cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.8319659
title: Inactivation of the RNA helicase CrhR impacts a specific subset of the transcriptome in the cyanobacterium <i>Synechocystis</i> sp. PCC 6803

description: DEAD-box RNA-helicases catalyze the reorganization of structured RNAs and the formation of RNP complexes. The cyanobacterium <i>Synechocystis</i> sp. PCC 6803 encodes a single DEAD-box RNA helicase, CrhR (Slr0083), whose expression is regulated by abiotic stresses that alter the redox potential of the photosynthetic electron transport chain, including temperature downshift. Despite its proposed effect on RNA metabolism and its known relevance in cold-stress adaptation, the reported impact of a CrhR knockout on the cold adaption of the transcriptome only identified eight affected genes. Here, we utilized a custom designed microarray to assess the impact of the absence of CrhR RNA helicase activity on the transcriptome, independent of cold stress. CrhR truncation impacts an RNA subset comprising ~10% of the ncRNA and also ~10% of the mRNA transcripts. While equal numbers of mRNAs showed increased as well as decreased abundance, more than 90% of the ncRNAs showed enhanced expression in the absence of CrhR, indicative of a negative effect on ncRNA transcription or stability. We further tested the effect of CrhR on the stability of strongly responding RNAs that identify examples of post-transcriptional and transcriptional regulation. The data suggest that CrhR impacts multiple aspects of RNA metabolism in <i>Synechocystis</i>.
DOI: 10.6084/m9.figshare.8319668.v2
title: Strand-specific affinity of host factor hnRNP C1/C2 guides positive to negative-strand ratio in Coxsackievirus B3 infection

description: Coxsackievirus B3 is an enterovirus, with positive-sense single-stranded RNA genome containing ‘Internal Ribosome Entry Site’ (IRES) in the 5ʹUTR. Once sufficient viral proteins are synthesized in the cell from the input RNA, viral template switches from translation to replication to synthesize negative-strand RNA. Inhibition of translation is a key step in regulating this switch as the positive-strand RNA template should be free of ribosomes to enable polymerase movement. In this study, we show how a host protein hnRNP C1/C2 inhibits viral RNA translation. hnRNP C1/C2 interacts with stem-loop V in the IRES and displaces poly-pyrimidine tract binding protein, a positive regulator of translation. We further demonstrate that hnRNP C1/C2 induces translation to replication switch, independently from the already known role of the ternary complex (PCBP2-3CD-cloverleaf RNA). These results suggest a novel function of hnRNP C1/C2 in template switching of positive-strand from translation to replication by a new mechanism. Using mathematical modelling, we show that the differential affinity of hnRNP C1/C2 for positive and negative-strand RNAs guides the final ± RNA ratio, providing first insight in the regulation of the positive to negative-strand RNA ratio in enteroviruses.
DOI: 10.6084/m9.figshare.8319668.v1
title: Strand-specific affinity of host factor hnRNP C1/C2 guides positive to negative-strand ratio in Coxsackievirus B3 infection

description: Coxsackievirus B3 is an enterovirus, with positive-sense single-stranded RNA genome containing ‘Internal Ribosome Entry Site’ (IRES) in the 5ʹUTR. Once sufficient viral proteins are synthesized in the cell from the input RNA, viral template switches from translation to replication to synthesize negative-strand RNA. Inhibition of translation is a key step in regulating this switch as the positive-strand RNA template should be free of ribosomes to enable polymerase movement. In this study, we show how a host protein hnRNP C1/C2 inhibits viral RNA translation. hnRNP C1/C2 interacts with stem-loop V in the IRES and displaces poly-pyrimidine tract binding protein, a positive regulator of translation. We further demonstrate that hnRNP C1/C2 induces translation to replication switch, independently from the already known role of the ternary complex (PCBP2-3CD-cloverleaf RNA). These results suggest a novel function of hnRNP C1/C2 in template switching of positive-strand from translation to replication by a new mechanism. Using mathematical modelling, we show that the differential affinity of hnRNP C1/C2 for positive and negative-strand RNAs guides the final ± RNA ratio, providing first insight in the regulation of the positive to negative-strand RNA ratio in enteroviruses.
DOI: 10.6084/m9.figshare.8319659.v2
title: Inactivation of the RNA helicase CrhR impacts a specific subset of the transcriptome in the cyanobacterium <i>Synechocystis</i> sp. PCC 6803

