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The 636-bp-long cDNA sequence of OsCu/Zn-SOD (AK059841) was cloned from Oryza sativa var. Longjing11 via reverse transcription polymerase chain reaction (RT-PCR). The encoded protein comprised of 211 amino acids is highly homologous to Cu/Zn-SOD proteins from tuscacera rice and millet. Quantitative RT-PCR revealed that in rice, the level of OsCu/Zn-SOD gene expression was lowest in roots and was highest in petals and during the S5 leaf stage. Moreover, the expression level of OsCu/Zn-SOD gene expression decreased during the L5 leaf stage to maturity. The level of OsCu/Zn-SOD gene expression, however, was increased under saline–sodic stress and NaHCO3 stress. Germination tests under 125, 150, and 175 mM NaCl revealed that OsCu/Zn-SOD-overexpressing lines performed better than the non-transgenic (NT) Longjing11 lines in terms of germination rate and height. Subjecting seedlings to NaHCO3 and water stress revealed that OsCu/Zn-SOD-overexpressing lines performed better than NT in terms of SOD activity, fresh weight, root length, and height. Under simulated NaHCO3 stress, OsCu/Zn-SOD-overexpressing lines performed better than NT in terms of survival rate (25.19% > 6.67%) and yield traits (average grain weight 20.6 > 18.15 g). This study showed that OsCu/Zn-SOD gene overexpression increases the detoxification capacity of reactive oxygen species in O. sativa and reduces salt-induced oxidative damage. We also revealed the regulatory mechanism of OsCu/Zn-SOD enzyme in saline–sodic stress resistance in O. sativa. Moreover, we provided an experimental foundation for studying the mechanism of OsCu/Zn-SOD enzymes in the chloroplast. [ABSTRACT FROM AUTHOR]

Boron (B) is an essential micronutrient for plants, but the molecular mechanisms underlying the uptake and distribution of B in allotetraploid rapeseed ( Brassica napus) are unclear. Here, we identified a B transporter of rapeseed, BnaC4.BOR1;1c, which is expressed in shoot nodes and involved in distributing B to the reproductive organs. Transgenic Arabidopsis plants containing a BnaC4.BOR1;1c promoter-driven GUS reporter gene showed strong GUS activity in roots, nodal regions of the shoots and immature floral buds. Overexpressing BnaC4.BOR1;1c in Arabidopsis wild type or in bor1-1 mutants promoted wild-type growth and rescued the bor1-1 mutant phenotype. Conversely, knockdown of BnaC4.BOR1;1c in a B-efficient rapeseed line reduced B accumulation in flower organs, eventually resulting in severe sterility and seed yield loss. BnaC4.BOR1;1c RNAi plants exhibited large amounts of disintegrated stigma papilla cells with thickened cell walls accompanied by abnormal proliferation of lignification under low-B conditions, indicating that the sterility may be a result of altered cell wall properties in flower organs. Taken together, our results demonstrate that BnaC4.BOR1;1c is a AtBOR1-homologous B transporter gene expressing in both roots and shoot nodes that is essential for the developing inflorescence tissues, which highlights its diverse functions in allotetraploid rapeseed compared with diploid model plant Arabidopsis. [ABSTRACT FROM AUTHOR]

[Display omitted] • Double modification can prompt the heterogeneous nucleation on the substrate. • Polydopamine can prevent the seeds from entering into the substrate pores. • Thin ZIF-8 membranes showed a high H 2 permeance of 1.8 × 10−6 mol·m−2·s−1·Pa−1. Heterogeneous nucleation on the substrate surface is an advantage for inducing the synthesis of a thin and continuous membrane. Here, high hydrogen permeable ZIF-8 membranes were fabricated by combining the dopamine functionalized substrate and seed-induced growth method. In addition to providing abundant functional groups, polydopamine also can chelate metal ions (Zn2+) to accelerate the nucleation on the substrate surface. Furthermore, polydopamine can anchor the seeds for promoting the heterogeneous nucleation on the substrate surfaces, and prevent the seeds from entering into the substrate porous. The characterization results by the X-ray diffraction and scanning electron microscopy showed a continuous and thin ZIF-8 layer was synthesized on the modified substrate, resulting in a low gas permeance resistance. For the single gas permeation performance, the membrane showed a marked hydrogen permeance of 1.8 × 10−6 mol·m−2·s−1·Pa−1, and the idea selectivity for H 2 /CO 2, H 2 /N 2 , H 2 /CH 4 and H 2 /C 3 H 8 is 4.1, 8.5, 11.3 and 294, respectively. The H 2 permeance of the obtained membrane is about one order of magnitude higher than that of similar substrate supported membrane. The membrane also demonstrated a comparable separation performance for mixed gas separation. [ABSTRACT FROM AUTHOR]

