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Polyploids are essential in plant evolution and species formation, providing a rich genetic reservoir and increasing species diversity. Complex polyploids with higher ploidy levels often have a dosage effect on the phenotype, which can be highly detrimental to gametes, making them rare. In this study, offspring plants resulting from an autoallotetraploid (RRRC) derived from the interspecific hybridization between allotetraploid Raphanobrassica (RRCC, 2n = 36) and diploid radish (RR, 2n = 18) were obtained. Fluorescence in situ hybridization (FISH) using C-genome-specific repeats as probes revealed two main genome configurations in these offspring plants: RRRCC (2n = 43, 44, 45) and RRRRCC (2n = 54, 55), showing more complex genome configurations and higher ploidy levels compared to the parental plants. These offspring plants exhibited extensive variation in phenotypic characteristics, including leaf type and flower type and color, as well as seed and pollen fertility. Analysis of chromosome behavior showed that homoeologous chromosome pairing events are widely observed at the diakinesis stage in the pollen mother cells (PMCs) of these allopolyploids, with a range of 58.73% to 78.33%. Moreover, the unreduced C subgenome at meiosis anaphase II in PMCs was observed, which provides compelling evidence for the formation of complex allopolyploid offspring. These complex allopolyploids serve as valuable genetic resources for further analysis and contribute to our understanding of the mechanisms underlying the formation of complex allopolyploids.
Subject(s)
Aneuploidy , Chromosomes, Plant , Polyploidy , Raphanus , Raphanus/genetics , Chromosomes, Plant/genetics , In Situ Hybridization, Fluorescence , Brassica/genetics , Hybridization, Genetic , Meiosis/genetics , Genome, Plant , Pollen/genetics , PhenotypeABSTRACT
BACKGROUND: Compassion fatigue in nursing interns contributes to career indecision and worsens the nursing shortage. While work environment and psychological factors are well-studied, the ethical dimension remains unexplored. Understanding these mechanisms, particularly the role of moral courage, is essential for designing interventions to combat compassion fatigue and address the workforce crisis. This study investigates the influence of moral courage on compassion fatigue among Chinese nursing interns, focusing on the mediating roles of moral sensitivity and professional identity. METHODS: A quantitative, cross-sectional study was conducted in accordance with the STROBE guidelines. We used the convenience sampling method to recruit 467 nursing interns from four public junior colleges in Hunan Province, China in February, 2024. Data were collected using Compassion Fatigue Short Scale, Moral Courage Scale, Revised Moral Sensitivity Questionnaire, and Professional Identity Scale. Data analyses were conducted using SPSS 22.0 and Amos 21.0. RESULTS: The modified model exhibited a good fit (χ2/df = 3.437, AGFI = 0.928, IFI = 0.984, TLI = 0.976, CFI = 0.984, NFI = 0.977, RMSEA = 0.072). Moral sensitivity positively influenced both moral courage and professional identity, while professional identity negatively impacted compassion fatigue. Importantly, the effect of moral courage on compassion fatigue was entirely mediated by moral sensitivity and professional identity (ß = -0.114, P = 0.001). CONCLUSION: This study suggests that moral courage in nursing interns mitigates compassion fatigue through the combined mediating effects of moral sensitivity and professional identity. Ethics education programs fostering moral courage, moral sensitivity, and professional values in nursing students could be crucial in alleviating compassion fatigue.
