CIP1, a CIPK23-interacting transporter, is implicated in Cd tolerance and phytoremediation.

Environmental pollution from cadmium (Cd) presents a serious threat to plant growth and development. Therefore, it's crucial to find out how plants resist this toxic metal to develop strategies for remediating Cd-contaminated soils. In this study, we identified CIP1, a transporter protein, by screening interactors of the protein kinase CIPK23. CIP1 is located in vesicles membranes and can transport Cd2+ when expressed in yeast cells. Cd stress specifically induced the accumulation of CIP1 transcripts and functional proteins, particularly in the epidermal cells of the root tip. CIKP23 could interact directly with the central loop region of CIP1, phosphorylating it, which is essential for the efficient transport of Cd2+. A loss-of-function mutation of CIP1 in wild-type plants led to increased sensitivity to Cd stress. Conversely, tobacco plants overexpressing CIP1 exhibited improved Cd tolerance and increased Cd accumulation capacity. Interestingly, this Cd accumulation was restricted to roots but not shoots, suggesting that manipulating CIP1 does not risk Cd contamination of plants' edible parts. Overall, this study characterizes a novel Cd transporter, CIP1, with potential to enhance plant tolerance to Cd toxicity while effectively eliminating environmental contamination without economic losses.

The plastid-localized lipoamide dehydrogenase 1 is crucial for redox homeostasis, tolerance to arsenic stress and fatty acid biosynthesis in rice.

Soil contamination with arsenic (As) can cause phytotoxicity and reduce crop yield. The mechanisms of As toxicity and tolerance are not fully understood. In this study, we used a forward genetics approach to isolate a rice mutant, ahs1, that exhibits hypersensitivity to both arsenate and arsenite. Through genomic resequencing and complementation tests, we identified OsLPD1 as the causal gene, which encodes a putative lipoamide dehydrogenase. OsLPD1 was expressed in the outer cell layer of roots, root meristem cells, and in the mesophyll and vascular tissues of leaves. Subcellular localization and immunoblot analysis demonstrated that OsLPD1 is localized in the stroma of plastids. In vitro assays showed that OsLPD1 exhibited lipoamide dehydrogenase (LPD) activity, which was strongly inhibited by arsenite, but not by arsenate. The ahs1 and OsLPD1 knockout mutants exhibited significantly reduced NADH/NAD+ and GSH/GSSG ratios, along with increased levels of reactive oxygen species and greater oxidative stress in the roots compared with wild-type (WT) plants under As treatment. Additionally, loss-of-function of OsLPD1 also resulted in decreased fatty acid concentrations in rice grain. Taken together, our finding reveals that OsLPD1 plays an important role for maintaining redox homeostasis, conferring tolerance to arsenic stress, and regulating fatty acid biosynthesis in rice.

OsMKK6 Regulates Disease Resistance in Rice.

Mitogen-activated protein kinase cascades play important roles in various biological programs in plants, including immune responses, but the underlying mechanisms remain elusive. Here, we identified the lesion mimic mutant rsr25 (rust spots rice 25) and determined that the mutant harbored a loss-of-function allele for OsMKK6 (MITOGEN-ACTIVATED KINASE KINASE 6). rsr25 developed reddish-brown spots on its leaves at the heading stage, as well as on husks. Compared to the wild type, the rsr25 mutant exhibited enhanced resistance to the fungal pathogen Magnaporthe oryzae (M. oryzae) and to the bacterial pathogen Xanthomonas oryzae pv. oryzae (Xoo). OsMKK6 interacted with OsMPK4 (MITOGEN-ACTIVATED KINASE 4) in vivo, and OsMKK6 phosphorylated OsMPK4 in vitro. The Osmpk4 mutant is also a lesion mimic mutant, with reddish-brown spots on its leaves and husks. Pathogen-related genes were significantly upregulated in Osmpk4, and this mutant exhibited enhanced resistance to M. oryzae compared to the wild type. Our results indicate that OsMKK6 and OsMPK4 form a cascade that regulates immune responses in rice.

