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Breeding rapeseed varieties with more main inflorescence siliques is an idea for developing rapeseed varieties that are suitable for light and simplified cultivation. The Brassica napus exhibited cluster bud of the main inflorescence (Bnclib) gene. At the fruiting stage, the main inflorescence had more siliques, higher density, and more main inflorescences. Moreover, the top of the main inflorescence bifurcated. Genetic analysis showed that the separation ratio between Bnclib and the wild type in the F2 generation was 3:1, which indicated that the trait was a single-gene-dominant inheritance. Among the 24 candidate genes, only one gene, BnaA03g53930D, showed differential expression between the groups (False discovery rate, FDR ≤ 0.05, |log2FC|≤ 1). qPCR verification of the BnaA03g53930D gene between Huyou 17 and its Bnclib near-isogenic line showed that BnaA03g53930D was significantly differentially expressed in the stem tissue of Huyou 17 and its Bnclib near-isogenic line (Bnclib NIL). The determination of gibberellin (GA), brassinolide (BR), cytokinin (CTK), jasmonic acid (JA), growth hormone (IAA), and strigolactone (SL) content in the shoot apex of Huyou 17 by Bnclib NIL and wild type showed that all six hormones significantly differed between the Bnclib NIL and Huyou 17. It is necessary to conduct further research on the interactions between JA and the other five hormones and the main inflorescence bud clustering in B. napus. [ABSTRACT FROM AUTHOR]

The high-resolution feature of single-cell transcriptome sequencing technology allows researchers to observe cellular gene expression profiles at the single-cell level, offering numerous possibilities for subsequent biomedical investigation. However, the unavoidable technical impact of high missing values in the gene-cell expression matrices generated by insufficient RNA input severely hampers the accuracy of downstream analysis. To address this problem, it is essential to develop a more rapid and stable imputation method with greater accuracy, which should not only be able to recover the missing data, but also effectively facilitate the following biological mechanism analysis. The existing imputation methods all have their drawbacks and limitations, some require pre-assumed data distribution, some cannot distinguish between technical and biological zeros, and some have poor computational performance. In this paper, we presented a novel imputation software FRMC for single-cell RNA-Seq data, which innovates a fast and accurate singular value thresholding approximation method. The experiments demonstrated that FRMC can not only precisely distinguish 'true zeros' from dropout events and correctly impute missing values attributed to technical noises, but also effectively enhance intracellular and intergenic connections and achieve accurate clustering of cells in biological applications. In summary, FRMC can be a powerful tool for analysing single-cell data because it ensures biological significance, accuracy, and rapidity simultaneously. FRMC is implemented in Python and is freely accessible to non-commercial users on GitHub: . [ABSTRACT FROM AUTHOR]

Breast cancer (BRCA) is the most common cancer among women. Adriamycin (ADR), also known as doxorubicin (Dox), is a commonly used chemotherapeutic agent for BRCA patients, however, the susceptibility of tumor cells to develop resistance to Dox has severely limited its clinical use. One new promising therapeutic target for breast cancer patients is exosomes. The objective of this study was to investigate the role of exosomes in regulating Dox resistance in BRCA. In this study, the exosomes from both types of cells were extracted by differential centrifugation. The effect of exosomes on drug resistance was assessed by laser confocal microscopy, MTT assay, and qRT-PCR. The miRNA was transfected into cells using Lipofectamine 2000, which was then evaluated for downstream genes and changes in drug resistance. Exosomes from MCF-7 cells (MCF-7/exo) and MCF-7/ADR cells (ADR/exo) were effectively extracted in this study. The ADR/exo was able to endocytose MCF-7 cells and make them considerably more resistant to Dox. Moreover, we observed a significant difference in miR-34a-5p expression in MCF-7/ADR and ADR/exo compared to MCF-7 and MCF-7/exo. Among the miR-34a-5p target genes, NOTCH1 displayed a clear change with a negative correlation. In addition, when miR-34a-5p expression was elevated in MCF-7/ADR cells, the expression of miR-34a-5p in ADR/exo was also enhanced alongside NOTCH1, implying that exosomes may carry miRNA into and out of cells and perform their function. In conclusion, exosomes can influence Dox resistance in breast cancer cells by regulating miR-34a-5p/NOTCH1. These findings provide novel insights for research into the causes of tumor resistance and the enhancement of chemotherapy efficacy in breast cancer. • This study indicated that ADR/exo can enter MCF-7 cells and regulate resistance. • Exosomes regulate miR-34-5p/NOTCH1 to reduce Dox resistance in breast cancer cells. • This study provides new ideas for therapeutic application of Dox-based chemotherapy. [ABSTRACT FROM AUTHOR]