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BACKGROUND: sTREM-1H and miR-126 play crucial roles in inflammation and immune responses, yet their involvement in patients with pulmonary infection following cranial injury remains understudied. OBJECTIVE: The distribution of pathogens causing infection in patients with pulmonary infection after craniocerebral injury was explored, and the changes in the levels of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) and miR-126 in peripheral blood were analyzed. METHODS: In this study, 60 patients (study group) with postoperative lung infection in craniocerebral injury treated from January 2019 to December 2, 2021, and 60 patients without lung infection were selected as the control group. The study group received anti-infection treatment. The infection pathogen of the study group was tested, and the changes of sTREM-1 and miR-126 levels in the peripheral blood of the study and control groups were recorded to explore the diagnosis and predictive Value of prognostic death. RESULTS: 66 pathogens were detected, including 18 gram-positive bacteria, 42 gram-negative bacteria, and 6 fungi. The sTREM-1 level was higher than the control group, and the miR-126 level was lower than the control group. By ROC curve analysis, the diagnostic AUC values of both patients were 0.907 and 0.848, respectively (P< 0.05). Compared to those in the study group, patients had decreased sTREM-1 levels and increased miR-126 levels after treatment (P< 0.05). Compared with the survival group, patients in the death group had increased sTREM-1 levels and decreased miR-126 levels, and ROC curve analysis, the predicted AUC death values were 0.854 and 0.862, respectively. CONCLUSION: Gram-negative bacteria, with increased peripheral sTREM-1 levels and decreased miR-126 levels. The levels of sTREM-1 and miR-126 have specific diagnostic and prognostic Values for pulmonary infection after craniocerebral injury. However, the study's conclusions are drawn from a limited sample and short-term data, which might limit their broader applicability. Future studies with larger populations and longitudinal designs are required to confirm these findings and determine these biomarkers' robustness across different settings. Further research should also explore how these biomarkers influence patient outcomes in craniocerebral injuries.
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BACKGROUND: Previous studies provide evidence that in vivo metabolites are associated with breast cancer (BC). However, the causal relationship between blood metabolites and BC remains unclear. METHOD: Comprehensive two-sample Mendelian randomization analysis was conducted to determine the causal association between 1400 publicly available genetic data on metabolic factors and human epidermal growth factor receptor positive (HER+) BC or HER- BC in this study. RESULT: Epiandrosterone sulfate levels (OR = 1.07, 95% CI = 1.02 ~ 1.10, p = 0.0013), 5alpha-androstan-3beta,17beta-diol monosulfate (2) levels (OR = 1.07, 95% CI = 1.03 ~ 1.12, p = 0.0012), glycohyocholate levels (OR = 0.85, 95% CI = 0.77 ~ 0.93, p = 0.0007) and etiocholanolone glucuronide levels (OR = 1.12, 95% CI = 1.05 ~ 1.20, p = 0.0013) were causally correlated with HER+ BC. 5 metabolites were causally correlated with HER- BC: Vanillic acid glycine levels (OR = 1.14, 95% CI = 1.06 ~ 1.22, p = 0.0003), Thyroxine levels (OR = 1.26, 95% CI = 1.11 ~ 1.44, p = 0.0004), 1-palmitoyl-2-linoleoyl-GPI (16:0/18:2) levels (OR = 0.86, 95% CI = 0.79 ~ 0.94, p = 0.0010), N-acetylphenylalanine levels (OR = 1.12, 95% CI = 1.05 ~ 1.19, p = 0.0007) and Glucose-to-mannose ratio (OR = 1.15, 95% CI = 1.06 ~ 1.24, p = 0.0008). Two common causally related metabolites were identified: Gamma-glutamyl glutamate and X-12849 levels. CONCLUSIONS: Our study has respectively demonstrated the connection between blood metabolites and HER+ or HER- BC by genetic means, thereby offering opportunities for therapeutic targets.
Subject(s)
Breast Neoplasms , Mendelian Randomization Analysis , Humans , Female , Breast Neoplasms/blood , Breast Neoplasms/genetics , Receptor, ErbB-2/genetics , Receptor, ErbB-2/metabolism , Polymorphism, Single NucleotideABSTRACT
Cells are the fundamental units of biological systems and exhibit unique development trajectories and molecular features. Our exploration of how the genomes orchestrate the formation and maintenance of each cell, and control the cellular phenotypes of various organismsis, is both captivating and intricate. Since the inception of the first single-cell RNA technology, technologies related to single-cell sequencing have experienced rapid advancements in recent years. These technologies have expanded horizontally to include single-cell genome, epigenome, proteome, and metabolome, while vertically, they have progressed to integrate multiple omics data and incorporate additional information such as spatial scRNA-seq and CRISPR screening. Single-cell omics represent a groundbreaking advancement in the biomedical field, offering profound insights into the understanding of complex diseases, including cancers. Here, we comprehensively summarize recent advances in single-cell omics technologies, with a specific focus on the methodology section. This overview aims to guide researchers in selecting appropriate methods for single-cell sequencing and related data analysis.