Liquid metal (LM) bioelectronics find widespread uses in healthcare devices and medical implants. However, the current LM‐based electrodes suffer from achieving a combination of features including stable conductivity, high tissue adhesion, stability, good biocompatibility, degradability, and recyclability. In this work, a stable LM electrode is prepared with an extremely high adhesion strength (8.9 MPa), which is tunable in a wide range by introducing an adhesive ureidopyrimidinone (UPy)‐based polymer to harvest the abovementioned properties. With the help of dynamic LM particle‐polymer interactions in the polymer matrix, LMs can not only enhance the adhesion properties but also form a percolated network at a low LM loading (38 vol%) to achieve a high conductance stability (R/R0 = 0.76 at 100% strain). The high adhesion strength provides a highly stable electrical connection with rigid components with a high stretchability of 1154% when mounting a resistor, while a relatively low adhesion makes it a comfortable wounded skin‐interfaced electrode for accelerating wound healing. Taking advantage of their tunable surface adhesion and biocompatibility, the as‐prepared LM electrodes provide a more reliable and friendly approach to the development of healthcare devices. [ABSTRACT FROM AUTHOR]

identify the specific nuclear scaffold-bound DNA sequence in rRNA gene clusters of silkworm Attacus ricini, the detergent-like salt lithium 3′, 5′ diiodosalicylate (LIS) was used for the preparation of nuclear scaffold. Through Southern hybridization, using different DNA stretches of rRNA gene as the probe, a scaffold-associated region (SAR) in the 5-non transcribed spacer (NTS) of rRNA gene has been identified. Exonuclease III digestion was used to narrow down the sequence of matrix attachment fragment. It was defined as a specific attachment site within the SacII-EcoRI fragment. It is about 1 kb in length and AT-rich (> 70%). Computer analysis of the SAR sequencing data showed that there are topoisomerase II cleavage sites, ATATTT box, and yeast autonomously replication sequence (ARS). The d(AT)18 specific DNA sequence of the SAR, which was determined previously, was an S1 nuclease hypersensitive site. It might be a cis-element of DNA-signal characteristic for SAR. [ABSTRACT FROM AUTHOR]

A single-stranded S1 nuclease hypersensitive site which contains a d(AT) sequence structure located in the 5′-non transcription spacer of silkworm A. ricini ribosomal RNA gene has been reported[1]. Using starved-refed silkworms, another S1 nuclease sensitive site was found existing in the rDNA chromatin, while under merely starving, this S1 sensitive site disappeared[2]. Recently this inducible S1 sensitive site has been further determined. It consists of a d(GT)10-d(AT)10 special DNA sequence at the transcription initiation region, and shows a behavior of ease in DNA-unwinding, indicating that S1 nuclease sensitive sites may have an important function in the regulation of rDNA transcription and replication. [ABSTRACT FROM AUTHOR]

Background: Recent evidences have shown that circular RNAs (circRNAs) are frequently dysregulated and play paramount roles in various cancers. circRNAs are abundant in central nervous system (CNS); however, few studies describe the clinical significance and role of circRNAs in gliomas, which is the most common and aggressive primary malignant tumor in the CNS. Methods: A bioinformatics analysis was performed to profile and screen the dyregulated circRNAs during early neural development. Quantitative real-time PCR was used to detect the expression of circ-MAPK4 and target miRNAs. Glioma cells were transfected with circ-MAPK4 siRNAs, then cell proliferation, apoptosis, transwell assays, as well as tumorigenesis and TUNEL assays, were performed to examine effect of circ-MAPK4 in vitro and vivo. Biotinylated-circ-MAPK4 probe based pull-down assay was conducted to confirm the relationship between circ-MAPK4 and miR-125-3p. Results: In this study, we identified a circRNA, circ-MAPK4 (has_circ_0047688), which was downregulated during early neural differentiation. In gliomas, circ-MAPK4 acted as an oncogene, was inversely upregulated and linked to clinical pathological stage of gliomas (P < 0.05). Next, we verified that circ-MAPK4 promoted the survival and inhibited the apoptosis of glioma cells in vitro and in vivo. Furthermore, we proved that circ-MAPK4 was involved in regulating p38/MAPK pathway, which affected glioma proliferation and apoptosis. Finally, miR-125a-3p, a miRNA exhibited tumor-suppressive function through impairing p38/MAPK pathway, which was increased by inhibiting circ-MAPK4 and could be pulled down by circ-MAPK4. Inhibition of miR-125a-3p could partly rescue the increased phosphorylation levels of p38/MAPK and the elevated amount of apoptosis inducing by knockdown of circ-MAPK4. Conclusions: Our findings suggest that circ-MAPK4 is a critical player in glioma cell survival and apoptosis via p38/MAPK signaling pathway through modulation of miR-125a-3p, which can serve as a new therapeutic target for treatment of gliomas. [ABSTRACT FROM AUTHOR]