CG hypermethylation of the bHLH39 promoter regulates its expression and Fe deficiency responses in tomato roots.

Iron (Fe) is an essential micronutrient for all organisms, including plants, whose limited bioavailability restricts plant growth, yield, and nutritional quality. While the transcriptional regulation of plant responses to Fe deficiency have been extensively studied, the contribution of epigenetic modulations, such as DNA methylation, remains poorly understood. Here, we report that treatment with a DNA methylase inhibitor repressed Fe deficiency-induced responses in tomato (Solanum lycopersicum) roots, suggesting the importance of DNA methylation in regulating Fe deficiency responses. Dynamic changes in the DNA methylome in tomato roots responding to short-term (12 hours) and long-term (72 hours) Fe deficiency identified many differentially methylated regions (DMRs) and DMR-associated genes. Most DMRs occurred at CHH sites under short-term Fe deficiency, whereas they were predominant at CG sites following long-term Fe deficiency. Furthermore, no correlation was detected between the changes in DNA methylation levels and the changes in transcript levels of the affected genes under either short-term or long-term treatments. Notably, one exception was CG hypermethylation at the bHLH39 promoter, which was positively correlated with its transcriptional induction. In agreement, we detected lower CG methylation at the bHLH39 promoter and lower bHLH39 expression in MET1-RNA interference lines compared with wild-type seedlings. Virus-induced gene silencing of bHLH39 and luciferase reporter assays revealed that bHLH39 is positively involved in the modulation of Fe homeostasis. Altogether, we propose that dynamic epigenetic DNA methylation in the CG context at the bHLH39 promoter is involved in its transcriptional regulation, thus contributing to the Fe deficiency response of tomato.

Rice chromatin protein OsHMGB1 is involved in phosphate homeostasis and plant growth by affecting chromatin accessibility.

Although phosphorus is one of the most important essential elements for plant growth and development, the epigenetic regulation of inorganic phosphate (Pi) signaling is poorly understood. In this study, we investigated the biological function and mode of action of the high-mobility-group box 1 protein OsHMGB1 in rice (Oryza sativa), using molecular and genetic approaches. We determined that OsHMGB1 expression is induced by Pi starvation and encodes a nucleus-localized protein. Phenotypic analysis of Oshmgb1 mutant and OsHMGB1 overexpression transgenic plants showed that OsHMGB1 positively regulates Pi homeostasis and plant growth. Transcriptome deep sequencing and chromatin immunoprecipitation followed by sequencing indicated that OsHMGB1 regulates the expression of a series of phosphate starvation-responsive (PSR) genes by binding to their promoters. Furthermore, an assay for transposase-accessible chromatin followed by sequencing revealed that OsHMGB1 is involved in maintaining chromatin accessibility. Indeed, OsHMGB1 occupancy positively correlated with genome-wide chromatin accessibility and gene expression levels. Our results demonstrate that OsHMGB1 is a transcriptional facilitator that regulates the expression of a set of PSR genes to maintain Pi homeostasis in rice by increasing the chromatin accessibility, revealing a key epigenetic mechanism that fine-tune plant acclimation responses to Pi-limited environments.

Integrated transcriptomic analysis identifies coordinated responses to nitrogen and phosphate deficiency in rice.

Nitrogen (N) and phosphorus (P) are two primary components of fertilizers for crop production. Coordinated acquisition and utilization of N and P are crucial for plants to achieve nutrient balance and optimal growth in a changing rhizospheric nutrient environment. However, little is known about how N and P signaling pathways are integrated. We performed transcriptomic analyses and physiological experiments to explore gene expression profiles and physiological homeostasis in the response of rice (Oryza sativa) to N and P deficiency. We revealed that N and P shortage inhibit rice growth and uptake of other nutrients. Gene Ontology (GO) analysis of differentially expressed genes (DEGs) suggested that N and Pi deficiency stimulate specific different physiological reactions and also some same physiological processes in rice. We established the transcriptional regulatory network between N and P signaling pathways based on all DEGs. We determined that the transcript levels of 763 core genes changed under both N or P starvation conditions. Among these core genes, we focused on the transcription factor gene NITRATE-INDUCIBLE, GARP-TYPE TRANSCRIPTIONAL REPRESSOR 1 (NIGT1) and show that its encoded protein is a positive regulator of P homeostasis and a negative regulator of N acquisition in rice. NIGT1 promoted Pi uptake but inhibited N absorption, induced the expression of Pi responsive genes PT2 and SPX1 and repressed the N responsive genes NLP1 and NRT2.1. These results provide new clues about the mechanisms underlying the interaction between plant N and P starvation responses.