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Fibroblast activation and extracellular matrix (ECM) deposition play an important role in the tracheal abnormal repair process and fibrosis. As a transcription factor, SOX9 is involved in fibroblast activation and ECM deposition. However, the mechanism of how SOX9 regulates fibrosis after tracheal injury remains unclear. We investigated the role of SOX9 in TGF-ß1-induced fibroblast activation and ECM deposition in rat tracheal fibroblast (RTF) cells. SOX9 overexpression adenovirus (Ad-SOX9) and siRNA were transfected into RTF cells. We found that SOX9 expression was up-regulated in RTF cells treated with TGF-ß1. SOX9 overexpression activated fibroblasts and promoted ECM deposition. Silencing SOX9 inhibited cell proliferation, migration, and ECM deposition, induced G2 arrest, and increased apoptosis in RTF cells. RNA-seq and chromatin immunoprecipitation sequencing (ChIP-seq) assays identified MMP10, a matrix metalloproteinase involved in ECM deposition, as a direct target of SOX9, which promotes ECM degradation by increasing MMP10 expression through the Wnt/ß-catenin signaling pathway. Furthermore, in vivo, SOX9 knockdown ameliorated granulation proliferation and tracheal fibrosis, as manifested by reduced tracheal stenosis. In conclusion, our findings indicate that SOX9 can drive fibroblast activation, cell proliferation, and apoptosis resistance in tracheal fibrosis via the Wnt/ß-catenin signaling pathway. The SOX9-MMP10-ECM biosynthesis axis plays an important role in tracheal injury and repair. Targeting SOX9 and its downstream target MMP10 may represent a promising therapeutic approach for tracheal fibrosis.
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Maize (Zea mays L.) is an important food crop with a wide range of uses in both industry and agriculture. Drought stress during its growth cycle can greatly reduce maize crop yield and quality. However, the molecular mechanisms underlying maize responses to drought stress remain unclear. In this work, a WRKY transcription factor-encoding gene, ZmWRKY30, from drought-treated maize leaves was screened out and characterized. ZmWRKY30 gene expression was induced by dehydration treatments. The ZmWRKY30 protein localized to the nucleus and displayed transactivation activity in yeast. Compared with wild-type (WT) plants, Arabidopsis lines overexpressing ZmWRKY30 exhibited a significantly enhanced drought stress tolerance, as evidenced by the improved survival rate, increased antioxidant enzyme activity by superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT), elevated proline content, and reduced lipid peroxidation recorded after drought stress treatment. In contrast, the mutator (Mu)-interrupted ZmWRKY30 homozygous mutant (zmwrky30) was more sensitive to drought stress than its null segregant (NS), characterized by the decreased survival rate, reduced antioxidant enzyme activity (SOD, POD, and CAT) and proline content, as well as increased malondialdehyde accumulation. RNA-Seq analysis further revealed that, under drought conditions, the knockout of the ZmWRKY30 gene in maize affected the expression of genes involved in reactive oxygen species (ROS), proline, and myo-inositol metabolism. Meanwhile, the zmwrky30 mutant exhibited significant downregulation of myo-inositol content in leaves under drought stress. Combined, our results suggest that ZmWRKY30 positively regulates maize responses to water scarcity. This work provides potential target genes for the breeding of drought-tolerant maize.