Background: Early metastasis is a key factor contributing to poor breast cancer (BC) prognosis. Circulating tumor cells (CTCs) are regarded as the precursor cells of metastasis, which are ultimately responsible for the main cause of death in BC. However, to date molecular mechanisms underlying CTC formation in BC have been insufficiently defined. Methods: RNA-seq was carried out in primary tissues from early-stage BC patients (with CTCs≥5 and CTCs = 0, respectively) and the validation study was conducted in untreated 80 BC patients. Multiple in vitro and in vivo models were used in functional studies. Luciferase reporter, ChIP-seq, CUT&Tag-seq, and GST-pulldown, etc. were utilized in mechanistic studies. CTCs were counted by the CanPatrol™ CTC classification system or LiquidBiospy™ microfluidic chips. ERK1/2 inhibitor SCH772984 was applied to in vivo treatment. Results: Highly expressed FOXD1 of primary BC tissues was observed to be significantly associated with increased CTCs in BC patients, particularly in early BC patients. Overexpressing FOXD1 enhanced the migration capability of BC cells, CTC formation and BC metastasis, via facilitating epithelial-mesenchymal transition of tumor cells. Mechanistically, FOXD1 was discovered to induce RalA expression by directly bound to RalA promotor. Then, RalA formed a complex with ANXA2 and Src, promoting the interaction between ANXA2 and Src, thus increasing the phosphorylation (Tyr23) of ANXA2. Inhibiting RalA-GTP form attenuated the interaction between ANXA2 and Src. This cascade culminated in the activation of ERK1/2 signal that enhanced metastatic ability of BC cells. In addition, in vivo treatment with SCH772984, a specific inhibitor of ERK1/2, was used to dramatically inhibit the CTC formation and BC metastasis. Conclusion: Here, we report a FOXD1-dependent RalA-ANXA2-Src complex that promotes CTC formation via activating ERK1/2 signal in BC. FOXD1 may serve as a prognostic factor in evaluation of BC metastasis risks. This signaling cascade is druggable and effective for overcoming CTC formation from the early stages of BC. [ABSTRACT FROM AUTHOR]

d-Xylose is a key component of lignocellulosic biomass and the second-most abundant carbohydrate on the planet. As one of the most powerful cyclo-lipopeptide antibiotics, fengycin displays strong wide-spectrum antifungal and antiviral, as well as potential anti-cancer activity. Pyruvate is a key metabolite linking the biosynthesis of fatty acids and amino acids, the precursors for fengycin. In this study, the genes encoding the Dahms xylose-utilization pathway were integrated into the amyE site of Bacillus subtilis 168, and based on the metabolic characteristics of the Dahms pathway, the acetate kinase (ackA) and lactate dehydrogenase (ldh) genes were knocked out. Then, the metabolic control module II was designed to convert glycolaldehyde, another intermediate of the Dahms pathway, in addition to pathways for the conversion of acetaldehyde into malic acid and oxaloacetic acid, resulting in strain BSU03. In the presence of module II, the content of acetic and lactic acid decreased significantly, and the xylose uptake efficiency increased. At the same time, the yield of fengycin increased by 87% compared to the original strain. Additionally, the underlying factors for the increase of fengycin titer were revealed through metabonomic analysis. This study therefore demonstrates that this regulation approach can not only optimize the intracellular fluxes for the Dahms pathway, but is also conducive to the synthesis of secondary metabolites similar to fengycin. Key points: • The expression and effect of the Dahms pathway on the synthesis of fengycin in Bacillus subtilis 168. • The expression of regulatory module II can promote the metabolic rate of the Dahms pathway and increase the synthesis of the fengycin. [ABSTRACT FROM AUTHOR]

