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According to the World Health Organization in 2022, 2.3 million women were diagnosed with breast cancer. Investigating the interaction networks between Bcl‐2‐associated athanogene (Bag)‐1 and other chaperone proteins may further the current understanding of the regulation of protein homeostasis in breast cancer cells and contribute to the development of treatment options. The present study aimed to determine the interactions between Bag‐1 and heat shock proteins (HSPs); namely, HSP90, HSP70 and HSP27, to elucidate their role in promoting heat shock factor‐1 (HSF1)‐dependent survival of breast cancer cells. HER2‐negative (MCF‐7) and HER2‐positive (BT‐474) cell lines were used to examine the impact of Bag‐1 expression on HSF1 and HSPs. We demonstrated that Bag‐1 overexpression promoted HER2 expression in breast cancer cells, thereby resulting in the concurrent constitutive activation of the HSF1–HSP axis. The activation of HSP results in the stabilization of several tumor‐promoting HSP clients such as AKT, mTOR and HSF1 itself, which substantially accelerates tumor development. Our results suggest that Bag‐1 can modulate the chaperone activity of HSPs, such as HSP27, by directly or indirectly regulating the phosphorylation of HSF1. This modulation of chaperone activity can influence the activation of genes involved in cellular homeostasis, thereby protecting cells against stress. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) poses significant therapeutic challenges, particularly OA that affects the hand. Currently available treatment strategies are often limited in terms of their efficacy in managing pain, regulating invasiveness, and restoring joint function. The APRICOTⓇ implant system developed by Aurora Medical Ltd (Chichester, UK) introduces a minimally invasive, bone-conserving approach for treating hand OA (https://apricot-project.eu/). By utilizing polycarbonate urethane (PCU), this implant incorporates a caterpillar track-inspired design to promote the restoration of natural movement to the joint. Surface modifications of PCU have been proposed for the biological fixation of the implant. This study investigated the biocompatibility of PCU alone or in combination with two surface modifications, namely dopamine-carboxymethylcellulose (dCMC) and calcium-phosphate (CaP) coatings. In a rat soft tissue model, native and CaP-coated PCU foils did not increase cellular migration or cytotoxicity at the implant–soft tissue interface after 3 d, showing gene expression of proinflammatory cytokines similar to that in non-implanted sham sites. However, dCMC induced an amplified initial inflammatory response that was characterized by increased chemotaxis and cytotoxicity, as well as pronounced gene activation of proinflammatory macrophages and neoangiogenesis. By 21 d, inflammation subsided in all the groups, allowing for implant encapsulation. In a rat bone model, 6 d and 28 d after release of the periosteum, all implant types were adapted to the bone surface with a surrounding fibrous capsule and no protracted inflammatory response was observed. These findings demonstrated the biocompatibility of native and CaP-coated PCU foils as components of APRICOTⓇ implants. Hand osteoarthritis treatments require materials that minimize irritation of the delicate finger joints. Differing from existing treatments, the APRICOTⓇ implant leverages polycarbonate urethane (PCU) for minimally invasive joint replacement. This interdisciplinary, preclinical study investigated the biocompatibility of thin polycarbonate urethane (PCU) foils and their surface modifications with calcium-phosphate (CaP) or dopamine-carboxymethylcellulose (dCMC). Cellular and morphological analyses revealed that both native and Ca-P coated PCU elicit transient inflammation, similar to sham sites, and a thin fibrous encapsulation in soft tissues and on bone surfaces. However, dCMC surface modification amplified initial chemotaxis and cytotoxicity, with pronounced activation of proinflammatory and neoangiogenesis genes. Therefore, native and CaP-coated PCU possess sought-for biocompatible properties, crucial for patient safety and performance of APRICOTⓇ implant. [Display omitted] [ABSTRACT FROM AUTHOR]

Aspergillus oryzae , also known as the yellow koji mold, produces various hydrolytic enzymes that are widely used in different industries. Its high capacity to produce secretory proteins makes this filamentous fungus a suitable host for heterologous protein production. Amylolytic gene promoter is widely used to express heterologous genes in A. oryzae. The expression of this promoter is strictly regulated by several transcription factors, whose activation involves various factors. Furthermore, the expression levels of amylolytic and heterologous genes are post-transcriptionally regulated by mRNA degradation mechanisms in response to aberrant transcriptional termination or endoplasmic reticulum stress. This review discusses the transcriptional and post-transcriptional regulatory mechanisms controlling the expression of genes encoding secretory proteins in A. oryzae. [ABSTRACT FROM AUTHOR]

Macrophage senescence, manifested by the special form of durable cell cycle arrest and chronic low-grade inflammation like senescence-associated secretory phenotype, has long been considered harmful. Persistent senescence of macrophages may lead to maladaptation, immune dysfunction, and finally the development of age-related diseases, infections, autoimmune diseases, and malignancies. However, it is a ubiquitous, multi-factorial, and dynamic complex phenomenon that also plays roles in remodeled processes, including wound repair and embryogenesis. In this review, we summarize some general molecular changes and several specific biomarkers during macrophage senescence, which may bring new sight to recognize senescent macrophages in different conditions. Also, we take an in-depth look at the functional changes in senescent macrophages, including metabolism, autophagy, polarization, phagocytosis, antigen presentation, and infiltration or recruitment. Furthermore, some degenerations and diseases associated with senescent macrophages as well as the mechanisms or relevant genetic regulations of senescent macrophages are integrated, not only emphasizing the possibility of regulating macrophage senescence to benefit age-associated diseases but also has an implication on the finding of potential targets or drugs clinically. Senescent macrophages are characterized by specific molecular and functional changes, leading to tissue degenerations and diseases. Targeting macrophage senescence is expected to be a novel strategy for disease intervention. [Display omitted] [ABSTRACT FROM AUTHOR]

FNDC3B (fibronectin type III domain containing 3B) is highly expressed in hepatocellular carcinoma (HCC) and other cancer types, and fusion genes involving FNDC3B have been identified in HCC and leukemia. Growing evidence suggests the significance of FNDC3B in tumorigenesis, particularly in cell migration and tumor metastasis. However, its regulatory mechanisms remain elusive. In this study, we employed bioinformatic, gene regulation, and protein‐DNA interaction screening to investigate the transcription factors (TFs) involved in regulating FNDC3B. Initially, 338 candidate TFs were selected based on previous chromatin immunoprecipitation (ChIP)‐seq experiments available in public domain databases. Through TF knockdown screening and ChIP coupled with Droplet Digital PCR assays, we identified that E2F1 (E2F transcription factor 1) is crucial for the activation of FNDC3B. Overexpression or knockdown of E2F1 significantly impacts the expression of FNDC3B. In conclusion, our study elucidated the mechanistic link between FNDC3B and E2F1. These findings contribute to a better understanding of FNDC3B in tumorigenesis and provide insights into potential therapeutic targets for cancer treatment. [ABSTRACT FROM AUTHOR]

The study aimed to observe molecular signaling, including reactive oxygen species (ROS) and mitochondrial membrane potential (ΔΨm), to evaluate the alteration of gene expression by low-level laser therapy (LLLT) and the correlation between its mechanisms and the NF-kB pathway in cells involved in orthodontic tooth movement. Osteoblast-like cells (MG63), immortalized periodontal ligament cells (iPDL), and M1 macrophage-like cells were irradiated by 980-nm LLLT with energy densities of 1 and 10 J/cm2 ΔΨm and intracellular ROS were monitored using fluorescent probes. The changes of mRNA expression were assessed using reverse transcription polymerase chain reaction (RT-PCR). NF-kB inhibitor, ROS scavenger, and ΔΨm suppressor were used to analyze signals associated with the regulation of gene expression. Finally, Western blot analysis was performed to confirm NF-kB signaling after LLLT. We found the increases of ΔΨm and ROS in all three cell types after LLLT, but no significant difference was observed between 1 and 10 J/cm2 LLLT. Regarding gene expression, some target genes were upregulated in MG63 6 h, 12 h, and 1 day after LLLT and in iPDL cells 12 h and 1 day after LLLT. However, no changes occurred in M1 cells. The inhibitor that significantly reduced most changes in gene expression was NF-kB inhibitor. Western blot analysis showed the increase in p-IkBα level after LLLT in iPDL and MG63, but not in M1. The 980-nm LLLT increased ΔΨm and ROS production in all three cell types. However, changes in gene regulation were found only in MG63 and iPDL cells, which related to the NF-kB pathway. [ABSTRACT FROM AUTHOR]