Subject(s)
Drought Resistance , Inositol , Plant Proteins , Reactive Oxygen Species , Zea mays , Antioxidants/metabolism , Arabidopsis/genetics , Arabidopsis/physiology , Gene Expression Regulation, Plant , Homeostasis , Inositol/metabolism , Plant Leaves/genetics , Plant Leaves/physiology , Plant Proteins/genetics , Plant Proteins/metabolism , Plants, Genetically Modified , Reactive Oxygen Species/metabolism , Stress, Physiological/genetics , Transcription Factors/genetics , Transcription Factors/metabolism , Zea mays/genetics , Zea mays/physiologyABSTRACT
Metal-halide perovskite nanocrystals (NCs) are one of the most promising emitters for the application of display and nanolight sources. The full width at half-maximum (FWHM) of photoluminescence (PL) emission is essential for color purity, which however remains a difficulty to further reduce the FWHM of the perovskite NCs at room temperature. Here, we show the quasi-sphere perovskite NCs with narrow PL emission at a deep-blue wavelength of â¼430 nm; its PL FWHM reaches â¼11 nm at room temperature, owing to the monodispersion in size distribution as well as the symmetric quasi-sphere morphology of NCs releasing the fine structure splitting-induced inhomogeneous broadening. Through regulating A cations with respect to the ratio of FA (or MA)-to-Cs and Cs-to-Pb, the PL emission of the NCs could be tuned from â¼505 to â¼430 nm combined with varied morphologies from large cube to small quasi-sphere. Such spectroscopic and morphological discrepancies are supposed to be attributed to the different crystalline kinetics that is strongly dependent on the synthetic condition. To be specific, in the case of increasing FA (or MA)-to-Cs, the growth rate of CsPbBr3 and FAPbBr3 (or MAPbBr3) perovskites is determined by the reactivity of transient species, while in the case of decreasing the Cs-to-Pb ratio, the growth rate of perovskites is slowed down by the serious reduction of Cs+ in the precursor. This study provides an effective strategy to adjust the emission across from green to deep-blue color and promotes the perovskite NCs with a narrow FWHM, and tunable PL emission facilitates in application of optoelectronic devices.
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Vaccinium duclouxii, a wild blueberry species native to the mountainous regions of southwestern China, is notable for its exceptionally high anthocyanin content, surpassing that of many cultivated varieties and offering significant research potential. Glutathione S-transferases (GSTs) are versatile enzymes crucial for anthocyanin transport in plants. Yet, the GST gene family had not been previously identified in V. duclouxii. This study utilized a genome-wide approach to identify and characterize the GST gene family in V. duclouxii, revealing 88 GST genes grouped into seven distinct subfamilies. This number is significantly higher than that found in closely related species, with these genes distributed across 12 chromosomes and exhibiting gene clustering. A total of 46 members are classified as tandem duplicates. The gene structure of VdGST is relatively conserved among related species, showing closer phylogenetic relations to V. bracteatum and evidence of purifying selection. Transcriptomic analysis and qRT-PCR indicated that VdGSTU22 and VdGSTU38 were highly expressed in flowers, VdGSTU29 in leaves, and VdGSTF11 showed significant expression in ripe and fully mature fruits, paralleling trends seen with anthocyanin accumulation. Subcellular localization identified VdGSTF11 primarily in the plasma membrane, suggesting a potential role in anthocyanin accumulation in V. duclouxii fruits. This study provides a foundational basis for further molecular-level functional analysis of the transport and accumulation of anthocyanins in V. duclouxii, enhancing our understanding of the molecular mechanisms underlying anthocyanin metabolism in this valuable species.
