cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.25848836.v1
title: Nm-Nano: a machine learning framework for transcriptome-wide single-molecule mapping of 2´-O-methylation (Nm) sites in nanopore direct RNA sequencing datasets

description: 2´-O-methylation (Nm) is one of the most abundant modifications found in both mRNAs and noncoding RNAs. It contributes to many biological processes, such as the normal functioning of tRNA, the protection of mRNA against degradation by the decapping and exoribonuclease (DXO) protein, and the biogenesis and specificity of rRNA. Recent advancements in single-molecule sequencing techniques for long read RNA sequencing data offered by Oxford Nanopore technologies have enabled the direct detection of RNA modifications from sequencing data. In this study, we propose a bio-computational framework, Nm-Nano, for predicting the presence of Nm sites in direct RNA sequencing data generated from two human cell lines. The Nm-Nano framework integrates two supervised machine learning (ML) models for predicting Nm sites: Extreme Gradient Boosting (XGBoost) and Random Forest (RF) with K-mer embedding. Evaluation on benchmark datasets from direct RNA sequecing of HeLa and HEK293 cell lines, demonstrates high accuracy (99% with XGBoost and 92% with RF) in identifying Nm sites. Deploying Nm-Nano on HeLa and HEK293 cell lines reveals genes that are frequently modified with Nm. In HeLa cell lines, 125 genes are identified as frequently Nm-modified, showing enrichment in 30 ontologies related to immune response and cellular processes. In HEK293 cell lines, 61 genes are identified as frequently Nm-modified, with enrichment in processes like glycolysis and protein localization. These findings underscore the diverse regulatory roles of Nm modifications in metabolic pathways, protein degradation, and cellular processes. The source code of Nm-Nano can be freely accessed at https://github.com/Janga-Lab/Nm-Nano.
DOI: 10.6084/m9.figshare.26827110
title: HNRNPD regulates the biogenesis of circRNAs and the ratio of mRNAs to circRNAs for a set of genes

description: Exonic circular RNAs (ecircRNAs) in animal cells are generated by backsplicing, and the biogenesis of ecircRNAs is regulated by an array of RNA binding proteins (RBPs). HNRNPD is a heterogeneous nuclear ribonucleoprotein family member with both cytoplasmic and nuclear roles, and whether HNRNPD regulates the biogenesis of circRNAs remains unknown. In this study, we examine the role of HNRNPD in the biogenesis of ecircRNAs. The levels of ecircRNAs are primarily increased upon depletion of HNRNPD. HNRNPD preferentially binds to motifs enriched with A and U nucleotides, and the flanking introns of ecircRNAs tend to have more numbers and higher intensity of HNRNPD binding sites. The levels of mRNAs are generally not significantly altered in HNRNPD knockout cells. For a small set of genes, the circRNA:mRNA ratio is substantially affected, and the mRNA levels of some of these genes demonstrate a significant decrease in HNRNPD knockout cells. CDK1 is identified as a key gene modulated by HNRNPD in the context of circRNA biogenesis. HNRNPD suppresses the biogenesis of circCDK1 and favours the generation of CDK1 mRNA, and the CDK1 protein is a critical regulator of the cell cycle and apoptosis. HNRNPD can participate in cellular physiology, including the cell cycle and apoptosis, and plays roles in clear cell renal cell carcinoma (ccRCC) by modulating circRNA biogenesis and the mRNA levels of key genes, such as CDK1.
DOI: 10.6084/m9.figshare.26827110.v2
title: HNRNPD regulates the biogenesis of circRNAs and the ratio of mRNAs to circRNAs for a set of genes

description: Exonic circular RNAs (ecircRNAs) in animal cells are generated by backsplicing, and the biogenesis of ecircRNAs is regulated by an array of RNA binding proteins (RBPs). HNRNPD is a heterogeneous nuclear ribonucleoprotein family member with both cytoplasmic and nuclear roles, and whether HNRNPD regulates the biogenesis of circRNAs remains unknown. In this study, we examine the role of HNRNPD in the biogenesis of ecircRNAs. The levels of ecircRNAs are primarily increased upon depletion of HNRNPD. HNRNPD preferentially binds to motifs enriched with A and U nucleotides, and the flanking introns of ecircRNAs tend to have more numbers and higher intensity of HNRNPD binding sites. The levels of mRNAs are generally not significantly altered in HNRNPD knockout cells. For a small set of genes, the circRNA:mRNA ratio is substantially affected, and the mRNA levels of some of these genes demonstrate a significant decrease in HNRNPD knockout cells. CDK1 is identified as a key gene modulated by HNRNPD in the context of circRNA biogenesis. HNRNPD suppresses the biogenesis of circCDK1 and favours the generation of CDK1 mRNA, and the CDK1 protein is a critical regulator of the cell cycle and apoptosis. HNRNPD can participate in cellular physiology, including the cell cycle and apoptosis, and plays roles in clear cell renal cell carcinoma (ccRCC) by modulating circRNA biogenesis and the mRNA levels of key genes, such as CDK1.
DOI: 10.6084/m9.figshare.26827110.v1
title: HNRNPD regulates the biogenesis of circRNAs and the ratio of mRNAs to circRNAs for a set of genes