Copyright of Cukurova Medical Journal / Çukurova Üniversitesi Tip Fakültesi Dergisi is the property of Cukurova University, Faculty of Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The cellobiose-responsive regulator ClbR, a Zn(II)2Cys6 binuclear-cluster transcription factor, is a positive regulator of carbohydrate-active enzyme (CAZyme) genes responsive to cellulose in Aspergillus aculeatus. Because Zn(II)2Cys6 transcription factors tend to dimerize with proteins of the same family, we searched for a counterpart of ClbR and identified ClbR2, which is 42% identical to ClbR, as an interacting partner of ClbR by yeast two-hybrid screening. Genetic analyses suggested that ClbR and ClbR2 cooperatively regulate the expression of CAZyme genes in response to cellulose and 1,4-β-mannobiose in A. aculeatus. CAZyme genes under the control of the transcription factor ManR were regulated by ClbR and ClbR2, whereas those controlled by the transcription factor XlnR were regulated by ClbR, but not ClbR2. These findings suggest that ClbR participates in multiple regulatory pathways in A. aculeatus by altering an interacting factor. [ABSTRACT FROM AUTHOR]

Clustered regularly interspaced short palindromic repeat activation (CRISPRa) technology has emerged as a precise genome editing tool for activating endogenous transgene expression. While it holds promise for precise cell modification, its translation into tissue engineering has been hampered by biosafety concerns and suboptimal delivery methods. To address these challenges, we have developed a CRISPRa non-viral gene delivery platform by immobilizing non-viral CRISPRa complexes into a biocompatible hydrogel/nanofiber (Gel/NF) composite scaffold. The Gel/NF scaffold facilitates the controlled and sustained release of CRISPRa complexes and also promotes cell recruitment to the scaffold for efficient and localized transfection. As a proof of concept, we employed this CRISPRa delivery platform to activate the vascular endothelial growth factor (VEGF) gene in a rat model with full-thickness skin defects. Our results demonstrate sustained upregulation of VEGF expression even at 21 days post-implantation, resulting in enhanced angiogenesis and improved skin regeneration. These findings underscore the potential of the Gel/NF scaffold-based CRISPRa delivery platform as an efficient and durable strategy for gene activation, offering promising prospects for tissue regeneration. Translation of clustered regularly interspaced short palindromic repeat activation (CRISPRa) therapy to tissue engineering is limited by biosafety concerns and unsatisfactory delivery strategy. To solve this issue, we have developed a CRISPRa non-viral gene delivery platform by immobilizing non-viral CRISPRa complexes into a biocompatible hydrogel/nanofiber (Gel/NF) composite scaffold. This scaffold enables controlled and sustained release of CRISPRa and can induce cell recruitment for localized transfection. As a proof of concept, we activated vascular endothelial growth factor (VEGF) in a rat model with full-thickness skin defects, leading to sustained upregulation of VEGF expression, enhanced angiogenesis and improved skin regeneration in vivo. These findings demonstrate the potential of this platform for gene activation, thereby offering promising prospects for tissue regeneration. [Display omitted] [ABSTRACT FROM AUTHOR]

This article, published in the Austral Journal of Veterinary Sciences, discusses a study on the effects of selenium on gene expression in in vitro follicles of ewes. The study found that selenium activated gene expression in the follicles, particularly genes related to the immune system. The researchers identified numerous differentially expressed genes, some of which were involved in apoptosis regulation. The study suggests that selenium treatment affects the transcriptome and has implications for immune processes in ovarian follicles. Additionally, a list of references to related scientific articles is provided, covering topics such as biological trace elements, CD4(+) T cells, ovarian granulosa cell death, selenium, and immune responses. [Extracted from the article]

We report the complete organellar genome sequences of an ultrasmall green alga, Medakamo hakoo strain M-hakoo 311, which has the smallest known nuclear genome in freshwater green algae. Medakamo hakoo has 90.8-kb chloroplast and 36.5-kb mitochondrial genomes containing 80 and 33 putative protein-coding genes, respectively. The mitochondrial genome is the smallest in the Trebouxiophyceae algae studied so far. The GC content of the nuclear genome is 73%, but those of chloroplast and mitochondrial genomes are 41% and 35%, respectively. Codon usages in the organellar genomes have a different tendency from that in the nuclear genome. The organellar genomes have unique characteristics, such as the biased encoding of mitochondrial genes on a single strand and the absence of operon structures in chloroplast ribosomal genes. Medakamo hakoo will be helpful for understanding the evolution of the organellar genome and the regulation of gene expression in chloroplasts and mitochondria. [ABSTRACT FROM AUTHOR]

Background Microsatellites or simple sequence repeats (SSR) consist of 1-6 nucleotide motifs of DNA or RNA which are ubiquitously present in tandem repeated sequences across genome in viruses: prokaryotes and eukaryotes. They may be localized to both the coding and non-coding regions. SSRs play an important role in replication, gene regulation, transcription, and protein function. The Caliciviridae (CLV) family of viruses have ss-RNA, non-enveloped, icosahedral symmetry 27-35 nm in diameter in size. The size of the genome lies between 6.4 and 8.6 kb. Results The incidence, composition, diversity, complexity, and host range of different microsatellites in 62 representatives of the family of Caliciviridae were systematically analyzed. The full-length genome sequences were assessed from NCBI (https://www.ncbi.nlm.nih.gov), and microsatellites were extracted through MISA software. The average genome size is about 7538 bp ranging from 6273 (CLV61) to 8798 (CLV47) bp. The average GC content of the genomes was ~ 51%. There are a total of 1317 SSRs and 53 cSSRs in the studied genomes. CLV 41 and CLV 49 contain the highest and lowest value of SSRs with 32 and 10 respectively, while CLV16 had maximum cSSR incidence of 4. There were 29 species which do not contain any cSSR. The incidence of mono-, di-, and tri-nucleotide SSRs was 219, 884, and 206, respectively. The most prevalent mono-, di-, and tri-nucleotide repeat motifs were "C" (126 SSRs), AC/CA (240 SSRs), and TGA/ACT (23 SSRs), respectively. Most of the SSRs and cSSRs are biased toward the coding region with a minimum of ~ 90% incident SSRs in the genomes' coding region. Viruses with similar host are found close to each other on the phylogenetic tree suggesting virus host being one of the driving forces for their evolution. Conclusions The Caliciviridae genomes does not conform to any pattern of SSR signature in terms of incidence, composition, and localization. This unique property of SSR plays an important role in viral evolution. Clustering of similar host in the phylogenetic tree is the evidence of the uniqueness of SSR signature. [ABSTRACT FROM AUTHOR]