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Resveratrol (RSV) is a polyphenol antioxidant that has been shown to have neuroprotective effects. We sought molecular mechanisms that emphasize the anti-inflammatory activity of RSV in traumatic brain injury (TBI) in mice associated with endoplasmic reticulum stress (ERS). After establishing three experimental groups (sham, TBI, and TBI+RSV), we explored the results of RSV after TBI on ERS and caspase-12 apoptotic pathways. The expression levels of C/EBP homologous protein (CHOP), glucose regulated protein 78kD (GRP78), caspase-3, and caspase-12 in cortical brain tissues were assessed by western blotting. The qPCR analysis was also performed on mRNA expression of tumor necrosis factor (TNF)-α and interleukin (IL)-1ß in cortical brain tissue. In addition, the expression of GRP78 in microglia (ionized calcium binding adaptor molecule 1; Iba-1) and neurons (neuronal nuclei; NeuN) was identified by immunofluorescence staining. The neurological function of mice was assessed by modified neurological severity scores (mNSS). After drug treatment, the expression of CHOP, GRP78, caspase-3 and caspase-12 decreased, and qPCR results showed that TNF-α and IL-1ß were down-regulated. Immunofluorescence staining showed down-regulation of Iba-1+/GRP78+ and NeuN+/GRP78+ cells after RSV treatment. The mNSS analysis confirmed improvement after RSV treatment. RSV improved apoptosis by downregulating the ERS signaling pathway and improved neurological prognosis in mice with TBI.
Subject(s)
Brain Injuries, Traumatic , Endoplasmic Reticulum Chaperone BiP , Endoplasmic Reticulum Stress , Resveratrol , Animals , Brain Injuries, Traumatic/drug therapy , Brain Injuries, Traumatic/pathology , Brain Injuries, Traumatic/metabolism , Resveratrol/pharmacology , Resveratrol/therapeutic use , Endoplasmic Reticulum Stress/drug effects , Mice , Male , Apoptosis/drug effects , Prognosis , Neuroprotective Agents/pharmacology , Neuroprotective Agents/therapeutic use , Neurons/drug effects , Neurons/pathology , Neurons/metabolism , Interleukin-1beta/metabolism , Interleukin-1beta/genetics , Caspase 12/metabolism , Caspase 12/genetics , Heat-Shock Proteins/metabolism , Heat-Shock Proteins/genetics , Tumor Necrosis Factor-alpha/metabolism , Mice, Inbred C57BL , Cell Death/drug effects , Microglia/drug effects , Microglia/metabolism , Microglia/pathology , Transcription Factor CHOP/metabolism , Transcription Factor CHOP/geneticsABSTRACT
Land use changes have profoundly influenced global environmental dynamics. The Yellow River (YR), as the world's fifth-longest river, significantly contributes to regional social and economic growth due to its extensive drainage area, making it a key global player. To ensure ecological stability and coordinate land use demand, modeling the future land allocation patterns of the Yellow River Basin (YRB) will assist in striking a balance between land use functions and the optimization of its spatial design, particularly in water and sand management. In this research, we used a multi-objective genetic algorithm (MOGA) with the PLUS model to simulate several different futures for the YRB's land use between 1990 and 2020 and predict its spatial pattern in 2030. An analysis of the spatiotemporal evolution of land use changes in the YRB indicated that construction land expansion is the primary driver of landscape pattern and structure changes and ecological degradation, with climate change also contributing to the expansion of the watershed area. On the other hand, the multi-scenario simulation, constrained by specific targets, revealed that economic development was mainly reflected in land expansion for construction. At the same time, grassland and woodland were essential pillars to support the region's ecological health, and increasing the development of unused land emerged as a potential pathway towards sustainable development in the region. This study could be used as a template for the long-term growth of other large river basins by elucidating the impacts of human activities on land use and rationalizing land resource allocation under various policy constraints.