[Display omitted] • A graphitization strategy was applied to re-build the edges and stacking of VG. • Such a reconstruction process achieves a long-term and reversible Na deposition and stripping electrochemistry. • The dendrite-free Na deposition and stripping mechanism of re-build VG is further revealed by theoretical calculation. Vertical graphene (VG) arrays, characteristic of particularly porous microscopic structures, are one promising host to accommodate Na deposition, relieve the formidable volume change and eliminate uncontrolled dendrite growth, by decreasing the local current density. However, in practice, the prepared VG arrays possess superabundant defect sites in the local tip positions, which would guide the accumulation of rampant Na-ion flux concentration on these tip defect sites, and thus result in strong local electric field distribution and the divisional dendritic growth. Herein, a novel reconstruction strategy is proposed to re-build the edges and stacking of VG, by removing some unstable carbon defects and changing turbostratic stacking structure of VG to a Bernal stacking mode of the graphited VG, which enables to guide the comparatively smaller and stable interface with Na. Benefiting from the synergistic effect of microscopic structure and defect chemistry design, the re-build VG achieves a long-term reversible Na plating/stripping over 6400 h at an areal capacity of 8 mAh cm−2 in half cell, as well as a long cycle life of up to 3300 h at 1 mA cm−2 with a plating capacity of 4 mAh cm−2 in symmetric cells. Concomitantly, the density functional theory calculations demonstrate that Na atoms tend to nucleate and grow into lateral Na plating on the re-build VG arrays at an atomic level. As a result, the full cell coupled with a P 2 -Na 2/3 Ni 1/3 Mn 1/3 Ti 1/3 O 2 cathode has a predominant improved cycling stability. This microscopic structure/defect chemistry engineering strategy provides new insight into guiding the uniform deposition of Na metal for high-performance sodium metal battery. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) is one of the major contributors to disability and death worldwide. Glutamate-mediated excitotoxicity, one of the secondary injuries occurring after TBI, leads to extreme neuronal apoptosis, and can be a potential target for intervention. Bone marrow mesenchymal stem cells-derived exosomes (BMSCs-Exos) have demonstrated neuroprotective effects on TBI. However, their precise role and the underlying mechanism by which they regulate glutamate-mediated excitotoxicity have not yet been determined. Therefore, this study aimed to determine whether BMSCs-Exos alleviate glutamate excitotoxicity post-TBI and their associated mechanism. BMSCs-Exos were extracted from the BMSCs incubation medium and identified by transmission electron microscopy, nanoparticle trafficking analysis, and western blotting. The neuroprotective effects of BMSCs-Exos on glutamate excitotoxicity were investigated in the glutamate-mediated excitotoxicity neuronal cell model and the TBI rat model (TBI induced by controlled cortical impact) using western blotting and TUNEL assay. Cortical lesion samples were collected post-TBI on day-1 and day-14 to study histology. In addition, cortical lesion volume on days 1, 3 and 7 following TBI was determined using T2-weighted magnetic resonance imaging (MRI), and cognitive function was assessed at 4 weeks following TBI using the Morris water maze (MWM) test. BMSCs-Exos were observed to be spherical with a mean diameter of 109.9 nm, and expressed exosomal markers CD9, CD81 and TSG101. BMSCs-Exos were efficiently endocytosed by astrocytes after co-incubation for 24 h. In vitro studies revealed that 125 μM of glutamate significantly induced neuronal apoptosis, which was attenuated by BMSCs-Exos in astrocyte–neuron co-cultures. This attenuation was mediated by the upregulation of glutamate transporter-1 (GLT-1) level and the downregulation of p-p38 MAPK level in astrocytes. Similar results were obtained in vivo, wherein we verified that PKH67-labeled BMSCs-Exos administered intravenously could reach the perilesional cortex crossing the blood-brain barrier and significantly reduce glutamate levels in the perilesional cortex of the TBI rat, accompanied by increased GLT-1 level and downregulation in p-p38 MAPK level. Additionally, western blotting and TUNEL staining also revealed that BMSCs-Exos significantly downregulated the expression of pro-apoptosis markers, including cleaved caspase-3 and cleaved caspase-9, and attenuated neuronal apoptosis following TBI. Immunohistochemical analysis and Nissl staining showed that BMSCs-Exos significantly increased GLT-1-positive cells, and the number of apoptotic neurons decreased in the perilesional cortex. Moreover, MRI and MWM results revealed that BMSCs-Exos significantly minimized cortical lesion volume and ameliorated cognitive function after TBI. The underlying neuroprotective mechanism of BMSCs-Exos may be due to an increase in GLT-1 level in astrocytes by blocking the p38 MAPK signaling pathway. Taken together, our findings demonstrate that the implementation of BMSCs-Exos may be an effective prospective therapy for attenuating post-TBI neurological damage. • BMSCs-Exos could be efficiently internalized by astrocytes. • BMSCs-Exos possess neuroprotective effects on TBI. • BMSCs-Exos attenuate post-TBI neurological damage by alleviating glutamate-mediated excitotoxicity. • The protective effects of BMSCs-Exos may be due to the increase of GLT-1 level by blocking the p38 MAPK signaling pathway. [ABSTRACT FROM AUTHOR]