As a prevalent neurodevelopmental disease, attention-deficit hyperactivity disorder (ADHD) impairs the learning and memory capacity, and so far, there has been no available treatment option for long-term efficacy. Alterations in gene regulation and synapse-related proteins influence learning and memory capacity; nevertheless, the regulatory mechanism of synapserelated protein synthesis is still unclear in ADHD. LncRNAs have been found participating in regulating genes in multiple disorders. For instance, lncRNA Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) has an essential regulatory function in numerous psychiatric diseases. However, how MALAT1 influences synapse-related protein synthesis in ADHD remains largely unknown. Here, our study found that MALAT1 decreased in the hippocampus tissue of spontaneously hypertensive rats (SHRs) compared to the standard controls, Wistar Kyoto (WKY) rats. Subsequent experiments revealed that MALAT1 enhanced the expression of neurexin 1 (NRXN1), which promoted the synapse-related genes (SYN1, PSD95, and GAP43) expression. Then, the bioinformatic analyses predicted that miR141-3p and miR-200a-3p, microRNAs belonging to miR-200 family and sharing same seed sequence, could interact with MALAT1 and NRXN1 mRNA, which were further confirmed by luciferase report assays. Finally, rescue experiments indicated that MALAT1 influenced the expression of NRXN1 by sponging miR-141-3p/200a-3p. All data verified our hypothesis that MALAT1 regulated synapse-related proteins (SYN1, PSD95, and GAP43) through the MALAT1-miR-141-3p/200a-3p-NRXN1 axis in ADHD. Our research underscored a novel role of MALAT1 in the pathogenesis of impaired learning and memory capacity in ADHD and may shed more light on developing diagnostic biomarkers and more effective therapeutic interventions for individuals with ADHD. [ABSTRACT FROM AUTHOR]

DNAzyme-based gene regulation shows great potential for the therapy of many cancers. However, ineffective delivery and insufficient cofactor supply pose challenges for potent gene therapy. In this study, we constructed a smart metal-polyphenol-DNAzyme nanoplatform (TA-Mn@Dz NPs) with intrinsic stability, effective delivery, and cofactor self-supply ability for gene-chemodynamic synergistic tumor therapy. Tannic acid, a plant-derived polyphenol, acts as an intermediate structural unit to mediate the assembly of Mn2+/DNAzyme and tumor acid environment-responsive nanocarriers. Intracellularly, the acidic environment triggers the decomposition of TA-Mn@Dz NPs to release DNAzyme and Mn2+. The Mn2+ ion not only boosts the catalytic cleavage of surviving mRNA for effective gene therapy but also activates chemodynamic therapy (CDT), generating highly toxic ·OH from endogenous H 2 O 2. When tail intravenously injected into MCF-7 tumor-bearing mice, the TA-Mn@Dz NPs display desirable synergistic gene-chemodynamic antitumor effects, paving the way for developing DNAzyme-based multifunctional theranostic platforms for biomedical applications. 1. A smart metal-polyphenol-DNAzyme nanoplatform was constructed for gene-chemodynamic synergistic tumor therapy. 2. Tannic acid act as intermediate structural units to mediate the assembly of Mn2+/DNAzyme and tumor acid environment-responsive nanocarriers. 3. The Mn2+-ion could not only boost the catalytic cleavage of surviving mRNA for effective gene therapy, but also catalyze endogenous H 2 O 2 to form cytotoxic hydroxyl radicals for chemodynamic therapy. 4. Our work paves an extremely simple way to integrate gene therapy with CDT for the dual-catalytic tumor treatment. [Display omitted] [ABSTRACT FROM AUTHOR]

Most somatic cells are diploid with 2 sets of chromosomes. These cells divide at regular intervals. At the time of division, called 'mitosis', each chromosome carries two chromatids. As they divide, the daughter cells get one chromatid from each chromosome. Thus though the cells retain their chromosome number, their DNA content gets half. Prior to the next division, these cells pass through a phase of DNA synthesis that recovers the lost DNA and adds a chromatid to each chromosome. 'Meiosis' is a division of cells that leads to the reduction in their chromosome number as well as the amount of DNA to haploidy (1 set of chromosomes and DNA). It is achieved by the cell undergoing two successive divisions without the intervening S phase. These haploid cells differentiate into gametes which when fused with another gamete make a diploid zygote, the progenitor of an organism. In higher organisms, cells specialised to undergo meiosis are germ cells. In several single-celled organisms too meiosis takes place. Essentially the process is conserved throughout the living world. In this article, we try to understand under what conditions and situations mitotically dividing cells initiate meiosis. We also unravel the genetic regulation of its initiation as well as the process that follows. In the unicellular mould, yeast, under conditions of stress (nutritional, environmental) a set of IME (inducers of meiosis) genes (IME1, IME2, IME4) get activated. These genes comprise regulators in their promoter regions that inhibit their expression in haploid and unstressed conditions. When activated, IME genes initiate cells into meiosis and induce a cascade of genes that steer the cells towards homologous pairing, recombination, and chromosomal segregation followed by another division without the S phase. We will also try to understand the mechanisms of other phenomena unique to meiosis viz., segregation of chromosomes instead of chromatid at anaphase I, entry into meiosis II and its execution without passing through the S phase. [ABSTRACT FROM AUTHOR]

Metabolic engineering has been widely used for production of natural medicinal molecules. However, engineering high-yield platforms is hindered in large part by limited knowledge of complex regulatory machinery of metabolic network. N 6-Methyladenosine (m6A) modification of RNA plays critical roles in regulation of gene expression. Herein, we identify 1470 putatively m6A peaks within 1151 genes from the haploid Saccharomyces cerevisiae strain. Among them, the transcript levels of 94 genes falling into the pathways which are frequently optimized for chemical production, are remarkably altered upon overexpression of IME4 (the yeast m6A methyltransferase). In particular, IME4 overexpression elevates the mRNA levels of the methylated genes in the glycolysis, acetyl-CoA synthesis and shikimate/aromatic amino acid synthesis modules. Furthermore, ACS1 and ADH2 , two key genes responsible for acetyl-CoA synthesis, are induced by IME4 overexpression in a transcription factor-mediated manner. Finally, we show IME4 overexpression can significantly increase the titers of isoprenoids and aromatic compounds. Manipulation of m6A therefore adds a new layer of metabolic regulatory machinery and may be broadly used in bioproduction of various medicinal molecules of terpenoid and phenol classes. Overexpression of IME4 (the yeast m6A methyltransferase) reinforces acetyl-CoA synthesis and shikimate pathway, and thereby increase the production of terpenoids (e.g. , santalols) and aromatic compounds (e.g. , p -coumaric acid). [Display omitted] [ABSTRACT FROM AUTHOR]

The dynamics of cell mechanics and epigenetic signatures direct cell behaviour and fate, thus influencing regenerative outcomes. In recent years, the utilisation of 2D geometric (i.e. square, circle, hexagon, triangle or round-shaped) substrates for investigating cell mechanics in response to the extracellular microenvironment have gained increasing interest in regenerative medicine due to their tunable physicochemical properties. In contrast, there is relatively limited knowledge of cell mechanobiology and epigenetics in the context of 3D biomaterial matrices, i.e., hydrogels and scaffolds. Scaffold geometry provides biophysical signals that trigger a nucleus response (regulation of gene expression) and modulates cell behaviour and function. In this review, we explore the potential of additive manufacturing to incorporate multi length-scale geometry features on a scaffold. Then, we discuss how scaffold geometry direct cell and nuclear mechanosensing. We further discuss how cell epigenetics, particularly DNA/histone methylation and histone acetylation, are modulated by scaffold features that lead to specific gene expression and ultimately influence the outcome of tissue regeneration. Overall, we highlight that geometry of different magnitude scales can facilitate the assembly of cells and multicellular tissues into desired functional architectures through the mechanotransduction pathway. Moving forward, the challenge confronting biomedical engineers is the distillation of the vast knowledge to incorporate multiscaled geometrical features that would collectively elicit a favourable tissue regeneration response by harnessing the design flexibility of additive manufacturing. It is well-established that cells sense and respond to their 2D geometric microenvironment by transmitting extracellular physiochemical forces through the cytoskeleton and biochemical signalling to the nucleus, facilitating epigenetic changes such as DNA methylation, histone acetylation, and microRNA expression. In this context, the current review presents a unique perspective and highlights the importance of 3D architectures (dimensionality and geometries) on cell and nuclear mechanics and epigenetics. Insight into current challenges around the study of mechanobiology and epigenetics utilising additively manufactured 3D scaffold geometries will progress biomaterials research in this space. [Display omitted] [ABSTRACT FROM AUTHOR]