Dual-stimulus phototherapeutic nanogel for triggering pyroptosis to promote cancer immunotherapy.

Pyroptosis is a highly inflammatory programmed cell death that activates inflammatory response, reverses immunosuppression and promotes systemic immune response for solid tumors treatment. However, the uncontrollable and imprecise process of pyroptosis stimulation leads to a scanty therapeutic effect. Here, we report a GSH/ROS dual response nanogel system (IMs) that can actively target the overexpressed mannose receptor (MR) of cancer cells, serve ultra-stable photothermal capacity of indocyanine green (ICG), induce cell pyroptosis and achieve enhanced tumor immune response. Photo-triggered IMs induce cytoplasmic Ca2+ introgression and activate caspase-3 through photo-activated ICG. The disconnect of SeSe bonds can break the oxidation and reduction balance of tumor cells, causing oxidative stress and synergistically enhancing caspase-3 cleavage, and regulating cell pyroptosis ultimately. Combined with anti-programmed death receptor 1 (anti-PD-1), the nanogel system not only effectivly suppress both primary tumor and distance tumor but also prolong the survival period of mice. This work introduces a strategy to optimize the photothermal performance of ICG and enhances tumor immune response mediated by triggering pyroptosis, which provides an impressive option for immune checkpoint blockade therapy.

Reduction-triggered polycyclodextrin supramolecular nanocage induces immunogenic cell death for improved chemotherapy.

Polycyclodextrin-based supramolecular nanoplatform crosslinked by stimuli-responsive moiety shows great promise in cancer therapy owing to its superior bio-stability and feasible modification of architectures. Here, the endogenous glutathione (GSH)-responsive polycyclodextrin supramolecular nanocages (PDOP NCs) are constructed by covalent crosslinking of multiple ß-cyclodextrin (ß-CD) molecules. The polycyclodextrin provide sites for conjugation of chemotherapeutic doxorubicin (DOX). Meanwhile, the PDOP NCs are stabilized by multiple interactions including host-guest interaction between DOX and ß-CD and hydrogen bonds between ß-CD units. The supramolecular crosslinked structure endowed the nanocage with high stability and drug loading capacity. Tons of GSH-sensitive disulfide linkages in PDOP NCs were broken at tumor cells, promoting tumor-specific DOX release. Besides, the redox equilibrium in tumor microenvironment could be disturbed due to GSH depletion, which further sensitized the DOX effects and alleviated drug resistance, facilitating inducing immunogenic cell death effect for enhanced chemotherapy, thereby achieving efficient tumor suppression and prolonged survival. Thus, the versatile polycyclodextrin-based supramolecular nanocage provides a novel and efficient drug delivery strategy for cancer treatment.

A novel protein domain is important for photosystem II complex assembly and photoautotrophic growth in angiosperms.