Background: The homologous proteins identified as cellular retinoic acid-binding proteins I and II ( CRABP-I and CRABP-II ) belong to a subset of intracellular proteins characterized by their robust affinity for retinoic acid, which plays an indispensable role in the development of hair follicle, including differentiation, proliferation, and apoptosis in keratinocytes. Previous research on Hu sheep hair follicles revealed the specific expression CRABP1 in dermal papilla cells (DPCs), suggesting that CRABP1 has a potential role in regulating the DPC population. Therefore, the main purpose of this study is to expose the performance of the CRABP1 genes in the development and proliferation of DPCs., Methods: Initially, overexpression and inhibition of CRABP1 in the DPCs were conducted through overexpression vector and siRNA. CCK-8, EDU, and RT-PCR cell cycle assays and immunostaining were performed to evaluate the proliferation and cell cycle of dermal papilla cells (DPCs). Although, the influence of CRABP1 upon β-catenin in dermal papilla cells (DPCs) was found using immunofluorescence labeling. Finally, RT-PCR was conducted to assess the impact of CRABP1 on the expression levels of CTNNB1, TCF4, and LEF1 in DPCs involved in the Wnt/β-catenin signaling pathway., Results: The results showed that CRABP1 overexpression promotes the growth rates of DPCs and significantly enhances the proportion of S-phase cells compared with the control group ( p < 0.05). The results were the opposite when CRABP1 was a knockdown. In contrast, there was a significant decline in the mRNA expression levels of CTNNβ1 , LEF1 ( p < 0.05), and TCF4 ( p < 0.01) by CRABP1 knockdown., Conclusions: This study found that CRABP1 influences the expression of important genes within the Wnt/β-catenin signaling pathway and promotes DPC proliferation. This investigation provides a theoretical framework to explain the mechanisms that control hair follicle morphogenesis and development.

Previous studies have shown that the BMP7 gene is differentially expressed in Hu sheep lamb skin of different pattern types, and its expression level is significantly correlated with hair follicle indices of different pattern types, but the molecular mechanism of the differential expression of the BMP7 gene remains unclear. This study investigated the effect of DNA methylation on the transcriptional expression of BMP7 . Firstly, we found that the mRNA expression of the BMP7 gene and the activity of the core promoter of the BMP7 gene were upregulated after 5-Aza-Deoxycytidine-induced demethylation treatment using qRT-PCR and double luciferase reporter assay. Then, we found that the proliferation of Hu sheep DPCs in vitro was promoted after 5-Aza-Deoxycytidine-induced demethylation treatment through qRT-PCR, CCK-8, and EdU assay, and that the overexpression of DNMT1 in DPCs induced the opposite effect. In addition, the results of the cell cycle assay reveal that the percentage of cells in the S phase was increased after 5-Aza-Deoxycytidine-induced demethylation treatment, and that the percentage of cells in the S phase was decreased after overexpression of DNMT1 in DPCs. This study indicated that the differential expression of the BMP7 gene in different patterns of Hu sheep lamb skin may be regulated by DNA methylation modification. In addition, DNA methylation can regulate the proliferation and cell cycle of DPCs in Hu sheep.