Background: Epigenome, genetic variants, and other environmental factors involved in gene regulation are highly inter-dependent in several chronic diseases, including obesity, cardiovascular disease, and diabetes. The present study aimed at testing the associations and the mechanism involved in silencing of CYP2R1 gene in normal and obese Saudi women patients. Height, weight, BMI, 25-hydroxy vitamin D, parathyroid hormone, glycemic status, and lipid profile (TG, LDL, HDL, and TC) of CYP2R1 were measured in 100 women (31 normal and 69 obese patients). Results: Our result shows that hypermethylation in site 2 of the CYP2R1 gene with body weight (p < 0.004), BMI (p < 0.002), waist circumference (p < 0.002), total-LDL (p < 0.027), total cholesterol (p < 0.022), and vitamin D (VD) (close to borderline significance p < 0.06) and site 4 of CYP2R1 with LDL (p < 0.041) in the four tested sites among normal and obese women was significantly associated. Moreover, we tested five different CpG sites in the CYP27B1 gene where site 5 correlated significantly with VD levels. Conclusion: Our present study clearly indicates that hypermethylation of specific sites in the CYP2R1 and CYP27B1 genes might regulate gene expression with special reference to the risk of obesity and vitamin D metabolism. [ABSTRACT FROM AUTHOR]

Background: Prostate cancer (PC) is a silent but potent killer among men. In 2018, PC accounted for more than 350, 000 death cases while more than 1.2 million cases were diagnosed. Docetaxel, a chemotherapeutic drug belonging to the taxane family of drugs, is one of the most potent drugs in combating advanced PC. However, PC cells often evolve resistance against the regimen. Hence, necessitating the search for complementary and alternative therapies. Quercetin, a ubiquitous phytocompound with numerous pharmacological properties, has been reported to reverse docetaxel resistance (DR) in docetaxel-resistant prostate cancer (DRPC). Therefore, this study aimed to explore the mechanism via which quercetin reverses DR in DRPC using an integrative functional network and exploratory cancer genomic data analyses. Results: The putative targets of quercetin were retrieved from relevant databases, while the differentially expressed genes (DEGs) in docetaxel-resistant prostate cancer (DRPC) were identified by analysing microarray data retrieved from the Gene Expression Omnibus (GEO) database. Subsequently, the protein-protein interaction (PPI) network of the overlapping genes between the DEGs and quercetin targets was retrieved from STRING, while the hub genes, which represent the key interacting genes of the network, were identified using the CytoHubba plug-in of Cytoscape. The hub genes were further subjected to a comprehensive analysis aimed at identifying their contribution to the immune microenvironment and overall survival (OS) of PC patients, while their alterations in PC patients were also revealed. The biological roles played by the hub genes in chemotherapeutic resistance include the positive regulation of developmental process, positive regulation of gene expression, negative regulation of cell death, and epithelial cell differentiation among others. Conclusion: Further analysis revealed epidermal growth factor receptor (EGFR) as the most pertinent target of quercetin in reversing DR in DRPC, while molecular docking simulation revealed an effective interaction between quercetin and EGFR. Ultimately, this study provides a scientific rationale for the further exploration of quercetin as a combinational therapy with docetaxel. [ABSTRACT FROM AUTHOR]

Background: MicroRNAs (miRNAs) are small endogenous RNAs with an approximate length of 18–22 nucleotides and involved in the regulation of gene expression in transcriptional or post-transcriptional levels. They were found to be associated with leaf morphogenesis, flowering time, vegetative phase change, and response to environmental cues in plants, where they act as a critical regulatory factor. The nature of high conservancy of plant miRNAs within the plant species made it possible to detect the conserved miRNAs by computational approaches. Expressed Sequence Tags (EST) based comparative genomic approaches provide advantages over wet lab approaches as it is convenient, easy to carry out and less time consuming. EST-based in silico approach can unravel new conserved miRNAs in plants, even when the complete genome sequence is not available. Results: To identify the novel miRNAs, a total of 46,865 ESTs from Jatropha curcas were searched for homology to all available 6746 mature miRNAs of plant eudicotyledons. Finally, we ended up with 12 novel miRNAs in Jatropha that range from 18 to 19 nucleotides where their respective precursor miRNAs had 54.11–71.76% (A + U) content. The putative miRNAs belong to 12 individual miRNA family and most of them have higher (A + U) content ranging from 47.36 to 77.77% than their respective miRNA homologs. Many of the target genes by the newly identified miRNAs were associated with plant growth and development, stress response, defense and hormone signaling, and oil synthesis pathways. Conclusion: These findings have the potential to speed up miRNA identification and expand our understanding of miRNA functions in J. curcas. [ABSTRACT FROM AUTHOR]

Copyright of Revista de la Academia Colombiana de Ciencias Exactas, Físicas y Naturales is the property of Academia Colombiana de Ciencias Exactas, Fisicas y Naturales and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

MYOCD is a transcription factor important for cardiac and smooth muscle development. We previously identified that actin‐related protein 5 (ARP5) binds to the N‐terminus of MYOCD. Here, we demonstrate that ARP5 inhibits the cooperative action of the cardiac‐specific isoform of MYOCD with MEF2. ARP5 overexpression in murine hearts induced cardiac hypertrophy and fibrosis, whereas ARP5 knockdown in P19CL6 cells significantly increased cardiac gene expression. ARP5 was found to bind to a MEF2‐binding motif of cardiac MYOCD and inhibit MEF2‐mediated transactivation by MYOCD. RNA‐seq analysis revealed 849 genes that are upregulated by MYOCD‐MEF2 and 650 genes that are repressed by ARP5. ARP5 expression increased with cardiomyopathy and was negatively correlated with the expression of Tnnt2 and Ttn, which were regulated by cardiac MYOCD‐MEF2. Overall, our data suggest that ARP5 is a potential suppressor of cardiac MYOCD during physiological and pathological processes. [ABSTRACT FROM AUTHOR]

Copyright of Brazilian Journal of Biology is the property of Instituto Internacional de Ecologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Osteosarcomas are prevalent in children and young adults and have a high recurrence rate. Cisplatin, doxorubicin, and methotrexate are common adjuvant chemotherapy drugs for treatment of osteosarcoma, but multidrug resistance is a growing problem. Therefore, understanding the molecular mechanisms of chemotherapy resistance in osteosarcoma cells is crucial for developing new therapeutic approaches and ultimately improving the prognosis of osteosarcoma patients. To identify genes associated with cisplatin resistance in osteosarcoma, we screened a large‐scale mutant library generated by transfecting human osteosarcoma cells with a piggyBac (PB) transposon‐based gene activation vector. Several candidate genes were identified by using Splinkerette‐PCR paired with Next Generation Sequencing. We created a disease‐free survival predictor model, which includes ZNF720, REEP3, CNNM2, and CGREF1, using TARGET (Therapeutically Applicable Research to Generate Effective Treatments) datasets. Additionally, the results of our enrichment analysis between the Four_genes_high group and Low_group suggested that these four genes may participate in cisplatin resistance in osteosarcoma through cross talk between various signaling pathways, especially the signaling pathway related to bone formation. These data may help guide future studies into chemotherapy for osteosarcoma. [ABSTRACT FROM AUTHOR]

Gene expression data represents a condition matrix where each row represents the gene and the column shows the condition. Micro array used to detect gene expression in lab for thousands of gene at a time. Genes encode proteins which in turn will dictate the cell function. The production of messenger RNA along with processing the same are the two main stages involved in the process of gene expression. The biological networks complexity added with the volume of data containing imprecision and outliers increases the challenges in dealing with them. Clustering methods are hence essential to identify the patterns present in massive gene data. Many techniques involve hierarchical, partitioning, grid based, density based, model based and soft clustering approaches for dealing with the gene expression data. Understanding the gene regulation and other useful information from this data can be possible only through effective clustering algorithms. Though many methods are discussed in the literature, we concentrate on providing a soft clustering approach for analyzing the gene expression data. The population elements are grouped based on the fuzziness principle and a degree of membership is assigned to all the elements. An improved Fuzzy clustering by Local Approximation of Memberships (FLAME) is proposed in this work which overcomes the limitations of the other approaches while dealing with the non-linear relationships and provide better segregation of biological functions. [ABSTRACT FROM AUTHOR]