description: Exonic circular RNAs (ecircRNAs) in animal cells are generated by backsplicing, and the biogenesis of ecircRNAs is regulated by an array of RNA binding proteins (RBPs). HNRNPD is a heterogeneous nuclear ribonucleoprotein family member with both cytoplasmic and nuclear roles, and whether HNRNPD regulates the biogenesis of circRNAs remains unknown. In this study, we examine the role of HNRNPD in the biogenesis of ecircRNAs. The levels of ecircRNAs are primarily increased upon depletion of HNRNPD. HNRNPD preferentially binds to motifs enriched with A and U nucleotides, and the flanking introns of ecircRNAs tend to have more numbers and higher intensity of HNRNPD binding sites. The levels of mRNAs are generally not significantly altered in HNRNPD knockout cells. For a small set of genes, the circRNA:mRNA ratio is substantially affected, and the mRNA levels of some of these genes demonstrate a significant decrease in HNRNPD knockout cells. CDK1 is identified as a key gene modulated by HNRNPD in the context of circRNA biogenesis. HNRNPD suppresses the biogenesis of circCDK1 and favours the generation of CDK1 mRNA, and the CDK1 protein is a critical regulator of the cell cycle and apoptosis. HNRNPD can participate in cellular physiology, including the cell cycle and apoptosis, and plays roles in clear cell renal cell carcinoma (ccRCC) by modulating circRNA biogenesis and the mRNA levels of key genes, such as CDK1.
DOI: 10.6084/m9.figshare.26982897
title: An orthology-based methodology as a complementary approach to retrieve evolutionarily conserved A-to-I RNA editing sites

description: Adar-mediated adenosine-to-inosine (A-to-I) mRNA editing is a conserved mechanism that exerts diverse regulatory functions during the development, evolution, and adaptation of metazoans. The accurate detection of RNA editing sites helps us understand their biological significance. In this work, with an improved genome assembly of honeybee (<i>Apis mellifera</i>), we used a new orthology-based methodology to complement the traditional pipeline of (<i>de novo</i>) RNA editing detection. Compared to the outcome of traditional pipeline, we retrieved many novel editing sites in CDS that are deeply conserved between honeybee and other distantly related insects. The newly retrieved sites were missed by the traditional <i>de novo</i> identification due to the stringent criteria for controlling false-positive rate. Caste-specific editing sites are identified, including an Ile&gt;Met auto-recoding site in <i>Adar</i>. This recoding was even conserved between honeybee and bumblebee, suggesting its putative regulatory role in shaping the phenotypic plasticity of eusocial Hymenoptera. In summary, we proposed a complementary approach to the traditional pipeline and retrieved several previously unnoticed CDS editing sites. From both technical and biological aspects, our works facilitate future researches on finding the functional editing sites and advance our understanding on the connection between RNA editing and the great phenotypic diversity of organisms.
DOI: 10.6084/m9.figshare.26982897.v1
title: An orthology-based methodology as a complementary approach to retrieve evolutionarily conserved A-to-I RNA editing sites