The high-resolution feature of single-cell transcriptome sequencing technology allows researchers to observe cellular gene expression profiles at the single-cell level, offering numerous possibilities for subsequent biomedical investigation. However, the unavoidable technical impact of high missing values in the gene-cell expression matrices generated by insufficient RNA input severely hampers the accuracy of downstream analysis. To address this problem, it is essential to develop a more rapid and stable imputation method with greater accuracy, which should not only be able to recover the missing data, but also effectively facilitate the following biological mechanism analysis. The existing imputation methods all have their drawbacks and limitations, some require pre-assumed data distribution, some cannot distinguish between technical and biological zeros, and some have poor computational performance. In this paper, we presented a novel imputation software FRMC for single-cell RNA-Seq data, which innovates a fast and accurate singular value thresholding approximation method. The experiments demonstrated that FRMC can not only precisely distinguish 'true zeros' from dropout events and correctly impute missing values attributed to technical noises, but also effectively enhance intracellular and intergenic connections and achieve accurate clustering of cells in biological applications. In summary, FRMC can be a powerful tool for analysing single-cell data because it ensures biological significance, accuracy, and rapidity simultaneously. FRMC is implemented in Python and is freely accessible to non-commercial users on GitHub: . [ABSTRACT FROM AUTHOR]

Background/Aims: HOX transcript antisense RNA (HOTAIR) plays a vital role in carcinogenesis. However, its functional and regulatory roles remain unclear. In this study, we aimed to investigate its biological function and clinical significance in human colorectal cancer (CRC). Methods: We examined the expression levels of lncRNA HOTAIR and miR-203a-3p in CRC tissues and CRC cell lines by qRT-PCR. Gain and loss-of-function assays were performed to examine the effects of HOTAIR and miR-203a-3p on the proliferation and chemoresistance of CRC cells. The possible mechanisms of HOTAIR were also explored by fluorescence reporter assay and Western blot. Results: The expressions of HOTAIR were upregulated in CRC tissue tissues compared to adjacent control tissues. We also found HOTAIR was downregulated by miR-203a-3p in CRC cell lines. Both HOTAIR knockdown and miR-203a-3p overexpression in CRC cell lines led to inhibited cell proliferation and reduced chemoresistance. We also determined that β-catenin and GRG5 were inhibitory targets of miR-203a-3p, and that Wnt/β-catenin signaling was inhibited by both HOTAIR knockdown and miR-203a-3p overexpression. Significantly, we found that increased expression of miR-203a-3p is essential for cell proliferation repression, chemoresistance reduction, and Wnt/β-catenin signaling inhibition induced by HOTAIR knockdown. Conclusions: Our study demonstrated that the lncRNA HOTAIR could regulate the progression and chemoresistance of CRC via modulating the expression levels of miR-203a-3p and the activity of Wnt/β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

Toxin-antitoxin (TA) systems are widespread in both bacteria and archaea, where they enable cells to adapt to environmental cues. TA systems play crucial roles in various cellular processes, such as programmed cell death, cell growth, persistence and virulence. Here, two distinct forms of the type II toxin-antitoxin complex HicAB were identified and characterized in Escherichia coli K-12, and both were successfully overexpressed and purified. The two proposed forms, HicABL and HicABS, differed in the presence or absence of a seven-amino-acid segment at the N-terminus in the antitoxin HicB. The short form HicABS readily crystallized under the conditions 0.1 M Tris-HCl pH 8.0, 20%( w/ v) PEG 6000, 0.2 M ammonium sulfate. The HicABS crystal diffracted and data were collected to 2.5 Å resolution. The crystal belonged to space group I222 or I212121, with unit-cell parameters a = 67.04, b = 66.31, c = 120.78 Å. Matthews coefficient calculation suggested the presence of two molecules each of HicA and HicBS in the asymmetric unit, with a solvent content of 55.28% and a Matthews coefficient ( VM) of 2.75 Å3 Da−1. [ABSTRACT FROM AUTHOR]