Microbial production of chiral γ-decalactone has received considerable attention due to its high market value. However, the inhibition of substrates and products on microorganisms has significantly limited the production of chiral γ-decalactone. In this study, a green biphasic fermentation system containing 1-butyl-3-methylimidazolium tetrafluoroborate ([C 4 MIM]PF 6) was developed to increase the synthesis of (R)-γ-decalactone from ricinoleic acid catalyzed by Clavispora lusitaniae YJ26. Under optimal conditions, the titer of γ-decalactone obtained using the biphasic system reached 2.04 g/L, which is 2.4 times that of the traditional aqueous fermentation system, and showed high enantioselectivity (e.e. > 99.0%). Fluorescence microscopy and flow cytometry results demonstrated that the addition of [C 4 MIM]PF 6 significantly alleviated the damage of substrate and product to cell membrane and improved cell viability, thus increasing the titer of γ-decalactone. Furthermore, comparative transcriptomic analysis results suggested that the improved mechanism may be attributed to the up-regulation of genes associated with cell membrane component synthesis or cell tolerance enhancement. Overall, the experimental results provide valuable insights into the efficient microbial production of chiral decalactone in an ionic liquids–containing biphasic fermentation system. The addition of ionic liquid increases the cell membrane integrity through gene regulation, thus enhancing its capacity to produce (R)-γ-decalactone. [Display omitted] [ABSTRACT FROM AUTHOR]

Research on anti-aging activity primarily focuses on crude extracts of anthocyanins, while relatively less attention has been given to anthocyanin monomers. This study was focused on exploring the anti-aging properties of the main anthocyanin monomer, petunidin-3- O -[rhamnopyranosyl-(trans - p -coumaroyl)]-5- O -(β -D-glucopyranoside) (P3G), from the fruits of Lycium ruthenicum Murray. The effects of P3G on stress endurance, lifespan, and gut microbiota in Caenorhabditis elegans were investigated. It was found that P3G significantly extended the mean lifespan by 19.50%, enhanced fitness through increased motility (30.39%) and pharyngeal pumping (18.33%), and reduced lipofuscin accumulation by 43.61% while maintaining fecundity. P3G prolonged lifespan by 20.13% and 18.82% during oxidative and heat stress, correspondingly. This effect was attributed to the activation of stress-related genes and the antioxidant system. The transcriptome results showed the enrichment in the longevity pathway and biosynthesis pathway of nematodes. The prominent role of the DAF-16 pathway was highlighted, as P3G enhanced the expression of daf-16 gene and downstream genes (sod-2 , sod-3 , and mlt-1), promoting nuclear accumulation of DAF-16. Moreover, modifications in the gut microbiota induced by P3G played a role in its anti-aging properties by governing gut microbial composition. Overall, P3G appeared to contribute to promoting the health of nematodes and might help delay their aging to some extent. [Display omitted] • P3G from Lycium ruthenicum improves nematode gut microbiota, impacting key bacteria. • P3G exhibits anti-aging effects via DAF-16 gene in nematodes. • P3G is associated with nematode microbiota and gene targets. [ABSTRACT FROM AUTHOR]

T-2 toxin, a trichothecene mycotoxin, is an important environmental pollutant that poses a threat globally to the health of humans and animals. It has been found to induce nephrotoxicity; however, the precise molecular mechanism involved remains unclear. In this study, mice were administered at a single dose of 2 mg/kg body weight T-2 toxin intraperitoneally, and kidney function and ultrastructural observations were assessed after 1 d, 3 d, and 7 d. Histopathological findings revealed that exposure to T-2 toxin caused noticeable tubular degeneration, necrosis and epithelial cell shedding in mouse kidneys. Transmission electron microscopy indicated that exposure to T-2 toxin caused mitochondrial swelling and vacuolization. Transcriptomic data revealed significant differences in the expression of 1122, 58, and 391 genes in kidney tissues 1 d, 3 d, or 7 d after T-2 toxin exposure, respectively. Moreover, after 1 d, the downregulated differentially expressed genes (DEGs) were found to be involved in the cell cycle, p53 signaling, and cellular senescence pathways, while the upregulated DEGs were found to be associated with the ribosomal pathway. Temporal changes in gene expression patterns (i.e. , after 3 d and 7 d) and disturbances in cellular metabolism during the recovery period (7 d) were detected in mouse kidneys after exposure to T-2 toxin. In conclusion, this study is the first to provide a comprehensive comparative transcriptomic analysis of T-2 toxin exposure-induced nephrotoxicity-related gene regulation at different time points and to investigate the mechanism underlying the nephrotoxicity of T-2 toxin at the mRNA expression level. • A comprehensive comparative transcriptomic analysis was used to investigate T-2 toxin -induced nephrotoxicity. • A signal dose of T-2 toxin exposure could result in mitochondrial damage and nephrotoxicity in mice. • Cell cycle, p53 signaling, cellular senescence, and ribosomal pathways were involved in T-2 toxin-induced nephrotoxicity. [ABSTRACT FROM AUTHOR]

Associations between indoor air pollution from fine particulate matter (PM with aerodynamic diameter d p < 2.5 μm) and human health are poorly understood. Here, we analyse the concentration-response curves for fine and ultrafine PM, the gene expression, and the methylation patterns in human bronchial epithelial cells (BEAS-2B) exposed at the air-liquid interface (ALI) within a classroom in downtown Rome. Our results document the upregulation of aryl hydrocarbon receptor (AhR) and genes associated with xenobiotic metabolism (CYP1A1 and CYP1B1) in response to single exposure of cells to fresh urban aerosols at low fine PM mass concentrations within the classroom. This is evidenced by concentrations of ultrafine particles (UFPs, dp < 0.1 μm), polycyclic aromatic hydrocarbons (PAH), and ratios of black carbon (BC) to organic aerosol (OA). Additionally, an interleukin 18 (IL-18) down-regulation was found during periods of high human occupancy. Despite the observed gene expression dysregulation, no changes were detected in the methylation levels of the promoter regions of these genes, indicating that the altered gene expression is not linked to changes in DNA methylation and suggesting the involvement of another epigenetic mechanism in the gene regulation. Gene expression changes at low exposure doses have been previously reported. Here, we add the possibility that lung epithelial cells, when singly exposed to real environmental concentrations of fine PM that translate into ultra-low doses of treatment, may undergo epigenetic alteration in the expression of genes related to xenobiotic metabolism. Our findings provide a perspective for future indoor air quality regulations. We underscore the potential role of indoor UFPs as carriers of toxic molecules with low-pressure weather conditions, when rainfall and strong winds may favour low levels of fine PM. [Display omitted] • No significant correlation was found between PM 1 and gene regulation of BEAS-2B cell. • AhR and CYP upregulation was linked to fresh urban aerosol and low condensation sink. • IL-18 was down-regulated during periods of high human occupancy. • The promoter methylation levels of AhR, CYP1A1, CYP1B1 and IL-18 were not changes. [ABSTRACT FROM AUTHOR]