description: Adar-mediated adenosine-to-inosine (A-to-I) mRNA editing is a conserved mechanism that exerts diverse regulatory functions during the development, evolution, and adaptation of metazoans. The accurate detection of RNA editing sites helps us understand their biological significance. In this work, with an improved genome assembly of honeybee (<i>Apis mellifera</i>), we used a new orthology-based methodology to complement the traditional pipeline of (<i>de novo</i>) RNA editing detection. Compared to the outcome of traditional pipeline, we retrieved many novel editing sites in CDS that are deeply conserved between honeybee and other distantly related insects. The newly retrieved sites were missed by the traditional <i>de novo</i> identification due to the stringent criteria for controlling false-positive rate. Caste-specific editing sites are identified, including an Ile&gt;Met auto-recoding site in <i>Adar</i>. This recoding was even conserved between honeybee and bumblebee, suggesting its putative regulatory role in shaping the phenotypic plasticity of eusocial Hymenoptera. In summary, we proposed a complementary approach to the traditional pipeline and retrieved several previously unnoticed CDS editing sites. From both technical and biological aspects, our works facilitate future researches on finding the functional editing sites and advance our understanding on the connection between RNA editing and the great phenotypic diversity of organisms.
DOI: 10.6084/m9.figshare.26829764
title: Endogenous ZAP affects Zika virus RNA interactome

description: One of the most recent advances in the analysis of viral RNA-cellular protein interactions is the Comprehensive Identification of RNA-binding Proteins by Mass Spectrometry (ChIRP-MS). Here, we used ChIRP-MS in mock-infected and Zika-infected wild-type cells and cells knockout for the zinc finger CCCH-type antiviral protein 1 (ZAP). We characterized ‘ZAP-independent’ and ‘ZAP-dependent’ cellular protein interactomes associated with flavivirus RNA and found that ZAP affects cellular proteins associated with Zika virus RNA. The ZAP-dependent interactome identified with ChIRP-MS provides potential ZAP co-factors for antiviral activity against Zika virus and possibly other viruses. Identifying the full spectrum of ZAP co-factors and mechanisms of how they act will be critical to understanding the ZAP antiviral system and may contribute to the development of antivirals.
DOI: 10.6084/m9.figshare.26829764.v1
title: Endogenous ZAP affects Zika virus RNA interactome

description: One of the most recent advances in the analysis of viral RNA-cellular protein interactions is the Comprehensive Identification of RNA-binding Proteins by Mass Spectrometry (ChIRP-MS). Here, we used ChIRP-MS in mock-infected and Zika-infected wild-type cells and cells knockout for the zinc finger CCCH-type antiviral protein 1 (ZAP). We characterized ‘ZAP-independent’ and ‘ZAP-dependent’ cellular protein interactomes associated with flavivirus RNA and found that ZAP affects cellular proteins associated with Zika virus RNA. The ZAP-dependent interactome identified with ChIRP-MS provides potential ZAP co-factors for antiviral activity against Zika virus and possibly other viruses. Identifying the full spectrum of ZAP co-factors and mechanisms of how they act will be critical to understanding the ZAP antiviral system and may contribute to the development of antivirals.
DOI: 10.6084/m9.figshare.25243307
title: Mature microRNA-binding protein QKI promotes microRNA-mediated gene silencing

description: Although Argonaute (AGO) proteins have been the focus of microRNA (miRNA) studies, we observed AGO-free mature miRNAs directly interacting with RNA-binding proteins, implying the sophisticated nature of fine-tuning gene regulation by miRNAs. To investigate microRNA-binding proteins (miRBPs) globally, we analyzed PAR-CLIP data sets to identify RBP quaking (QKI) as a novel miRBP for let-7b. Potential existence of AGO-free miRNAs were further verified by measuring miRNA levels in genetically engineered AGO-depleted human and mouse cells. We have shown that QKI regulates miRNA-mediated gene silencing at multiple steps, and collectively serves as an auxiliary factor empowering AGO2/let-7b-mediated gene silencing. Depletion of QKI decreases interaction of AGO2 with let-7b and target mRNA, consequently controlling target mRNA decay. This finding indicates that QKI is a complementary factor in miRNA-mediated mRNA decay. QKI, however, also suppresses the dissociation of let-7b from AGO2, and slows the assembly of AGO2/miRNA/target mRNA complexes at the single-molecule level. We also revealed that QKI overexpression suppresses cMYC expression at post-transcriptional level, and decreases proliferation and migration of HeLa cells, demonstrating that QKI is a tumour suppressor gene by in part augmenting let-7b activity. Our data show that QKI is a new type of RBP implicated in the versatile regulation of miRNA-mediated gene silencing.
DOI: 10.6084/m9.figshare.25243307.v1
title: Mature microRNA-binding protein QKI promotes microRNA-mediated gene silencing