Correction to: I Nature Communications i https://doi.org/10.1038/s41467-020-19922-3, published online 27 November 2020 In this article the author name Ke-Ren Zhou was incorrectly written as Ke-Reng Zhou. These authors contributed equally: Yu-Chan Zhang, Meng-Qi Lei. [Extracted from the article]

The aim of this study was to investigate the relationship between cell cycle reentry and apoptosis in cultured cortical neurons following oxygen-glucose deprivation (OGD). We found that the percentage of neurons with BrdU uptake, TUNEL staining, and colocalized BrdU uptake and TUNEL staining was increased relative to control 6, 12 and 24 h after 1 h of OGD. The number of neurons with colocalized BrdU and TUNEL staining was decreased relative to the number of TUNEL-positive neurons at 24 h. The expression of phosphorylated retinoblastoma protein (phospho-Rb) was significantly increased 6, 12 and 24 h after OGD, parallel with the changes in BrdU uptake. Phospho-Rb and TUNEL staining were colocalized in neurons 6 and 12 h after OGD. This colocalization was strikingly decreased 24 h after OGD. Treatment with the cyclin-dependent kinase inhibitor roscovitine (100 μM) decreased the expression of phospho-Rb and reduced neuronal apoptosis in vitro. These results demonstrated that attempted cell cycle reentry with phosphorylation of Rb induce early apoptosis in neurons after OGD and there must be other mechanisms involved in the later stages of neuronal apoptosis besides cell cycle reentry. Phosphoralated Rb may be an important factor which closely associates aberrant cell cycle reentry with the early stages of neuronal apoptosis following ischemia/hypoxia in vitro, and pharmacological interventions for neuroprotection may be useful directed at this keypoint. [ABSTRACT FROM AUTHOR]

Abstract: Background: Primary osteoarthritis (OA) is a polygenic disease. To investigate the gene expression profile of cartilage and synovium from osteoarthritis and healthy rats using cDNA microarray is beneficial to recognize the pathogenesis of osteoarthritis and provide evidence for gene therapy of osteoarthritis. Objective: The present study aimed to investigate the gene expression profile of the cartilage and synovium of chronic arthritis and healthy rats through cDNA microarray assay, and identify the differentially expressed genes. This study may be helpful for understanding the role of differentially expressed genes in osteoarthritis and the gene polymorphism of osteoarthritis. Methods: A total of 24 male Wistar rats were randomly divided into control group and osteoarthritis group (n == 12 per group). The synovial and cartilage were obtained and total RNA was extracted. cDNA microarray assay was performed to identify the differentially expressed genes, and cluster analysis was conducted. Results and Conclusion: A total of 82 differentially expressed genes were identified, among which 27 were up-regulated and 55 down-regulated. Gene microarray assay is effective to identify differentially expressed genes and may find out novel osteoarthritis associated genes. Multiple genes are involved in the pathogenesis of osteoarthritis. The differentially expressed genes provide important information for further studies on the pathogenesis of osteoarthritis and gene therapy of osteoarthritis. [ABSTRACT FROM AUTHOR]

