLR) immune receptor, has been cloned, yet Ne1 remains elusive. Here, we report that Ne1 , which encodes an alpha/beta hydrolase (ABH) protein generated by structural variation, triggers hybrid necrosis with Ne2 by activating autoimmune responses. We further verify that not only allelic variation but also copy number variation (CNV) of Ne1 are pivotal for hybrid necrosis diversity in wheat. Ne1 likely originates from wild emmer wheat, potentially through duplication and ectopic recombination events. Unlike Ne2 , which is frequently selected for rust resistance in wheat breeding, the lower prevalence of Ne1 in modern wheat cultivars is attributed to its association with hybrid necrosis. Altogether, these findings illuminate the co-evolution of the NLR / ABH gene pair in plant development and innate immunity, offering potential benefits for wheat breeding. Hybrid necrosis in wheat is caused by the complementary genes Ne1 and Ne2 . The underlying mechanism remains enigmatic. Here, Si et al. demonstrated that a genetic interaction between the α/β hydrolase (Ne1) and the NLR immune receptor (Ne2) triggers autoimmune responses, inducing hybrid necrosis.

Type 1 diabetes mellitus (T1DM), known as insulin-dependent diabetes mellitus, is characterized by persistent hyperglycemia resulting from damage to the pancreatic β cells and an absolute deficiency of insulin, leading to multi-organ involvement and a poor prognosis. The progression of T1DM is significantly influenced by oxidative stress and apoptosis. The natural compound eugenol (EUG) possesses anti-inflammatory, anti-oxidant, and anti-apoptotic properties. However, the potential effects of EUG on T1DM had not been investigated. In this study, we established the streptozotocin (STZ)-induced T1DM mouse model in vivo and STZ-induced pancreatic β cell MIN6 cell model in vitro to investigate the protective effects of EUG on T1DM, and tried to elucidate its potential mechanism. Our findings demonstrated that the intervention of EUG could effectively induce the activation of nuclear factor E2-related factor 2 (NRF2), leading to an up-regulation in the expressions of downstream proteins NQO1 and HMOX1, which are regulated by NRF2. Moreover, this intervention exhibited a significant amelioration in pancreatic β cell damage associated with T1DM, accompanied by an elevation in insulin secretion and a reduction in the expression levels of apoptosis and oxidative stress-related markers. Furthermore, ML385, an NRF2 inhibitor, reversed these effects of EUG. The present study suggested that EUG exerted protective effects on pancreatic β cells in T1DM by attenuating apoptosis and oxidative stress through the activation of the NRF2 signaling pathway. Consequently, EUG holds great promise as a potential therapeutic candidate for T1DM.

Based on the Integrated Land–Sea Management, this study established a theoretical framework for the sustainability of coastal regions by combining sustainable development with coupling coordination theory. The improved coupling coordination model was used to analyze the sustainable development of the Bohai Rim and its coastal provinces and cities from 2006 to 2020. Our implications were as follows: (1) The theoretical framework showed an S -shaped spiral trend, and the empirical results on the Bohai Rim were consistent with the trajectory conclusions. (2) The economic subsystem played a crucial role in the system’s evolution toward sustainable development. (3) The region and city models demonstrated consistent coupling and coordination development degrees. However, the consistency was not completely synchronous. Conscious eco-environmental governance activities can promote benign interactions among systems and improve this relationship. (4) The sustainable development of coastal cities is different from that of the provinces in which they are located. It merely demonstrates their relative status among all coastal cities and does not fully represent the wider region in which they are located. The findings suggest that adaptive policies, whether economic, social or environmental, can promote sustainable development. Economic stimulus policies can promote a transition of sustainable development; in the economic downturn, the adaptive environmental policy is realized by adjusting the relationship between subsystems to promote the coordination of regional systems, preparing for the next sustainable system transition. The established theoretical model and improvised mathematical method can be extended to study various coastal regions

Objective Bisphenol A (BPA), a pervasive environmental pollutant, is increasingly associated with osteoarthritis (OA) development, yet its molecular mechanisms remain unknown. Currently, there is no definitive cure for OA. Methods BPA targets were predicted using STITCH and Swiss Target Prediction, while OA-related targets were collected from GeneCards, OMIM, and the Therapeutic Target Database (TTD). Protein-protein interaction (PPI) networks were constructed using STRING and visualized in Cytoscape to identify hub targets. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed, and molecular docking with AutoDock evaluated BPA-core target interactions. We employed our Computational Analysis of Novel Drug Opportunities (CANDO) platform for de novo drug prediction. Results Systematic bioinformatics analysis identified 26 candidate targets, with ESR1, PTGS2, CCL2, FLNA, and TRPV1 as key hubs. Pathway analysis revealed involvement in calcium ion transport, muscle contraction, IL-17 signaling, and estrogen signaling. Molecular docking confirmed strong BPA-target binding affinities. CANDO predicted 14 potential OA treatments, including glucosamine, ibuprofen, celecoxib, indomethacin, palmitic acid, and linoleic acid. Notably, qRT-PCR validation revealed that ESR1, PTGS2, CCL2, and TRPV1 were highly expressed, whereas FLNA was expressed at lower levels in the osteoarthritis blood samples. Conclusions This study elucidates BPA’s molecular mechanisms in OA and identifies promising therapeutic candidates. The integration of network toxicology, molecular docking, and computational drug discovery provides a robust framework for understanding environmental toxicants and advancing OA therapies.