Subject(s)
Conservation of Natural Resources , Rivers , Models, Theoretical , Climate Change , ChinaABSTRACT
Ferroptosis, a type of programmed cell death that relies on iron, is distinct in terms of its morphological, biochemical and genetic features. Unlike other forms of cell death, such as autophagy, apoptosis, necrosis, and pyroptosis, ferroptosis is primarily caused by lipid peroxidation. Cells that die due to iron can potentially trigger an immune response which intensifies inflammation and causes severe inflammatory reactions that eventually lead to multiple organ failure. In recent years, ferroptosis has been identified in an increasing number of medical fields, including neurological pathologies, chronic liver diseases and sepsis. Ferroptosis has the potential to cause an inflammatory tempest, with many of the catalysts and pathological indications of respiratory ailments being linked to inflammatory reactions. The growing investigation into ferroptosis in respiratory disorders has also garnered significant interest to better understand the mechanism of ferroptosis in these diseases. In this review, the recent progress in understanding the molecular control of ferroptosis and its mechanism in different respiratory disorders is examined. In addition, this review discusses current challenges and prospects for understanding the link between respiratory diseases and ferroptosis.
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Acute liver failure (ALF) is a critical condition that can lead to substantial liver dysfunction. It is characterized by complex clinical manifestations and rapid progression, presenting significant challenges in diagnosis and treatment. We investigated the protective effect of mefunidone (MFD), a novel antifibrosis pyridone agent, on ALF in mice, and explored its potential mechanism of action. MFD pretreatment can alleviate lipopolysaccharide (LPS) and d-galactosamine (D-GalN)-induced ALF, reduce hepatocyte apoptosis, and reduce inflammation and oxidative stress. Additionally, MFD alleviated LPS/D-GalN-stimulated reactive oxygen species (ROS) production and cell death in AML12 cells. RNA sequencing enrichment analysis showed that MFD significantly affected the Mitogen-Activated Protein Kinase (MAPK) pathway. In vivo and in vitro experiments showed that MFD inhibited MKK4 and JNK phosphorylation. JNK activation caused by MKK4 and JNK activators could eliminate the therapeutic effect of MFD on AML12. In addition, MFD pretreatment alleviated ConA-induced ALF, reduced inflammation and oxidative stress in mice, and reduced mouse mortality. These results suggest that MFD can potentially protect against ALF, partially by inhibiting the MKK4-JNK pathway, and is a promising new therapeutic drug for ALF.
Subject(s)
Liver Failure, Acute , MAP Kinase Kinase 4 , Piperazines , Pyridones , Animals , Male , Mice , Cell Line , Galactosamine/toxicity , Lipopolysaccharides/toxicity , Liver Failure, Acute/drug therapy , Liver Failure, Acute/chemically induced , Liver Failure, Acute/metabolism , Liver Failure, Acute/pathology , MAP Kinase Kinase 4/metabolism , MAP Kinase Kinase 4/antagonists & inhibitors , MAP Kinase Signaling System/drug effects , MAP Kinase Signaling System/physiology , Mice, Inbred C57BL , Oxidative Stress/drug effects , Pyridones/pharmacology , Pyridones/therapeutic use , Piperazines/pharmacology , Piperazines/therapeutic useABSTRACT
Long-range ordered phases in most high-entropy and medium-entropy alloys (HEAs/MEAs) exhibit poor ductility, stemming from their brittle nature of complex crystal structure with specific bonding state. Here, we propose a design strategy to severalfold strengthen a single-phase face-centered cubic (fcc) Ni2CoFeV MEA by introducing trigonal κ and cubic L12 intermetallic phases via hierarchical ordering. The tri-phase MEA has an ultrahigh tensile strength exceeding 1.6 GPa and an outstanding ductility of 30% at room temperature, which surpasses the strength-ductility synergy of most reported HEAs/MEAs. The simultaneous activation of unusual dislocation multiple slip and stacking faults (SFs) in the κ phase, along with nano-SF networks, Lomer-Cottrell locks, and high-density dislocations in the coupled L12 and fcc phases, contributes to enhanced strain hardening and excellent ductility. This work offers a promising prototype to design super-strong and ductile structural materials by harnessing the hierarchical ordered phases.