description: DEAD-box RNA-helicases catalyze the reorganization of structured RNAs and the formation of RNP complexes. The cyanobacterium <i>Synechocystis</i> sp. PCC 6803 encodes a single DEAD-box RNA helicase, CrhR (Slr0083), whose expression is regulated by abiotic stresses that alter the redox potential of the photosynthetic electron transport chain, including temperature downshift. Despite its proposed effect on RNA metabolism and its known relevance in cold-stress adaptation, the reported impact of a CrhR knockout on the cold adaption of the transcriptome only identified eight affected genes. Here, we utilized a custom designed microarray to assess the impact of the absence of CrhR RNA helicase activity on the transcriptome, independent of cold stress. CrhR truncation impacts an RNA subset comprising ~10% of the ncRNA and also ~10% of the mRNA transcripts. While equal numbers of mRNAs showed increased as well as decreased abundance, more than 90% of the ncRNAs showed enhanced expression in the absence of CrhR, indicative of a negative effect on ncRNA transcription or stability. We further tested the effect of CrhR on the stability of strongly responding RNAs that identify examples of post-transcriptional and transcriptional regulation. The data suggest that CrhR impacts multiple aspects of RNA metabolism in <i>Synechocystis</i>.
DOI: 10.6084/m9.figshare.8319659.v1
title: Inactivation of the RNA helicase CrhR impacts a specific subset of the transcriptome in the cyanobacterium <i>Synechocystis</i> sp. PCC 6803

description: DEAD-box RNA-helicases catalyze the reorganization of structured RNAs and the formation of RNP complexes. The cyanobacterium <i>Synechocystis</i> sp. PCC 6803 encodes a single DEAD-box RNA helicase, CrhR (Slr0083), whose expression is regulated by abiotic stresses that alter the redox potential of the photosynthetic electron transport chain, including temperature downshift. Despite its proposed effect on RNA metabolism and its known relevance in cold-stress adaptation, the reported impact of a CrhR knockout on the cold adaption of the transcriptome only identified eight affected genes. Here, we utilized a custom designed microarray to assess the impact of the absence of CrhR RNA helicase activity on the transcriptome, independent of cold stress. CrhR truncation impacts an RNA subset comprising ~10% of the ncRNA and also ~10% of the mRNA transcripts. While equal numbers of mRNAs showed increased as well as decreased abundance, more than 90% of the ncRNAs showed enhanced expression in the absence of CrhR, indicative of a negative effect on ncRNA transcription or stability. We further tested the effect of CrhR on the stability of strongly responding RNAs that identify examples of post-transcriptional and transcriptional regulation. The data suggest that CrhR impacts multiple aspects of RNA metabolism in <i>Synechocystis</i>.
DOI: 10.6084/m9.figshare.8319635
title: <i>Talking in Time</i>: The development of a self-administered conversation analysis based training programme for cochlear implant users

description: <b>Objectives:</b> Training software to facilitate participation in conversations where overlapping talk is common was to be developed with the involvement of Cochlear implant (CI) users. <b>Methods:</b> Examples of common types of overlap were extracted from a recorded corpus of 3.5 hours of British English conversation. In eight meetings, an expert panel of five CI users tried out ideas for a computer-based training programme addressing difficulties in turn-taking. <b>Results:</b> Based on feedback from the panel, a training programme was devised. The first module consists of introductory videos. The three remaining modules, implemented in interactive software, focus on non-overlapped turn-taking, competitive overlaps and accidental overlaps. <b>Discussion:</b> The development process is considered in light of feedback from panel members and from an end of project dissemination event. Benefits, limitations and challenges of the present approach to user involvement and to the design of self-administered communication training programmes are discussed. <b>Conclusion:</b> The project was characterized by two innovative features: the involvement of service users not only at its outset and conclusion but throughout its course; and the exclusive use of naturally occurring conversational speech in the training programme. While both present practical challenges, the project has demonstrated the potential for ecologically valid speech rehabilitation training.
DOI: 10.6084/m9.figshare.8319635.v1
title: <i>Talking in Time</i>: The development of a self-administered conversation analysis based training programme for cochlear implant users