Photosystem II (PSII) is a multi-subunit protein complex of the photosynthetic electron transport chain that is vital to photosynthesis. Although the structure, composition, and function of PSII have been extensively studied, its biogenesis mechanism remains less understood. Thylakoid rhodanese-like (TROL) provides an anchor for leaf-type ferredoxin:NADP+ oxidoreductase. Here, we report the chacterizaton of a second type of TROL protein, TROL2, encoded by seed plant genomes whose function has not previously been reported. We show that TROL2 is a PSII assembly cofactor with essential roles in the establishment of photoautotrophy. TROL2 contains a 45-amino-acid domain, termed the chlorotic lethal seedling (CLS) domain, that is both necessary and sufficient for TROL2 function in PSII assembly and photoautotrophic growth. Phylogenetic analyses suggest that TROL2 may have arisen from ancestral TROL1 via gene duplication before the emergence of seed plants and acquired the CLS domain via evolution of the sequence encoding its N-terminal portion. We further reveal that TROL2 (or CLS) forms an assembly cofactor complex with the intrinsic thylakoid membrane protein LOW PSII ACCUMULATION2 and interacts with small PSII subunits to facilitate PSII complex assembly. Collectively, our study not only shows that TROL2 (CLS) is essential for photoautotrophy in angiosperms but also reveals its mechanistic role in PSII complex assembly, shedding light on the molecular and evolutionary mechanisms of photosynthetic complex assemblyin angiosperms.

The hot science in rice research: How rice plants cope with heat stress.

Global climate change has great impacts on plant growth and development, reducing crop productivity worldwide. Rice (Oryza sativa L.), one of the world's most important food crops, is susceptible to high-temperature stress from seedling stage to reproductive stage. In this review, we summarize recent advances in understanding the molecular mechanisms underlying heat stress responses in rice, including heat sensing and signalling, transcriptional regulation, transcript processing, protein translation, and post-translational regulation. We also highlight the irreversible effects of high temperature on reproduction and grain quality in rice. Finally, we discuss challenges and opportunities for future research on heat stress responses in rice.

Diselenide-Based Dual-Responsive Prodrug as Pyroptosis Inducer Potentiates Cancer Immunotherapy.

Pyroptosis is demonstrated to trigger antitumor immunity and represents a promising new strategy to potentiate cancer immunotherapy. The number of potent pyroptosis inducers, however, is limited and without tumor-targeting capability, which inevitably causes damage in normal tissues. Herein, a small molecular prodrug of paclitaxel-oxaliplatin is rationally synthesized, which can be covalently self-assembled with diselenide-containing cross-linking (Dse11), producing a diselenide nanoprodrug (DSe@POC) to induce pyroptosis for the first time. The diselenide bonds within DSe@POC can be split by high glutathione in the tumor microenvironment (TME) and reactive oxygen species induced by photodynamic therapy, thus possessing excellent TME on-target effects. Additionally, DSe@POC is able to elicit intense pyroptosis to remodel the immunostimulated TME and trigger a robust immune response. Furthermore, combined αPD-1 therapy effectively inhibits the growth of remote tumors through the abscopal effect, amplifies a long-term immune memory response to reject rechallenged tumors, and prolongs survival. Collectively, DSe@POC, as the first TME dual-responsive diselenide-based pyroptosis inducer, will open up an attractive approach for cancer immunotherapy.

A Dual-Responsive STAT3 Inhibitor Nanoprodrug Combined with Oncolytic Virus Elicits Synergistic Antitumor Immune Responses by Igniting Pyroptosis.

Immune checkpoint blockade (ICB) therapy shows excellent efficacy against malignancies; however, insufficient tumor immunogenicity and the immunosuppressive tumor microenvironment (TME) are considered as the two major stumbling blocks to a broad ICB response. Here, a combinational therapeutic strategy is reported, wherein TME-reactive oxygen species/pH dual-responsive signal transducers and activators of transcription 3 inhibitor nanoprodrugs MPNPs are combined with oncolytic herpes simplex virus 1 virotherapy to synergistically ignite pyroptosis for enhancing immunotherapy. MPNPs exhibit a certain level of tumor accumulation, reduce tumor cell stemness, and enhance antitumor immune responses. Furthermore, the simultaneous application of oncolytic viruses (OVs) confers MPNPs with higher tumor penetration capacity and remarkable gasdermin-E-mediated pyroptosis, thereby reshaping the TME and transforming "cold" tumors into "hot" ones. This "fire of immunity" strategy successfully activates robust T-cell-dependent antitumor responses, potentiating ICB effects against local recurrence and pulmonary metastasis in preclinical "cold" murine triple-negative breast cancer and syngeneic oral cancer models. Collectively, this work may pave a new way and offer an unprecedented opportunity for the combination of OVs with nanomedicine for cancer immunotherapy.