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Aqueous calcium (Ca) decline is threatening freshwater ecosystems worldwide. There are great concerns about the possible ecological consequences of Ca limitation combined with biological pressures like predation. Here we investigated the interactions between Ca restriction and fish predation risk on the phenotypic plasticity in the keystone herbivore Daphnia, together with physiological responses underlying the plastic trait changes. Fish predation risk induced D. pulex to mature earlier and produce more but smaller offspring at adequate Ca. Declining Ca inhibited the expression of defensive traits, with the inhibitive degree showing a linear or threshold-limited dynamic. The presence of predation risk mitigated the negative effect of declining Ca on reducing body size but exacerbated the delay in maturity, indicating a life history trade-off for larger body size rather than the current reproduction in multi-stressed Daphnia. Actin 3-mediated cytoskeleton and AMPK ß-mediated energy metabolism were highly correlated with these plastic trait changes. Altered phenotypic plasticity in planktonic animals is expected to trigger many ecological impacts from individual fitness to community structure, thus providing new insights into the mechanisms underlying decreased Ca affecting lake ecosystems.
Subject(s)
Calcium , Daphnia , Fishes , Predatory Behavior , Animals , Daphnia/physiology , Calcium/metabolism , Water Pollutants, Chemical/toxicity , Ecosystem , Food Chain , Lakes/chemistry , Body Size , Phenotype , Reproduction/drug effects , Daphnia pulexABSTRACT
BACKGROUND: Calcium-dependent protein kinases (CPKs) are crucial for recognizing and transmitting Ca2+ signals in plant cells, playing a vital role in growth, development, and stress response. This study aimed to identify and detect the potential roles of the CPK gene family in the amphidiploid Brassica carinata (BBCC, 2n = 34) using bioinformatics methods. RESULTS: Based on the published genomic information of B. carinata, a total of 123 CPK genes were identified, comprising 70 CPK genes on the B subgenome and 53 on the C subgenome. To further investigate the homologous evolutionary relationship between B. carinata and other plants, the phylogenetic tree was constructed using CPKs in B. carinata and Arabidopsis thaliana. The phylogenetic analysis classified 123 family members into four subfamilies, where gene members within the same subfamily exhibited similar conserved motifs. Each BcaCPK member possesses a core protein kinase domain and four EF-hand domains. Most of the BcaCPK genes contain 5 to 8 introns, and these 123 BcaCPK genes are unevenly distributed across 17 chromosomes. Among these BcaCPK genes, 120 replicated gene pairs were found, whereas only 8 genes were tandem duplication, suggesting that dispersed duplication mainly drove the family amplification. The results of the Ka/Ks analysis indicated that the CPK gene family of B. carinata was primarily underwent purification selection in evolutionary selection. The promoter region of most BcaCPK genes contained various stress-related cis-acting elements. qRT-PCR analysis of 12 selected CPK genes conducted under cadmium and salt stress at various points revealed distinct expression patterns among different family members in response to different stresses. Specifically, the expression levels of BcaCPK2.B01a, BcaCPK16.B02b, and BcaCPK26.B02 were down-regulated under both stresses, whereas the expression levels of other members were significantly up-regulated under at least one stress. CONCLUSION: This study systematically identified the BcaCPK gene family in B. carinata, which contributes to a better understanding the CPK genes in this species. The findings also serve as a reference for analyzing stress responses, particularly in relation to cadmium and salt stress in B. carinata.