description: <b>Objectives:</b> Training software to facilitate participation in conversations where overlapping talk is common was to be developed with the involvement of Cochlear implant (CI) users. <b>Methods:</b> Examples of common types of overlap were extracted from a recorded corpus of 3.5 hours of British English conversation. In eight meetings, an expert panel of five CI users tried out ideas for a computer-based training programme addressing difficulties in turn-taking. <b>Results:</b> Based on feedback from the panel, a training programme was devised. The first module consists of introductory videos. The three remaining modules, implemented in interactive software, focus on non-overlapped turn-taking, competitive overlaps and accidental overlaps. <b>Discussion:</b> The development process is considered in light of feedback from panel members and from an end of project dissemination event. Benefits, limitations and challenges of the present approach to user involvement and to the design of self-administered communication training programmes are discussed. <b>Conclusion:</b> The project was characterized by two innovative features: the involvement of service users not only at its outset and conclusion but throughout its course; and the exclusive use of naturally occurring conversational speech in the training programme. While both present practical challenges, the project has demonstrated the potential for ecologically valid speech rehabilitation training.
DOI: 10.6084/m9.figshare.8319530
title: MOESM2 of Cheminformatics approach to exploring and modeling trait-associated metabolite profiles

description: Additional file 2. The scripts and additional data necessary to recreate our analyses.
DOI: 10.6084/m9.figshare.8319530.v1
title: MOESM2 of Cheminformatics approach to exploring and modeling trait-associated metabolite profiles

description: Additional file 2. The scripts and additional data necessary to recreate our analyses.
DOI: 10.6084/m9.figshare.8319506
title: Additional file 2 of Performance of neural network basecalling tools for Oxford Nanopore sequencing

description: Supplementary tables. This spreadsheet contains tables with information on each test read set, basecaller commands, all accuracy and error data results, and information on the training sets used for the custom models. (XLSX 85 kb)
DOI: 10.6084/m9.figshare.8319506.v1
title: Additional file 2 of Performance of neural network basecalling tools for Oxford Nanopore sequencing

description: Supplementary tables. This spreadsheet contains tables with information on each test read set, basecaller commands, all accuracy and error data results, and information on the training sets used for the custom models. (XLSX 85 kb)
DOI: 10.6084/m9.figshare.8319335
title: Additional file 1: of Genomic characterization of MDR/XDR-TB in Kazakhstan by a combination of high-throughput methods predominantly shows the ongoing transmission of L2/Beijing 94–32 central Asian/Russian clusters

description: Table S1. detailed TB-SPRINT results on 700 MTC DNA samples from Kazakhstan (n = 677 spoligotypes including 3 potential “mixed infection”, 23 failed). Table S2. detailed TB-SNPID results on 470 MTC DNA samples from Kazakhstan (n = 543 analysed, 73 failed). Table S3. Lineage and Sublineage assignation of Spoligotyping results (n = 677). Table S4. All isolates (n = 93) of “set1” (i.e. chronologically first set) typed by two methods: TB-SPRINT and TB-SNPID. Table S5. Detailed results for n = 391 samples run both by TB-SPRINT and TB-SNPID. Table S6. Analysis of discrepant drug-resistance results between TB-SPRINT and TB-SNPID on the 391 set of isolates. Table S7. congruence between SigE and RD131 (TB-SNPID) results in Aktobe suggests the presence of a single DST L2/Beijing 94–32 clone. Table S8. Chi2 square statistics on L2/L4 prevalence in some regions of Kazakhstan. (XLSX 318 kb)
DOI: 10.6084/m9.figshare.8319335.v1
title: Additional file 1: of Genomic characterization of MDR/XDR-TB in Kazakhstan by a combination of high-throughput methods predominantly shows the ongoing transmission of L2/Beijing 94–32 central Asian/Russian clusters