The environmental transmission of antibiotic resistance genes (ARGs) and metal resistance genes (MRGs) exerted devastating threats to global public health, and their interactions with other emerging contaminants (ECs) have raised increasing concern. This study investigated that the abundances of ARGs and MRGs with the predominant type of efflux pump were simultaneously increased (8.4–59.1%) by disinfectant polyhexamethylene guanidine (PHMG) during waste activated sludge (WAS) anaerobic digestion. The aggregation of the same microorganisms (i.e., Hymenobacter and Comamonas) and different host bacteria (i.e., Azoarcus and Thauera) were occurred upon exposure to PHMG, thereby increasing the co-selection and propagation of MRGs and ARGs by vertical gene transfer. Moreover, PHMG enhanced the process of horizontal gene transfer (HGT), facilitating their co-transmission by the same mobile genetic elements (20.2–223.7%). Additionally, PHMG up-regulated the expression of critical genes (i.e., glnB , trpG and gspM) associated with the HGT of ARGs and MRGs (i.e., two-component regulatory system and quorum sensing) and exocytosis system (i.e., bacterial secretion system). Structural equation model analysis further verified that the key driver for the simultaneous enrichment of ARGs and MRGs under PHMG stress was microbial community structure. The study gives new insights into the aggravated environmental risks and mechanisms of ECs in sludge digestion system, providing guidance for subsequent regulation and control of ECs. [Display omitted] • PHMG induces the co-enrichment of MRGs and ARGs (8.4–59.1%). • MRGs and ARGs share similar microbial hosts, MGEs and transmission pathway. • PHMG promotes the transmission of ARGs and MRGs through simultaneous VGT and HGT. • The genetic regulation (i.e., tnpA and trpG) of TCS, QS and BSS cause the MRGs and ARGs co-selection. • Microbial community is the primary factor driving the MRGs and ARGs co-propagation. [ABSTRACT FROM AUTHOR]

Jumonji domain-containing protein D3 (JMJD3) is a 2-oxoglutarate-dependent dioxygenase that specifically removes transcriptional repression marks di- and tri-methylated groups from lysine 27 on histone 3 (H3K27me2/3). The erasure of these marks leads to the activation of some associated genes, thereby influencing various biological processes, such as development, differentiation, and immune response. However, comprehensive descriptions regarding the relationship between JMJD3 and inflammation are lacking. Here, we provide a comprehensive overview of JMJD3, including its structure, functions, and involvement in inflammatory pathways. In addition, we summarize the evidence supporting JMJD3's role in several inflammatory diseases, as well as the potential therapeutic applications of JMJD3 inhibitors. Additionally, we also discuss the challenges and opportunities associated with investigating the functions of JMJD3 and developing targeted inhibitors and propose feasible solutions to provide valuable insights into the functional exploration and discovery of potential drugs targeting JMJD3 for inflammatory diseases. [Display omitted] • JMJD3 is an H3K27me2/3 demethylase mediating transcriptional activation of associated genes. • JMJD3 is implicated in various physiological and pathological processes, including inflammation. • JMJD3 is a potential therapeutic target for multiple inflammatory diseases. • No JMJD3 inhibitor is clinically available up to now. [ABSTRACT FROM AUTHOR]

Primary headache disorders (PHD), specifically migraine, are strongly associated with temporomandibular disorders (TMD), sharing some patterns of orofacial pain. Both disorders have significant genetic contributions already studied. PRISMA guidelines were followed to conduct this systematic review, which comprehensively summarize and discuss the genetic overlap between TMD and PHD to aid future research in potential therapy targets. This review included eight original articles published between 2015 and 2020, written in English and related to either TMD and/or PHD. The genes simultaneously assessed in PHD and TMD studies were COMT, MTHFR, and ESR1. COMT was proved to play a critical role in TMD pathogenesis, as all studies have concluded about its impact on the occurrence of the disease, although no association with PHD was found. No proof on the impact of MTHFR gene regulation on either TMD or PHD was found. The most robust results are concerning the ESR1 gene, which is present in the genetic profile of both clinical conditions. This novel systematic review highlights not only the need for a clear understanding of the role of ESR1 and COMT genes in pain pathogenesis, but it also evaluates their potential as a promising therapeutic target to treat both pathologies. [ABSTRACT FROM AUTHOR]

Root nodule symbiosis is promoted in nitrogen-deficient environments, whereas host plants cease the symbiosis if they can obtain enough nitrogen from their surrounding soil. In Lotus japonicus, recent reports indicate that two NODULE INCEPTION (NIN)-LIKE PROTEIN (NLP) transcription factors, LjNLPl and LjNLP4, play important roles in the regulation of gene expression and nodulation in response to nitrate. To characterize the redundant and unique roles of LjNLPl and LjNLP4 in more detail, we reanalyzed our previous transcriptome data using Ljnlpl and Ljnlp4 mutants. Although downstream genes of LjNLPl and LjNLP4 mostly overlapped, we found that nitrate-induced expression of NITRATE TRANSPORTER 2 (LjNRT2) family genes was specifically regulated by LjNLPl. In contrast, LjNRTl gene family expression was regulated by both LjNLPl and LjNLP4. Therefore, it is likely that the two NLPs play distinct roles in the regulation of nitrate transport. [ABSTRACT FROM AUTHOR]

Background: Small RNAs (sRNAs) that do not get untranslated into proteins exhibit a pivotal role in the expression regulation of their cognate gene(s) in almost all eukaryotic lineages, including plants. Hitherto, numerous protein families such as Dicer, a unique class of Ribonuclease III, have been reported to be involved in sRNAs processing pathways and silencing. In this study, we aimed to investigate the phylogenetic relationship and evolutionary history of the DCL protein family. Results: Our results illustrated the DCL family of proteins grouped into four main subfamilies (DCLs 1–4) presented in either Eudicotyledons or Liliopsids. The accurate observation of the phylogenetic trees supports the independent expansion of DCL proteins among the Eudicotyledons and Liliopsids species. They share the common origin, and the main duplication events for the formation of the DCL subfamilies occurred before the Eudicotyledons/Liliopsids split from their ancestral DCL. In addition, shreds of evidence revealed that the divergence happened when multicellularization started and since the need for complex gene regulation considered being a necessity by organisms. At that time, they have evolved independently among the monophyletic lineages. The other finding was that the combination of DCL protein subfamilies bears several highly conserved functional domains in plant species that originated from their ancestor architecture. The conservation of these domains happens to be both lineage-specific and inter lineage-specific. Conclusions: DCL subfamilies (i.e., DCL1-DCL4) distribute in their single clades after diverging from their common ancestor and before emerging into higher plants. Therefore, it seems that the main duplication events for the formation of the DCL subfamilies occurred before the Eudicotyledons/Liliopsida split and before the appearance of moss, and after the single-cell green algae. We also observed the same trends among the main DCL subfamilies from functional unit composition and architecture. Despite the long evolutionary course from the divergence of Liliopsida lineage from the Eudicotyledons, a significant diversifying force to domain composition and orientation was absent. The results of this study provide a deeper insight into DCL protein evolutionary history and possible sequence and structural relationships between DCL protein subfamilies in the main higher plant monophyletic lineages; i.e., Eudicotyledons and Liliopsida. [ABSTRACT FROM AUTHOR]

Heterogeneous nuclear ribonucleoproteins (hnRNPs) are essential players in the regulation of gene expression. The majority of the twenty different hnRNP proteins act through the modulation of pre-mRNA splicing. Most have been shown to regulate the expression of critical genes for the progression of tumorigenic processes and were also observed to be overexpressed in several types of cancer. Moreover, these proteins were described as essential components for the maturation of some microRNAs (miRNAs). In the human genome, over 70% of miRNAs are transcribed from introns; therefore, we hypothesized that regulatory proteins involved with splicing could be important for their maturation. Increased expression of the miR-17-92 cluster has already been shown to be related to the development of many cancers, such as thyroid, lung, and lymphoma. In this article, we show that overexpression of hnRNP A1 and hnRNP C in BCPAP thyroid cancer cells directly affects the expression of miR-17-92 miRNAs. Both proteins associate with the 50-end of this cluster, strongly precipitate miRNAs miR-17 and miR-18a and upregulate the expression of miR-92a. Upon overexpression of these hnRNPs, BCPAP cells also show increased proliferation, migration, and invasion rates, suggesting upregulation of these proteins and miRNAs is related to an enhanced tumorigenic phenotype. [ABSTRACT FROM AUTHOR]