The occurrence of osteoarthritis in the knee joint is regulated by a complex network, and there is currently no specific therapeutic drug available. Functional exercises and treatments targeting inflammatory factors have shown the potential to alleviate knee osteoarthritis to some extent. Therefore, the aim of this study was to assess the intra-articular injection (IAI) of autologous platelet-rich plasma (PRP) combined with physical therapy (PT) in treating knee osteoarthritis. A total of 128 patients with knee osteoarthritis were included in the study, including 64 males and 64 females. A total of 128 patients were divided into sodium hyaluronate group (HA group), PRP group, PRP + PT group, and PT group, with 32 cases in each group. Visual analog scale (VAS), Western Ontario and McMaster University Osteoarthritis Index (WOMAC), and Japanese Orthopaedic Association (JOA) were employed to evaluate the recovery of patients from pain and osteoarthritis. Color Doppler ultrasound imaging technology was utilized to assess joint effusion, synovial membrane thickness, and articular cartilage thickness in patients with knee osteoarthritis. Enzyme-linked immunosorbent assay (ELISA) was employed to detect the levels of interleukin-1β (IL-1β), transforming growth factor-β1 (TGF-β1), and matrix metallopeptidase 3 (MMP-3) in the synovial fluid. Compared to the HA group, the PT group, PRP group, and PRP combined with PT (PRP + PT) group all showed reduced VAS and WOMAC scores, increased JOA scores, decreased joint effusion, synovial membrane thickness, and articular cartilage thickness in the knee joint. Additionally, levels of IL-1β and MMP-3 in the synovial fluid decreased, while TGF-β1 levels increased (P < 0.05). Compared with the PT group, the VAS and WOMAC scores of the knee joint in the PRP group decreased, JOA scores increased, joint effusion, synovial thickness, and articular cartilage thickness decreased, but there was no statistically significant difference (P > 0.05), and the PRP + PT group showed decreased VAS and WOMAC scores, increased JOA scores, reduced joint effusion, synovial membrane thickness, and articular cartilage thickness in the knee joint. Moreover, levels of IL-1β and MMP-3 in the synovial fluid decreased, while TGF-β1 levels increased (P < 0.05). No severe adverse reactions were observed in any of the four groups, but the pain rate in the PRP + TP group was significantly lower than PT group, PRP group, and PRP + PT group (P < 0.05). The efficacy of intra-articular injection of PRP combined with exercise therapy in the treatment of knee osteoarthritis is superior to that of single interventions such as simple interventions of HA, PRP injection, and PT. Furthermore, intra-articular injection of PRP combined with exercise therapy demonstrates enhanced effectiveness in improving the inflammatory levels associated with knee osteoarthritis and facilitating the rehabilitation process., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Main Conclusion: The rice SnRK2 members SAPK4, SAPK5, SAPK7 and SAPK10 are positive regulators involved in the regulation of rice flowering, while other single mutants exhibited no effect on rice flowering. The rice SnRK2 family, comprising 10 members known as SAPK (SnRK2-Associated Protein Kinase), is pivotal in the abscisic acid (ABA) pathway and crucial for various biological processes, such as drought resistance and salt tolerance. Additionally, these members have been implicated in the regulation of rice heading date, a key trait influencing planting area and yield. In this study, we utilized gene editing technology to create mutants in the Songjing 2 (SJ2) background, enabling a comprehensive analyze the role of each SAPK member in rice flowering. We found that SAPK1, SAPK2, and SAPK3 may not directly participate in the regulatory network of rice heading date, while SAPK4, SAPK5, and SAPK7 play positive roles in rice flowering regulation. Notably, polygene deletion resulted in an additive effect on delaying flowering. Our findings corroborate the previous studies indicating the positive regulatory role of SAPK10 in rice flowering, as evidenced by delayed flowering observed in sapk9/10 double mutants. Moving forward, our future research will focus on analyzing the molecular mechanisms underlying SAPKs involvement in rice flowering regulation, aiming to enhance our understanding of the rice heading date relationship network and lay a theoretical foundation for breeding efforts to alter rice ripening dates., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Rice flowering time determines its geographical distribution and yield traits. As a short-day plant, rice can grow in the northern long-day conditions due to the functional mutations of many photosensitive genes. In this study, to identify novel genes or alleles that regulate flowering time in high latitude region, two cultivar, Dongnong 413 (DN413) and Yukimochi (XN) showing extreme early flowering were used for investigation. DN413 is around 4.0 days earlier than XN, and both cultivars can be grown in II (2500 ℃-2700 ℃) to III (2300 ℃-2500 ℃) accumulated temperature zones. We found that the two cultivars shared the same genotype of heading date genes, including Hd1/2/4/5/6/16/17/18 , Ehd2 , DTH2 , SE5 , Hd3a . Importantly, a novel Ehd3 allele characterized by a A1146C substitution was identified, which results in the E382D substitution, hereafter the 382 position E is defined as Hap&#95;E and the 382 position D is defined as Hap&#95;D. Association analysis showed that Hap&#95;E is earlier flowering than Hap&#95;D. Subsequently, we construct DN413 Hap&#95;D line by three times back-crossing DN413 with XN, and found the heading date of DN413 Hap&#95;D was 1.7-3.5 days later than DN413. Moreover, Hap&#95;E and Hap&#95;D of Ehd3 were transformed into ehd3 mutant, respectively, and the Ehd3pro:Ehd3D/ehd3 flowered later than that Ehd3pro:Ehd3E/ehd3 by around 4.3 days. Furthermore, we showed Ehd3 functions as a transcriptional suppressor and the substitution of Asp-382 lost the inhibition activity in protoplasts. Finally, a CAPS marker was developed and used for genotyping and marker assistant breeding. Collectively, we discovered a novel functional allele of Ehd3 , which can used as a valuable breeding target., Supplementary Information: The online version contains supplementary material available at 10.1007/s11032-024-01472-x., Competing Interests: Competing interestsThe author(s) declare that they have no conflict of interest., (© The Author(s), under exclusive licence to Springer Nature B.V. 2024.)