• We identified 110 DEGs in PBMCs from cardioembolic patients and healthy controls. • Integrated bioinformatics analyses identified CTNNB1 and MDM2 as central hub genes. • Ischemic neuron-exposed neutrophils show Mdm2/p53-mediated β-catenin degradation. • Neutrophils upregulate pro-survival Ctnnb1 to compensate for this degradation. A better understanding of the mechanism(s) underlying cardioembolic stroke can promote recovery and reduce the risk of recurrent embolisms. Peripheral blood mononuclear cell (PBMC) gene expression datasets from cardioembolic patients and healthy controls were obtained from the Gene Expression Omnibus (GEO) database (GSE58294). The Limma software package was utilized to identify differentially-expressed genes (DEGs). Protein-protein interaction (PPI) analysis of the DEGs was performed using STRING. A weighted gene co-expression network analysis (WGCNA) was used to build a gene co-expression network. In vitro experiments assessed the effects on neutrophils exposed to oxygen and glucose-deprived (OGD) cortical neurons. An in vivo murine model of thromboembolic stroke was constructed through thrombin injection to examine effects on circulating neutrophils. Mechanistic in vitro studies were conducted using the proteasome inhibitor MG132, the p53-Mdm2 binding inhibitor Nutlin-3a, Mdm2 small-interfering RNA (siRNA), and Ctnnb1 siRNA. DEG analysis identified 44 upregulated and 66 downregulated genes in cardioembolic stroke PBMCs. PPI analysis of these DEGs yielded one eight-node protein module with β-catenin (CTNNB1) as the central hub protein. Integration of the DEGs with WGCNA-derived hub genes revealed the key hub DEGs CTNNB1 and mouse double minute 2 (MDM2). Follow-up experiments revealed Mdm2, p53, and phospho-β-catenin upregulation in neutrophils exposed to OGD neurons in vitro and following thromboembolic stroke in vivo. Mechanistic studies revealed that neutrophils transcriptionally upregulate Ctnnb1 expression to compensate for Mdm2/p53-mediated β-catenin degradation induced by exposure to OGD neurons, thereby promoting neutrophil survival. Compensatory Ctnnb1 transcriptional upregulation in neutrophils induced by ischemic neuron exposure may be involved in promoting neutrophil survival following cardioembolic stroke. [ABSTRACT FROM AUTHOR]

Plant spermatogenesis is a complex process that directly affects crop breeding. A rapid change in gene abundance occurs at early meiosis prophase, when gene regulation is selective. However, how these genes are regulated remains unknown. Here, we show that rice reproductive phasiRNAs are essential for the elimination of a specific set of RNAs during meiotic prophase I. These phasiRNAs cleave target mRNAs in a regulatory manner such that one phasiRNA can target more than one gene, and/or a single gene can be targeted by more than one phasiRNA to efficiently silence target genes. Our investigation of phasiRNA-knockdown and PHAS-edited transgenic plants demonstrates that phasiRNAs and their nucleotide variations are required for meiosis progression and fertility. This study highlights the importance of reproductive phasiRNAs for the reprogramming of gene expression during meiotic progression and establishes a basis for future studies on the roles of phasiRNAs with a goal of crop improvement. 21-nucleotide phased secondary siRNAs are expressed in the developing rice anthers during meiosis. Here, the authors show that phasiRNAs can cleave target mRNA and act to ensure the progression of meiosis and fertility in rice. [ABSTRACT FROM AUTHOR]

Background: A better understanding of the molecular mechanism involving lncRNA-miRNA-mRNA network underlying glioma genesis is beneficial to the treatment of glioma. This study was designed to investigate the role of lncRNA NEAT1, miR-132 and SOX2 interaction in glioma. Methods: Microarray analysis was conducted to identify the differentially expressed lncRNAs in glioma tissues. The expression levels of NEAT1, miR-132 and SOX2 were determined by qRT-PCR and western blot. Proliferation of glioma cells was detected by MTT assay, while migration and invasion were determined by transwell assay. The target relationships were predicted by miRcode algorithm, and confirmed by dual luciferase reporter gene assay. Results: NEAT1 was up-regulated in glioma. Knockdown of NEAT1 inhibited glioma cells' viability, migration and invasion. MiR-132 was down-regulated while SOX2 was up-regulated in glioma cells. NEAT1 negatively regulated the expression of miR-132 in glioma while miR-132 targeted SOX2 to down-regulate its expression. Conclusion: NEAT1 promoted glioma development by promoting SOX2 expression through suppressing miR-132. [ABSTRACT FROM AUTHOR]