Characterizing membrane anchoring of leaf-form ferredoxin-NADP+ oxidoreductase in rice.

Leaf-form ferredoxin-NADP+ oxidoreductases (LFNRs) function in the last step of the photosynthetic electron transport chain, exist as soluble proteins in the chloroplast stroma and are weakly associated with thylakoids or tightly anchored to chloroplast membranes. Arabidopsis thaliana has two LFNRs, and the chloroplast proteins AtTROL and AtTIC62 participate in anchoring AtLFNRs to the thylakoid membrane. By contrast, the membrane anchoring mechanism of rice (Oryza sativa) LFNRs has not been elucidated. Here, we investigated the membrane-anchoring mechanism of LFNRs and its physiological roles in rice. We characterized the rice protein OsTROL1 based on its homology to AtTROL. We determined that OsTROL1 is also a thylakoid membrane anchor and its loss leads to a compensatory increase in OsTIC62. OsLFNR1 attachment through a membrane anchor depends on OsLFNR2, unlike the Arabidopsis counterparts. In addition, OsTIC62 was more highly expressed in the dark than under light conditions, consistent with the increased membrane binding of OsLFNR in the dark. Moreover, we observed reciprocal stabilization between OsLFNRs and their membrane anchors. In addition, unlike in Arabidopsis, the loss of LFNR membrane anchor affects photosynthesis in rice. Overall, our study sheds light on the mechanisms anchoring LFNRs to membranes in rice and highlights differences with Arabidopsis.

Ubiquitin-Specific Protease 2 (OsUBP2) Negatively Regulates Cell Death and Disease Resistance in Rice.

Lesion mimic mutants (LMMs) are great materials for studying programmed cell death and immune mechanisms in plants. Various mechanisms are involved in the phenotypes of different LMMs, but few studies have explored the mechanisms linking deubiquitination and LMMs in rice (Oryza sativa). Here, we identified a rice LMM, rust spots rice (rsr1), resulting from the mutation of a single recessive gene. This LMM has spontaneous reddish-brown spots on its leaves, and displays enhanced resistance to both fungal leaf blast (caused by Magnaporthe oryzae) and bacterial blight (caused by Xanthomonas oryzae pv. oryzae). Map-based cloning showed that the mutated gene in rsr1 encodes a Ubiquitin-Specific Protease 2 (OsUBP2). The mutation of OsUBP2 was shown to result in reactive oxygen species (ROS) accumulation, chloroplast structural defects, and programmed cell death, while the overexpression of OsUBP2 weakened rice resistance to leaf blast. OsUBP2 is therefore a negative regulator of immune processes and ROS production. OsUBP2 has deubiquitinating enzyme activity in vitro, and the enzyme active site includes a cysteine at the 234th residue. The ubiquitinated proteomics data of rsr1 and WT provide some possible target protein candidates for OsUBP2.

Immunomodulatory-Photodynamic Nanostimulators for Invoking Pyroptosis to Augment Tumor Immunotherapy.