Rice is a chilling-sensitive plant, and extremely low temperatures seriously decrease rice production. Several genes involved in chilling stress have been reported in rice; however, the chilling signaling in rice remains largely unknown. Here, we investigated the chilling tolerance phenotype of overexpression of constitutive active OsMAPK6 (CAMAPK6-OE) and OsMAPK6 mutant dsg1, and demonstrated that OsMAPK6 positively regulated rice chilling tolerance. It was shown that, under cold stress, the survival rate of dsg1 was significantly lower than that of WT, whereas CAMAPK6-OE display higher survival rate than WT. Physiological assays indicate that ion leakage and dead cell in dsg1 was much more severe than those in WT and CAMAPK6-OE. Consistently, expression of chilling responsive genes in dsg1, including OsCBFs and OsTPP1, was significantly lower than that of in WT and CAMAPK6-OE. Biochemical analyses revealed that chilling stress promotes phosphorylation of OsMAPK6. Besides, we found that OsMAPK6 interacts with and phosphorylates two key regulators in rice cold signaling, OsIPA1 and OsICE1, and then enhance their protein stability. Overall, our results revealed a cold-induced OsMAPK6-OsICE1/OsIPA1 signaling cascade by which OsMAPK6 was involved in rice chilling tolerance, which provides novel insights to understand rice cold response at seedling stage., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Flowering time is one of the most fundamental factors that determine the distribution and final yield of rice. Ehd1 (Early heading date 1) is a B-type response regulator which functions as a flowering time activator. Although diverse flowering time genes have been reported as regulatory factors of Ehd1 expression, the potential regulators of Ehd1 largely remain to be identified. Here, we identified a basic leucine zipper transcription factor bZIP65, a homolog of bZIP71, as a new negative regulator of Ehd1 . The overexpression of bZIP65 delays flowering, while bzip65 mutants have similar flowering time to SJ2 (Songjing2) in both long-day and short-day conditions. Biochemically, bZIP65 associates with Ehd1 promoter and transcriptionally represses the expression of Ehd1 . Moreover, we found that bZIP65 enhances H3K27me3 level of Ehd1 . Taken together, we cloned a new gene, bZIP65 , regulating rice heading date, and uncovered the mechanism of bZIP65 delaying flowering time, where bZIP65 increases the H3K27me3 level of Ehd1 and transcriptionally represses the expression of Ehd1 , similar to its homolog bZIP71., Supplementary Information: The online version contains supplementary material available at 10.1007/s11032-022-01334-4., Competing Interests: Competing interestsThe authors declare no competing interests., (© The Author(s), under exclusive licence to Springer Nature B.V. 2022.)