Subject(s)
Brassica , Brassica/genetics , Phylogeny , Cadmium/metabolism , Multigene Family , Genomics , Gene Expression Regulation, Plant , Stress, Physiological/genetics , Plant Proteins/genetics , Genome, PlantABSTRACT
Acyl carrier proteins (ACPs) have been reported to play a crucial role in responding to biotic and abiotic stresses, regulating growth and development. However, the biological function of the ACP gene family in the Brassica genus has been limited until now. In this study, we conducted a comprehensive analysis and identified a total of 120 ACP genes across six species in the Brassica genus. Among these, there were 27, 26, and 30 ACP genes in the allotetraploid B. napus, B. juncea, and B. carinata, respectively, and 14, 13, and 10 ACP genes in the diploid B. rapa, B. oleracea, and B. nigra, respectively. These ACP genes were further classified into six subclades, each containing conserved motifs and domains. Interestingly, the majority of ACP genes exhibited high conservation among the six species, suggesting that the genome evolution and polyploidization processes had relatively minor effects on the ACP gene family. The duplication modes of the six Brassica species were diverse, and the expansion of most ACPs in Brassica occurred primarily through dispersed duplication (DSD) events. Furthermore, most of the ACP genes were under purifying selection during the process of evolution. Subcellular localization experiments demonstrated that ACP genes in Brassica species are localized in chloroplasts and mitochondria. Cis-acting element analysis revealed that most of the ACP genes were associated with various abiotic stresses. Additionally, RNA-seq data revealed differential expression levels of BnaACP genes across various tissues in B. napus, with particularly high expression in seeds and buds. qRT-PCR analysis further indicated that BnaACP genes play a significant role in salt stress tolerance. These findings provide a comprehensive understanding of ACP genes in Brassica plants and will facilitate further functional analysis of these genes.
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The serotonin signaling system plays a crucial role in regulating the ontogeny of crustaceans. Here, we describe the effects of different concentrations of the 5-hydroxytryptamine 1A receptor antagonist (WAY-100635) on the induced antipredation (Rhodeus ocellatus as the predator), morphological, behavioral, and life-history defenses of Daphnia magna and use transcriptomics to analyze the underlying molecular mechanisms. Our results indicate that exposure to WAY-100635 leads to changes in the expression of different defensive traits in D. magna when faced with fish predation risks. Specifically, as the length of exposure to WAY-100635 increases, high concentrations of WAY-100635 inhibit defensive responses associated with morphological and reproductive activities but promote the immediate negative phototactic behavioral defense of D. magna. This change is related to the underlying mechanism through which WAY-100635 interferes with gene expression of G-protein-coupled GABA receptors by affecting GABBR1 but promotes serotonin receptor signaling and ecdysteroid signaling pathways. In addition, we also find for the first time that fish kairomone can significantly activate the HIF-1α signaling pathway, which may lead to an increase in the rate of immediate movement. These results can help assess the potential impacts of serotonin-disrupting psychotropic drugs on zooplankton in aquatic ecosystems.
Subject(s)
Daphnia magna , Serotonin 5-HT1 Receptor Agonists , Transcriptome , Animals , Daphnia magna/drug effects , Predatory Behavior , Transcriptome/drug effects , Serotonin 5-HT1 Receptor Agonists/pharmacologyABSTRACT
Liver metastasis (LM) is an important factor leading to colorectal cancer (CRC) mortality. However, the effect of T-cell exhaustion on LM in CRC is unclear. Single-cell sequencing data derived from the Gene Expression Omnibus database. Data were normalized using the Seurat package and subsequently clustered and annotated into different cell clusters. The differentiation trajectories of epithelial cells and T cells were characterized based on pseudo-time analysis. Single-sample gene set enrichment analysis (ssGSEA) was used to calculate enrichment scores for different cell clusters and to identify enriched biological pathways. Finally, cell communication analysis was performed. Nine cell subpopulations were identified from CRC samples with LM. The proportion of T cells increased in LM. T cells can be subdivided into NK/T cells, regulatory T cells (Treg) and exhausted T cells (Tex). In LM, cell adhesion and proliferation activity of Tex were promoted. Epithelial cells can be categorized into six subpopulations. The transformation of primary CRC into LM involved two evolutionary branches of Tex cells. Epithelial cells two were at the beginning of the trajectory in CRC but at the end of the trajectory in CRC with LM. The receptor ligands CEACAM5 and ADGRE5-CD55 played critical roles in the interactions between Tex and Treg cell-epithelial cell, which may promote the epithelial-mesenchymal transition process in CRC. Tex cells are able to promote the process of LM in CRC, which in turn promotes tumour development. This provides a new perspective on the treatment and diagnosis of CRC.