Research on gene expression, as well as the regulatory interactions governing it, has been considered one of the significant challenges in recent decades. The process of regulating gene expression determines which genes should be turned on and turned off at specific times. Microarray data provide a wealth of information regarding gene expression levels. Due to the large volume of such data, their analysis requires robust computational methods for identifying and analyzing gene regulation networks. However, scholars in this field encounter numerous challenges, including the high number of genes to be considered, the limited number of samples, and the inherently noisy nature of the data. Accordingly, the main purpose of the present study is to propose a modeling approach for inferring gene regulatory networks using regression-based and rotation forest methods. In this method, after initial processing, the data are divided into different clusters using clustering approaches. This categorization is utilized in the next step to extract the knowledge matrix. Subsequently, regulatory interactions governing genes are identified using an improved version of rotation forest based on t-SNE. Furthermore, the proposed approach has been compared with some significant methods commonly used in this discipline to evaluate its efficiency. The analysis results demonstrate that, due to the incorporation of hidden biological knowledge within the dataset during the network modeling process, the proposed model excels in identifying regulatory mechanisms. It not only aligns with top methods in the discipline but can also, at times, outperform them in identifying gene regulatory networks. [ABSTRACT FROM AUTHOR]

Although polarized light can assist many animals in performing special visual tasks, current polarized light pollution (PLP) caused by urban construction has been shown to induce maladaptive behaviors of PL-sensitive animals and change ecological interactions. However, the underlying mechanisms remain unclear. Our previous work hypothesized that linearly polarized light (LPL) is an ecological trap for Oratosquilla oratoria , a common Stomatopoda species in the China Sea. Here we explored the underlying negative effects of artificially LPL on O. oratoria based on comparative transcriptomics. We identified 3616 differentially expressed genes (DEGs) in O. oratoria compound eyes continuous exposed to natural light (NL) and LPL scenarios. In comparison with the NL scenario, a total of 1972 up- and 1644 down- regulated genes were obtained from the O. oratoria compound eyes under LPL scenario, respectively. Furthermore, we performed functional annotation of those DEGs described above and identified 65 DEGs related to phototransduction, reproduction, immunity, and synapse. Based on the functional information, we suspected that continuous LPL exposure could block the light transmission, disrupt the reproductive process, and lead to the progressive failure of the immune response of O. oratoria. In conclusion, this study is the first to systematically describe the negative effects of artificial LPL exposure on O. oratoria at the genetic level, and it can improve the biological conservation theory behind PLP. [Display omitted] • Linearly polarized light (LPL) may be an ecological trap for Oratosquilla oratoria. • There were 3616 differentially expressed genes in O. oratoria compound eyes under natural light and LPL. • Phototransduction, reproduction, immunity, and synapse-related genes determines the response of O. oratoria to LPL. [ABSTRACT FROM AUTHOR]

Methylosome protein 50 (Mep50) functions as a partner to protein arginine methyltransferase 5. MEP50 serves as a coactivator for both the androgen receptor and estrogen receptor in humans. Mep50 plays a crucial role in the development of germ cells in Drosophila. The precise role of Mep50 in oogenesis remains unclear in vertebrates. The objective of this study was to investigate the role of Mep50 in oogenesis in medaka fish. Disruption of Mep50 resulted in impaired oogenesis and the formation of multiple oocyte follicles in medaka. RNA-seq analysis revealed significant differential gene expression in the mutant ovary, with 4542 genes up-regulated and 1264 genes down-regulated. The regulated genes were found to be enriched in cellular matrices and ECM-receptor interaction, the Notch signaling pathway, the PI3K-Akt signaling pathway, the MAPK signaling pathway, the Hippo signaling pathway, and the Jak-Stat pathway, among others. In addition, the genes related to the hypothalamus-pituitary-gonad axis, steroid metabolism, and IGF system were impacted. Furthermore, the mutation of mep50 caused significant alterations in alternative splicing of pre-mRNA in ovarian cells. Quantitative RT-PCR results validated the findings from RNA-seq analysis in the specific genes, including akt2 , map3k5 , yap1 , fshr , cyp17a , igf1 , ythdc2 , cdk6 , and col1 , among others. The findings of this study demonstrate that Mep50 plays a crucial role in oogenesis, participating in a diverse range of biological processes such as steroid metabolism, cell matrix regulation, and signal pathways. This may be achieved through the regulation of gene expression via mRNA splicing in medaka ovarian cells. [Display omitted] • Loss of mep50 resulted in the formation of multiple oocyte follicles in medaka. • The mep50 mutation interfered with alternative splicing events. • Mutation of mep50 disrupted gene expression involved in steroidogenesis, and cyclin regulation, etc. • Mep50 plays a role in oogenesis, possibly by regulating gene expression through mRNA splicing. [ABSTRACT FROM AUTHOR]

Israel represents the southern limit of the distribution of the banded newt (Ommatotriton vittatus). The life cycle of O. vittatus includes several distinct phases: eggs, aquatic larvae, a terrestrial phase and an aquatic reproductive phase. We investigated differences in gene expression during the life cycle and transition of banded newts between terrestrial and aquatic habitats using mRNA-seq. We identified ∼10 k genes that were differentially expressed (DE) in one of the pairwise comparisons between 3 groups: 1 - terrestrial newts (males and females), 2 - aquatic newts (males and females), 3 - aquatic larvae before metamorphosis. The groups were clearly defined by Principal Components Analysis (PCA). The greatest difference was between aquatic newts (males and females) and aquatic larvae: ∼7.4 k DE genes. Of special interest were the ∼2.4 k genes DE between the aquatic and terrestrial phenotypes. These included prominent candidates with known roles in kidney function (uromodulin homologs were strongly associated with aquatic lifestyle), tissue structure (keratins), and the thyroid hormone signaling modulator DUOXA1. Additional developmental and metabolic pathways overrepresented among the identified DE genes included "epidermis development", "nervous system development", "nucleotide-sugar biosynthesis". Overall, both metamorphosis and environmental transition of banded newts involve extensive transcriptomic remodeling involving developmental, metabolic, and cellular pathways. Understanding the roles of these pathways and individual genes is instrumental for studies of transition between habitats, especially those affected by climate change. Furthermore, the phenotypic flexibility of the newt and the underlying regulation of gene expression can shed light on the evolution of terrestrial vertebrates. [Display omitted] • The banded newt has several distinct phases: eggs, aquatic larvae, a terrestrial phase and an aquatic reproductive phase. • These transitions cause extensive transcriptomic remodeling of developmental, metabolic, and cellular pathways. • Identified DE genes have known roles in kidney function, tissue structure, and hormone signaling. [ABSTRACT FROM AUTHOR]

The current photodynamic performance of CuS nanoparticles (CuS NPs) alone is still greatly challenged by the low quantum yield of reactive oxygen species (ROS). At the same time, the efficiency of photothermal therapy (PTT) and photodynamic therapy (PDT) is reduced due to the self-protective ability of tumor cells when attacked by hyperthermia and ROS. To address this issue, we synthesized D Cu x S NPs using customized DNA templates through a surface vacancy-rich engineering strategy. In addition to their inherent photothermal properties, the surface vacancy-rich of D Cu x S NPs effectively hinders electron-hole pair complexation, thereby enhancing their photodynamic properties. Furthermore, the tumor-targeting NC3S aptamer and the i-motif DNA/Nrf2 siRNA chimera were attached to both ends of the DNA template. The final ND Cu x S@siRNA NPs were highly enriched in tumor cells, while the i-motif undergoes a conformational change to release Nrf2 siRNA upon acidic stimulation for Nrf2 pathway blocking to decrease tumor cell protection effect against ROS and high temperature, creating a favorable tumor microenvironment for enhanced PTT and PDT effects. In this study, we explored the potential of DNA templates for engineering nanomaterials, enhanced the photodynamic properties of D Cu x S NPs through a surface vacancy-rich strategy, and exploited the versatility of DNA templates to combine phototherapy with gene regulation, providing a promising approach for clinical tumor treatment. [Display omitted] • A dual modulation strategy for phototherapy and gene therapy is reported using DNA template synthesis strategy for engineering nanomaterials. • D Cu X S has the enhanced photodynamic properties due to the presence of oxygen vacancies and sulfur vacancies. • ND Cu X S@siRNA NPs release Nrf2 siRNA in response to acidic condition to achieve gene silencing, which in turn enhances PTT and PDT. [ABSTRACT FROM AUTHOR]