Glioblastoma multiforme (GBM) is the most malignant type of primary brain tumor in adults and can diffusely infiltrate adjacent normal tissue. GBM is therefore rarely cured by surgery or radiation therapy. Matrix metalloproteinases (MMPs) are involved in tissue remodeling and numerous other physiological progresses. The MMPs MMP-2 and MMP-9 are associated with the invasion ability of GBM. PT93 is a novel caffeic acid amide derivative that was first synthesized in 2013. In the present study, the human GBM T98G, U87 and U251 cell lines and the normal mouse neuron HT22 cell line were used to investigate the anticancer and cytotoxic effects of PT93 in vitro . The cytotoxicity of PT93 was measured using MTT and lactate dehydrogenase assays. The anti-proliferation effect was tested using a cell colony formation assay. Gelatin zymography analysis and a scratch test were used to investigate the anti-migration mechanism of PT93. Western blot analysis was used to measure the expression of MMP-2/-9. The experimental results showed that PT93 suppressed the proliferation of T98G cells, and showed cytotoxicity effects at high concentration in T98G, U87, U251 and HT22 cell lines. Furthermore, PT93 limited the migration ability of the cells and inhibited the extracellular MMP-2 and MMP-9 activity of T98G and U251 cells. Finally, the present study confirmed that PT93 affects the level of MMP-2/-9 expression in T98G cells in a concentration-dependent manner. The present study indicates that PT93, as a novel caffeic acid amide derivative, may be used in the treatment of GBM.

The Hippo pathway plays an important role in the development of hepatocellular carcinoma (HCC). The present study aimed at exploring the genetic variants of Hippo pathway-related genes and their association with HCC prognosis. A total of 331 HCC patients who tested positive for hepatitis B surface antigen were recruited in this study. None of the patients had prior surgical treatment. Twelve potentially functional single-nucleotide polymorphisms (rs7317471 and rs9509492 in LATS2; rs4810446, rs2267853, rs8000, and rs6073627 in MST1; rs10955176 in MST2; and rs16861979, rs2043550, rs16861985, rs1055153, and rs7630434 in TAZ) in the Hippo pathway were genotyped from patients' peripheral leukocytes using the Sequenom MassARRAY iPLEX platform. Cox proportional hazard models and log-rank test were used for the survival analyses. LATS2 rs7317471 C>T polymorphism was significantly associated with decreased risk of death in HCC using the dominant model (adjusted hazard ratio [HR] =0.63, 95% confidence interval [CI] =0.46-0.87, P=0.004). Furthermore, using stratified analysis, LATS2 rs7317471 CT/TT genotypes were found to be significantly associated with decreased risk of death in patients who were below 53 years of age (adjusted HR =0.50), females (adjusted HR =0.60), smokers (adjusted HR =0.56), drinkers (adjusted HR =0.58), have Barcelona clinic liver cancer stage B (adjusted HR =0.62), and received no prior chemotherapy or transcatheter hepatic arterial chemoembolization (adjusted HR =0.48). Our results suggested that LATS2 rs7317471 could be used as a potential biomarker for the prediction of HCC prognosis.

Glioblastoma (GBM) is the most common brain tumor with high abilities of proliferation, migration and invasion. As is well-known, the peritumoral excitotoxic neuronal cell loss caused by glutamate, secreted by GBM cells, through activated N-methyl-D aspartate receptor (NMDAR) of neuronal cell. What's more, glutamate benefits the migration of GBM cells. However, the glutamate will not kill the GBM cells itself, which may be due to the deficiency of NMDAR. Fasudil, a ROCK inhibitor, was applied for subarachnoid hemorrhage (SAH) in clinic for many years. And it was found to be of potential to inhibit the proliferation, migration and invasion of GBM cells. In present study, we applied fasudil on the primary human GBM cells to further investigate the reduction of cell viability combined with glutamate. Combination treatment of glutamate and fasudil could significantly decrease the cell viability and elevate the level of LDH compared with fasudil treatment alone. What's more, MK-801, a NMDAR antagonist, could partially abolish this death caused by combination treatment. Further study found that the expression level of NMDAR-2B was elevated after treatment with fasudil in GBM cells. These results demonstrated fasudil could increase the expression level of NMDAR, which is necessary for glutamate to work. In a word, our research has provided a new sight of medicine combination in the treatment of GBM.