Abstract In this study, a cDNA of ICE1 (inducer of CBF expression 1) gene, named BcICE1 , was isolated from Brassica campestris 'Longyou 6'. The deduced protein has 499 amino acids containing a typical bHLH domain and is highly identical with AtICE1 (85.9%) from Arabidopsis thaliana. BcICE1 is located in the nucleus. The activities of SOD, CAT, POD, and APX and the transcriptional levels of SOD , CAT , and POD genes were higher in BcICE1-transgenic tobacco than in wild-type (WT) tobacco under cold stress. Compared with WT tobacco, proline, soluble sugar, and chlorophyll were enhanced, whereas malondialdehyde and relative conductivity were decreased in BcICE1-transgenic tobacco. The overexpression of BcICE1 in tobacco increased the expression of CBF1 , CBF2 , and other stress-related genes. Moreover, under salt and PEG (25%) stress, the activities of APX and GPX and content of soluble sugar and chlorophyll in BcICE1-transgenic tobacco were higher than those in WT tobacco. Our results suggest that BcICE1 plays an important role in the response to abiotic stress. Highlights • We identified cDNA of the BcICE1 gene from Brassica campestris. • BcICE1 is localized in the nucleus. • Overexpression of BcICE1 increases antioxidant enzyme activity in tobacco. • Overexpression of BcICE1 improves abiotic stress resistance of transgenic tobacco. • Overexpression of BcICE1 alters the expression of antioxidant enzyme genes and stress response genes in tobacco. [ABSTRACT FROM AUTHOR]

Sijunzi Decoction (SJZD), a traditional Chinese herbal remedy, is frequently employed in the treatment of various cancers, including colon cancer. Previous research suggests that SJZD plays a pivotal role in modulating the immune system and enhancing immunity against tumors. However, the precise role of SJZD in combating colon cancer and its potential molecular functions in regulating natural killer cells remain elusive. To elucidate the potential mechanism underlying the anticolon cancer effects of SJZD in synergy with natural killer (NK) cells through both in vivo and in vitro experiments. In vivo experiments: A subcutaneous tumor mouse model of colon cancer and in vivo NK cell depletion experiments were conducted to observe the anticolon cancer effects of SJZD. Flow cytometry assessed immune cell depletion in mouse spleens, while immunohistochemical (IHC) staining detected the expression of apoptotic genes in tumor tissues. In vitro experiments: The mechanism by which SJZD regulates the sensitization of colon cancer cells to NK cells was investigated using real-time polymerase chain reaction (RT-PCR), western blotting (WB), and co-culture experiments with NK cells. Sijunzi Decoction (SJZD) significantly impeded tumor growth in mice; however, NK cell depletion markedly attenuated the tumor-suppressive effect of SJZD. Immunohistochemical (IHC) results indicated that SJZD increased the expression of P53, death receptor 4 (DR4), and death receptor 5 (DR5) in tumor tissues. In vitro experiments, 24 h SJZD-pretreated colon cancer cells showed a substantial elevation in P53, DR4, and DR5 levels, and the activity of colon cancer cells significantly diminished after co-culture with NK cells. These effects of SJZD were reversed with the addition of the P53 inhibitor pifithrin-α (PFT-α), resulting in reduced inhibition of colon cancer cells by NK cells. SJZD enhances the levels of DR4 and DR5 through the modulation of P53 expression, consequently increasing the sensitivity of colon cancer cells to NK cell-mediated killing. These findings provide a theoretical foundation for the clinical application of SJZD in patients with colon cancer. In this study, we first investigated the effect of SJZD on subcutaneous tumor growth in mice with colon cancer using in vivo assays and assessed the impact of NK cells on the anticolon cancer effect of SJZD in vivo through NK cell depletion. In vitro experiments were conducted to explore the potential mechanism of action of SJZD in NK cell-mediated anticolon cancer effects. Sijunzi Decoction (SJZD) augmented the anti-colon cancer efficacy of NK cells in a syngeneic mouse subcutaneous tumor model. The interaction of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) on the surface of NK cells with TRAILR1/TRAILR2 on the surface of colon cancer cells initiated an exogenous apoptotic pathway, leading to apoptosis in colon cancer cells. Notably, SJZD heightened the expression of TRAILR1/TRAILR2 by modulating the expression of P53, thereby amplifying the sensitivity of colon cancer cells to NK cell-mediated killing. [Display omitted] • Colon cancer is one of the leading causes of cancer-related deaths. • Anti-Tumor immunotherapy is a hot topic of current research. • Tumor microenvironment inhibits anti-tumor activity of NK cells. • Traditional Chinese medicine has multiple anti-tumor advantages. • P53 regulates the expression of death receptors DR4, DR5. [ABSTRACT FROM AUTHOR]