description: Although Argonaute (AGO) proteins have been the focus of microRNA (miRNA) studies, we observed AGO-free mature miRNAs directly interacting with RNA-binding proteins, implying the sophisticated nature of fine-tuning gene regulation by miRNAs. To investigate microRNA-binding proteins (miRBPs) globally, we analyzed PAR-CLIP data sets to identify RBP quaking (QKI) as a novel miRBP for let-7b. Potential existence of AGO-free miRNAs were further verified by measuring miRNA levels in genetically engineered AGO-depleted human and mouse cells. We have shown that QKI regulates miRNA-mediated gene silencing at multiple steps, and collectively serves as an auxiliary factor empowering AGO2/let-7b-mediated gene silencing. Depletion of QKI decreases interaction of AGO2 with let-7b and target mRNA, consequently controlling target mRNA decay. This finding indicates that QKI is a complementary factor in miRNA-mediated mRNA decay. QKI, however, also suppresses the dissociation of let-7b from AGO2, and slows the assembly of AGO2/miRNA/target mRNA complexes at the single-molecule level. We also revealed that QKI overexpression suppresses cMYC expression at post-transcriptional level, and decreases proliferation and migration of HeLa cells, demonstrating that QKI is a tumour suppressor gene by in part augmenting let-7b activity. Our data show that QKI is a new type of RBP implicated in the versatile regulation of miRNA-mediated gene silencing.
DOI: 10.6084/m9.figshare.27174460
title: m6A modification of RNA in cervical cancer: role and clinical perspectives

description: N6-methyladenosine (m6A) is widely recognized as the predominant form of RNA modification in higher organisms, with the capability to finely regulate RNA metabolism, thereby influencing a series of crucial physiological and pathological processes. These processes include regulation of gene expression, cell proliferation, invasion and metastasis, cell cycle control, programmed cell death, interactions within the tumour microenvironment, energy metabolism, and immune regulation. With advancing research into the mechanisms of RNA methylation, the pivotal role of m6A modification in the pathophysiology of reproductive system tumours, particularly cervical cancer, has been progressively unveiled. This discovery has opened new research avenues and presented significant potential for the diagnosis, prognostic evaluation, and treatment of diseases. This review delves deeply into the biological functions of m6A modification and its mechanisms of action in the onset and progression of cervical cancer. Furthermore, it explores the prospects of m6A modification in the precision diagnosis and treatment of cervical cancer, aiming to provide new perspectives and a theoretical basis for innovative and advanced treatment strategies for cervical cancer.
DOI: 10.6084/m9.figshare.27174460.v1
title: m6A modification of RNA in cervical cancer: role and clinical perspectives

description: N6-methyladenosine (m6A) is widely recognized as the predominant form of RNA modification in higher organisms, with the capability to finely regulate RNA metabolism, thereby influencing a series of crucial physiological and pathological processes. These processes include regulation of gene expression, cell proliferation, invasion and metastasis, cell cycle control, programmed cell death, interactions within the tumour microenvironment, energy metabolism, and immune regulation. With advancing research into the mechanisms of RNA methylation, the pivotal role of m6A modification in the pathophysiology of reproductive system tumours, particularly cervical cancer, has been progressively unveiled. This discovery has opened new research avenues and presented significant potential for the diagnosis, prognostic evaluation, and treatment of diseases. This review delves deeply into the biological functions of m6A modification and its mechanisms of action in the onset and progression of cervical cancer. Furthermore, it explores the prospects of m6A modification in the precision diagnosis and treatment of cervical cancer, aiming to provide new perspectives and a theoretical basis for innovative and advanced treatment strategies for cervical cancer.
DOI: 10.6084/m9.figshare.27203404
title: Rbm3 deficiency leads to transcriptome-wide splicing alterations

description: <i>Rbm3</i> (RNA-binding motif protein 3) is a stress responsive gene, which maintains cellular homeostasis and promotes survival upon various harmful cellular stimuli. Rbm3 protein shows conserved structural and molecular similarities to heterogeneous nuclear ribonucleoproteins (hnRNPs), which regulate all steps of the mRNA metabolism. Growing evidence is pointing towards a broader role of Rbm3 in various steps of gene expression. Here, we demonstrate that Rbm3 deficiency is linked to transcriptome-wide pre-mRNA splicing alterations, which can be reversed through Rbm3 co-expression from a cDNA. Using an MS2 tethering assay, we show that Rbm3 regulates splice site selection similar to other hnRNP proteins when recruited between two competing 5 ′ splice sites. Furthermore, we show that the N-terminal part of Rbm3 encompassing the RNA recognition motif (RRM), is sufficient to elicit changes in splice site selection. On the basis of these findings, we propose a novel, undescribed function of Rbm3 in RNA splicing that contributes to the preservation of transcriptome integrity.
DOI: 10.6084/m9.figshare.27203404.v1
title: Rbm3 deficiency leads to transcriptome-wide splicing alterations