Cancer immunotherapy is restricted to immune resistance caused by immunosuppressive tumor microenvironment. Pyroptosis involved in antitumor immunotherapy as a new schedule is prospective to reverse immunosuppression. Herein, acidic tumor microenvironment (TME)-evoked MRC nanoparticles (MRC NPs) co-delivering immune agonist RGX-104 and photosensitizer chlorine e6 (Ce6) are reported for pyroptosis-mediated immunotherapy. RGX-104 remodels TME by transcriptional activation of ApoE to regress myeloid-derived suppressor cells' (MDSCs) activity, which neatly creates foreshadowing for intensifying pyroptosis. Considering Ce6-triggered photodynamic therapy (PDT) can strengthen oxidative stress and organelles destruction to increase immunogenicity, immunomodulatory-photodynamic MRC nanodrugs will implement an aforementioned two-pronged strategy to enhance gasdermin E (GSDME)-dependent pyroptosis. RNA-seq analysis of MRC at the cellular level is introduced to first elucidate the intimate relationship between RGX-104 acting on LXR/ApoE axis and pyroptosis, where RGX-104 provides the prerequisite for pyroptosis participating in antitumor therapy. Briefly, MRC with favorable biocompatibility tackles the obstacle of hydrophobic drugs delivery, and becomes a powerful pyroptosis inducer to reinforce immune efficacy. MRC-elicited pyroptosis in combination with anti-PD-1 blockade therapy boosts immune response in solid tumors, successfully arresting invasive metastasis and extending survival based on remarkable antitumor immunity. MRC may initiate a new window for immuno-photo pyroptosis stimulators augmenting pyroptosis-based immunotherapy.

Sustained release of chlorogenic acid-loaded nanomicelles alleviates bone loss in mouse periodontitis.

Periodontitis is a prevalent chronic inflammatory disease that destroys the periodontal supporting tissues, impinges on oral health, and is correlated with an increased risk of systemic disease. Currently, the main drug treatment is antibiotic therapy; however, systemic antibiotic therapy still has various drawbacks such as bacterial resistance, low bioavailability and burst release. It is noteworthy that the local use of non-antibiotic drugs with sustained release characteristics can effectively overcome these problems. It has been documented that chlorogenic acid (CGA) has good anti-inflammatory and antioxidant properties. To achieve the sustained release of CGA, we synthesized CGA-PLGA@PVP nanomicelles by loading CGA onto poly(D,L-lactide-co-glycolide) (PLGA) and modified them with polyvinylpyrrolidone (PVP) for better dispersion. The results demonstrated that CGA-PLGA@PVP nanomicelles could prolong the release time of CGA, and could not only effectively remove reactive oxygen species (ROS) but also downregulate the overexpression of proinflammatory cytokines in lipopolysaccharide (LPS)-treated RAW264.7 cells. Moreover, CGA-PLGA@PVP nanomicelles could remain in gingival tissue for more than 24 hours after local injection, inhibit alveolar bone resorption and prevent the progression of periodontitis in a mouse model, showing good biocompatibility. Therefore, CGA-PLGA@PVP nanomicelles have great properties and are expected to be a novel therapeutic strategy for periodontitis.

Progress on methods for acquiring flanking genomic sequence.

Flanking genomic sequences refer to the DNA sequences flanking specific sites of known sequences in chromosome, which contain information such as candidate genes, transcriptional regulation, chromosome structure, and biosafety, and play an important role in genomics research. Flanking sequence acquisition technologies are mainly used in the cloning of regulatory sequences such as promoters and enhancers, identification of T-DNA or transposon insertion sites, chromosome walking, genome-wide gap filling, etc. It is an important means of structural genomics research and functional genomics research. It is applied in the identification of transgenic plants and animals and their safety management. With the development of molecular biology, many methods for obtaining flanking sequences have been established, including plasmid rescue, inverse PCR, ligation-mediated PCR, semi-random primer PCR, whole-genome resequencing etc. In this review, we summarize and compared different methods for acquiring flanking genomic sequence. The principles and research progress of each approach are discussed.

Functional redundancy of OsPIN1 paralogous genes in regulating plant growth and development in rice.