RNA interference (RNAi) is a gene silencing mechanism that occurs after transcription. It is induced by double stranded RNA which results in a sequence-specific gene regulation by small RNAs thus results in mRNA degradation. RNA silencing pathways in plants are small interfering RNA (siRNA), micro RNA (miRNA), short hairpin RNA (shRNA) that also involves enzymes, and protein complex for complete mechanism. RNAi applications have been used to increase biotic and abiotic resistance, alter plant architecture, improve fruit quality, enhanced nutritional values, enhanced secondary metabolites, seedless fruits, reduced anti-nutritional toxic compounds, reduced allergens and to develop high-value industrial products. Therefore, RNAi is a novel approach that can be exploited for functional analysis of target genes, regulation of gene expression, improved quality traits, alternative method for crop protection and production in vegetables. This review is an attempt to collect current information on the RNAi mechanism and its application in the improvement of vegetable crops. [ABSTRACT FROM AUTHOR]

The energy‐saving strategy of Djungarian hamsters (Phodopus sungorus, Cricetidae) to overcome harsh environmental conditions comprises of behavioral, morphological, and physiological adjustments, including spontaneous daily torpor, a metabolic downstate. These acclimatizations are triggered by short photoperiod and orchestrated by the hypothalamus. Key mechanisms of long‐term photoperiodic acclimatizations have partly been described, but specific mechanisms that acutely control torpor remain incomplete. Here, we performed comparative transcriptome analysis on hypothalamus of normometabolic hamsters in their summer‐ and winter‐like state to enable us to identify changes in gene expression during photoperiodic acclimations. Comparing nontorpid and torpid hamsters may also be able to pin down mechanisms relevant for torpor control. A de novo assembled transcriptome of the hypothalamus was generated from hamsters acclimated to long photoperiod or to short photoperiod. The hamsters were sampled either during long photoperiod normothermia, short photoperiod normothermia, or short photoperiod‐induced spontaneous torpor with a body temperature of 24.6 ± 1.0 °C, or. The mRNA‐seq analysis revealed that 32 and 759 genes were differentially expressed during photoperiod or torpor, respectively. Biological processes were not enriched during photoperiodic acclimatization but were during torpor, where transcriptional and metabolic processes were reinforced. Most extremely regulated genes (those genes with |log2(FC)| > 2.0 and padj < 0.05 of a pairwise group comparison) underpinned the role of known key players in photoperiodic comparison, but these genes exhibit adaptive and protective adjustments during torpor. Targeted analyses of genes from potentially involved hypothalamic systems identified gene regulation of previously described torpor‐relevant systems and a potential involvement of glucose transport. [ABSTRACT FROM AUTHOR]

Leaf morphogenesis in Vitis vinifera is closely associated with the biosynthesis of various metabolites, starch, and growth-related molecules. In the present study, Illumina RNA deep sequencing-based on transcriptome analysis was deployed to understand leaf morphogenesis in Vitis vinifera. The KEGG pathway analysis revealed the transcripts involved in the biosynthesis of major metabolites leading to leaf growth. The highest number of DEGs were down-regulated at young leave-vs-mature leaves stages (3,501) followed by large leaves-vs-mature leaves (2,364); however, the minimum number of up-regulated transcripts were recorded at young leaves-vs-immature leaves (195). The gene regulation in the starch biosynthetic pathway, young leaves-vs-mature leaves showed the highest number of transcripts (24 up-regulated and 60 down-regulated). For ABC Transporters, 224 transcripts were expressed, among which the maximum number of transcripts (59) were recorded in large leaves-vs-mature leaves. Amino and nucleotide sugar metabolism showed 112 transcripts (22 up-regulated and 90 down-regulated), in which immature leaves-vs-mature leaves expressed 30 DEGs. In addition, Flavonoid pathway showed the highest number of transcripts i.e. 903 were expressed among the studied pathways. The findings of this study will also help to a better understanding of the underlying process during grape leaf morphogenesis and to unravel the mechanism. [ABSTRACT FROM AUTHOR]

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Cardiac fibrotization is a well-known process characteristic of many cardiac pathological conditions. The key element is excessive activation of cardiac fibroblasts, their transdifferentiation into myofibroblasts, increased production, and accumulation of extracellular matrix proteins, resulting in cardiac stiffness. The exact cellular mechanisms and molecular components involved in the process are not fully elucidated, but the SOCE mechanism could play an important role. Its key molecules are the molecular sensor of calcium in ER/SR - STIM and the highly selective calcium channels Orai located in the plasma membrane. This study aims to evaluate selected SOCEassociated genes in the activation of HCF cell culture by several known substances (phenylephrine, isoprenaline) that represent cardiovascular overload. After cell cultivation, cell medium was collected to measure the soluble collagen content. From the harvested cells, qRT-PCR was performed to determine the mRNA levels of the corresponding genes. The activation of cells was based on changes in the relative expression of collagen genes as well as the collagen content in the medium of the cell culture. We detected an increase in the expression of the Orai2 isoform, a change in the Orai1/Orai3 ratio and also an increase in the expression of the STIM2 isoform. These results suggest an increased activation of the SOCE mechanism under stress conditions of fibroblasts, which supports the hypothesis of fibroblast activation in pathological processes by altering calcium homeostasis through the SOCE mechanism. [ABSTRACT FROM AUTHOR]

The mammalian skeleton develops through two distinct modes of ossification: intramembranous ossification and endochondral ossification. During the process of skeletal development, SRY-box containing gene 9 (Sox9), runt-related transcription factor 2 (Runx2), and Sp7 work as master transcription factors (TFs) or transcriptional regulators, underlying cell fate specification of the two distinct populations: bone-forming osteoblasts and cartilage-forming chondrocytes. In the past two decades, core transcriptional circuits underlying skeletal development have been identified mainly through mouse genetics and biochemical approaches. Recently emerging next-generation sequencer (NGS)-based studies have provided genome-scale views on the gene regulatory landscape programmed by the master TFs/transcriptional regulators. With particular focus on Sox9, Runx2, and Sp7, this review aims to discuss the gene regulatory landscape in skeletal development, which has been identified by genome-scale data, and provide future perspectives in this field. [ABSTRACT FROM AUTHOR]

Transcription factors (TFs) orchestrate the regulation of cellular gene expression and thereby determine cell functionality. In this study, we analyzed the distribution of TFs containing domains, which named as ZnFTFs, both in ascomycete and basidiomycete fungi. We found that ZnFTFs were widely distributed in these fungal species, but there was more expansion of the ZnFTF class in Ascomycota than Basidiomycota. We identified 40 ZnFTFs in Ustilaginoidea virens , and demonstrated the involvement of UvZnFTF1 in vegetative growth, conidiation, pigment biosynthesis and pathogenicity. RNA-Seq analysis suggested that UvZnFTF1 may regulate different nutrient metabolism pathways, the production of secondary metabolites, and the expression of pathogen-host interaction genes and secreted protein- encoding genes. Analysis of the distribution of different fungal TFs in U. virens further demonstrated that UvZnFTFs make up a large TF family and may play essential biological roles in U. virens. [ABSTRACT FROM AUTHOR]