description: <i>Rbm3</i> (RNA-binding motif protein 3) is a stress responsive gene, which maintains cellular homeostasis and promotes survival upon various harmful cellular stimuli. Rbm3 protein shows conserved structural and molecular similarities to heterogeneous nuclear ribonucleoproteins (hnRNPs), which regulate all steps of the mRNA metabolism. Growing evidence is pointing towards a broader role of Rbm3 in various steps of gene expression. Here, we demonstrate that Rbm3 deficiency is linked to transcriptome-wide pre-mRNA splicing alterations, which can be reversed through Rbm3 co-expression from a cDNA. Using an MS2 tethering assay, we show that Rbm3 regulates splice site selection similar to other hnRNP proteins when recruited between two competing 5 ′ splice sites. Furthermore, we show that the N-terminal part of Rbm3 encompassing the RNA recognition motif (RRM), is sufficient to elicit changes in splice site selection. On the basis of these findings, we propose a novel, undescribed function of Rbm3 in RNA splicing that contributes to the preservation of transcriptome integrity.
DOI: 10.21233/nkbb-yg34
title: LDDsite1124 ostracode surface sample dataset

description: Raw data for the LDDsite1124 ostracode surface sample dataset submitted to the Neotoma Paleoecology Database. Data is available through the landing page in JSON format. The landing page referenced by the DOI also contains links to publications and a map-based viewer for the dataset. The Neotoma Paleoecology Database maintains a homepage at https://www.neotomadb.org.
DOI: 10.15468/dl.djvmra
title: Occurrence Download

description: A dataset containing 1731 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Tadarida aegyptiaca (E.Geoffroy, 1818)"
 ]
}

 The dataset includes 1731 records from 47 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0026726-250426092105405/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.uxv3a7
title: Occurrence Download

description: A dataset containing 943 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Ambystoma mexicanum (Shaw & Nodder, 1798)"
 ]
}

 The dataset includes 943 records from 63 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0026727-250426092105405/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.21233/aj78-nd62
title: LDDsite3251 ostracode surface sample dataset

description: Raw data for the LDDsite3251 ostracode surface sample dataset submitted to the Neotoma Paleoecology Database. Data is available through the landing page in JSON format. The landing page referenced by the DOI also contains links to publications and a map-based viewer for the dataset. The Neotoma Paleoecology Database maintains a homepage at https://www.neotomadb.org.
DOI: 10.15468/dl.f5a5kp
title: Occurrence Download

description: A dataset containing 1731 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Tadarida aegyptiaca (E.Geoffroy, 1818)"
 ]
}

 The dataset includes 1731 records from 47 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0026728-250426092105405/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.21233/jxmp-pz39
title: Lake Mattoon water chemistry dataset

description: Raw data for the Lake Mattoon water chemistry dataset submitted to the Neotoma Paleoecology Database. Data is available through the landing page in JSON format. The landing page referenced by the DOI also contains links to publications and a map-based viewer for the dataset. The Neotoma Paleoecology Database maintains a homepage at https://www.neotomadb.org.
DOI: 10.6084/m9.figshare.28452551
title: Saltwater intrusion in coastal Lebanon: evolution of patterns, and database for groundwater quality monitoring and management

description: Half a century after the only national-scale report on saltwater intrusion (SWI) in Lebanon, the evolution of this hazard is re-examined. SWI proxies from 4000+ field measurements and chemical samplings are collected from a network of 276 sites. To interpret this dataset, the coast is divided into seven large coastal areas which are then sub-divided into 14 smaller coastal hydrogeological zones (CHZs) reflecting uniform hydrogeological conditions and properties. Hydrochemical analyses characterized the groundwater types of the coast. Fresh–brackish to brackish–salt NaCl or CaCl water types attaining elevated salt content are present in several zones, and ongoing salinization to variable extents affects four CHZs. Porous-unconsolidated aquifers suffered the largest salinization spread compared to fractured karstic aquifers. Over-pumping is the main SWI driver in many zones. Comparing to older results, fast-ascending SWI impacts most coastal groundwater resources. The database from this study is shared to serve urgently needed continuous monitoring of SWI proxies and groundwater resources management.