The OsPIN1 paralogous genes (OsPIN1a-1d) are important for root and panicle development in rice (Oryza sativa L.). However, the specific role of OsPIN1 paralogous genes is still not clear. To understand the specific roles of PIN1 paralogs in rice, we generated pin1 triple and quadruple mutants by crossing the pin1a pin1b and pin1c pin1d double mutants which we previously created. Compared with the 7-day-old wild type, the pin1a pin1c pin1d and pin1b pin1c pin1d triple mutants showed no obvious phenotype variation except that the pin1a pin1c pin1d triple mutant had shorter primary root and shoot. The pin1a pin1b pin1c and pin1a pin1b pin1d triple mutants exhibited a series of developmental abnormalities, including shorter primary roots, longer root hairs, fewer crown roots and lateral roots, shorter and curved shoots. Furthermore, the pin1a pin1b pin1c pin1d quadruple mutant displayed more severe phenotypic defects which was lethal. In addition, the expression levels of some hormone signal transduction and crown root development related genes, such as OsIAAs, OsARFs, OsRRs, and OsCRLs, were significantly altered in the stem base of all examined pin1 multiple mutants. Taken together, our results demonstrated that the four OsPIN1 paralogous genes function redundantly in regulating rice growth and development.

The miR157-SPL-CNR module acts upstream of bHLH101 to negatively regulate iron deficiency responses in tomato.

Iron (Fe) homeostasis is critical for plant growth, development, and stress responses. Fe levels are tightly controlled by intricate regulatory networks in which transcription factors (TFs) play a central role. A series of basic helix-loop-helix (bHLH) TFs have been shown to contribute to Fe homeostasis, but the regulatory layers beyond bHLH TFs remain largely unclear. Here, we demonstrate that the SQUAMOSA PROMOTER-BINDING PROTEIN-LIKE (SPL) TF SlSPL-CNR negatively regulates Fe-deficiency responses in tomato (Solanum lycopersicum) roots. Fe deficiency rapidly repressed the expression of SlSPL-CNR, and Fe deficiency responses were intensified in two clustered regularly interspaced palindromic repeats (CRISPR)/CRISPR-associated protein 9-generated SlSPL-CNR knock-out lines compared to the wild-type. Comparative transcriptome analysis identified 47 Fe deficiency-responsive genes the expression of which is negatively regulated by SlSPL-CNR, one of which, SlbHLH101, helps regulate Fe uptake genes. SlSPL-CNR localizes the nucleus and interacts with the GTAC and BOX 4 (ATTAAT) motifs in the SlbHLH101 promoter to repress its expression. Inhibition of SlSPL-CNR expression in response to Fe deficiency was well correlated with the expression of the microRNA SlymiR157. SlymiR157-overexpressing tomato lines displayed enhanced Fe deficiency responses, as did SlSPL-CNR loss-of-function mutants. We propose that the SlymiR157-SlSPL-CNR module represents a novel pathway that acts upstream of SlbHLH101 to regulate Fe homeostasis in tomato roots.

2D/3D S-scheme heterojunction of carbon nitride/iodine-deficient bismuth oxyiodide for photocatalytic hydrogen production and bisphenol A degradation.

A novel 2D/3D S-scheme carbon nitride/iodine-deficient bismuth oxyiodide (g-C3N4/BiO1.2I0.6) heterojunction was constructed for the first time by calcining a mixture of g-C3N4 nanosheets and flower-like BiOI. Irradiated by visible light, this g-C3N4/BiO1.2I0.6 heterojunction exhibited excellent photocatalytic hydrogen production and BPA degradation activity with high cycle stability. In particular, the photocatalytic activity of 0.2-C3N4/BiO1.2I0.6 could reach 1402.7 µmol g-1 h-1 (hydrogen production rate) and 0.01155 min-1 (apparent rate of bisphenol A degradation), which were 3.5 and 3.2 times that of g-C3N4 respectively. The remarkable photocatalytic performance was due to the efficient charge separation of g-C3N4/BiO1.2I0.6 and the formation of S-scheme heterojunction, which maintained strong photocatalytic reduction and oxidation potentials. Noticeably, the charge density difference and band offsets of the g-C3N4/BiO1.2I0.6 were calculated. The results revealed that a built-in electric field (IEF) was created. The values of the valence band offset (ΔEVBO) and the conduction band offset (ΔECBO) were -0.84 and -1.27 eV, respectively, which further demonstrated the formation of S-scheme photocatalytic charge transfer mechanism.