description: Table S1. detailed TB-SPRINT results on 700 MTC DNA samples from Kazakhstan (n = 677 spoligotypes including 3 potential “mixed infection”, 23 failed). Table S2. detailed TB-SNPID results on 470 MTC DNA samples from Kazakhstan (n = 543 analysed, 73 failed). Table S3. Lineage and Sublineage assignation of Spoligotyping results (n = 677). Table S4. All isolates (n = 93) of “set1” (i.e. chronologically first set) typed by two methods: TB-SPRINT and TB-SNPID. Table S5. Detailed results for n = 391 samples run both by TB-SPRINT and TB-SNPID. Table S6. Analysis of discrepant drug-resistance results between TB-SPRINT and TB-SNPID on the 391 set of isolates. Table S7. congruence between SigE and RD131 (TB-SNPID) results in Aktobe suggests the presence of a single DST L2/Beijing 94–32 clone. Table S8. Chi2 square statistics on L2/L4 prevalence in some regions of Kazakhstan. (XLSX 318 kb)
DOI: 10.6084/m9.figshare.8319281
title: Additional file 9: of A comparative study of microbial community and dynamics of Asaia in the brown planthopper from susceptible and resistant rice varieties

description: Bacterial sequences of the F6 generation BPHs from the resistant, IR36, rice variety. (TXT 22 kb)
DOI: 10.6084/m9.figshare.8319281.v1
title: Additional file 9: of A comparative study of microbial community and dynamics of Asaia in the brown planthopper from susceptible and resistant rice varieties

description: Bacterial sequences of the F6 generation BPHs from the resistant, IR36, rice variety. (TXT 22 kb)
DOI: 10.6084/m9.figshare.8319239
title: Additional file 11: of A comparative study of microbial community and dynamics of Asaia in the brown planthopper from susceptible and resistant rice varieties

description: Bacterial sequences of the F6 generation BPHs from the resistant, RH, rice variety. (XLSX 10 kb)
DOI: 10.6084/m9.figshare.8319239.v1
title: Additional file 11: of A comparative study of microbial community and dynamics of Asaia in the brown planthopper from susceptible and resistant rice varieties

description: Bacterial sequences of the F6 generation BPHs from the resistant, RH, rice variety. (XLSX 10 kb)
DOI: 10.6084/m9.figshare.8319233
title: Additional file 10: of A comparative study of microbial community and dynamics of Asaia in the brown planthopper from susceptible and resistant rice varieties

description: Bacterial sequences of the F16 generation BPHs from the IR36 rice variety. (XLSX 18 kb)
DOI: 10.6084/m9.figshare.8319233.v1
title: Additional file 10: of A comparative study of microbial community and dynamics of Asaia in the brown planthopper from susceptible and resistant rice varieties

description: Bacterial sequences of the F16 generation BPHs from the IR36 rice variety. (XLSX 18 kb)
DOI: 10.6084/m9.figshare.8319224
title: Additional file 9: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S9. MAML3 translocation-positive PPGL master regulators (dpiâ =â 0.05). (CSV 21 kb)
DOI: 10.6084/m9.figshare.8319218
title: Additional file 8: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S8. VHL-loss PPGL master regulators (dpiâ =â 0.05). (CSV 22 kb)
DOI: 10.6084/m9.figshare.8319224.v1
title: Additional file 9: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S9. MAML3 translocation-positive PPGL master regulators (dpiâ =â 0.05). (CSV 21 kb)
DOI: 10.6084/m9.figshare.8319218.v1
title: Additional file 8: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S8. VHL-loss PPGL master regulators (dpiâ =â 0.05). (CSV 22 kb)
DOI: 10.6084/m9.figshare.8319209
title: Additional file 6: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S6. MAML3 translocation-positive PPGL master regulators (dpiâ =â 0.00). (CSV 19 kb)
DOI: 10.6084/m9.figshare.8319212
title: Additional file 7: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S7. SDHB-loss PPGL master regulators (dpiâ =â 0.05). (CSV 22 kb)
DOI: 10.6084/m9.figshare.8319212.v1
title: Additional file 7: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S7. SDHB-loss PPGL master regulators (dpiâ =â 0.05). (CSV 22 kb)
DOI: 10.6084/m9.figshare.8319203
title: Additional file 5: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S5. VHL-loss PPGL master regulators (dpiâ =â 0.00). (CSV 18 kb)
DOI: 10.6084/m9.figshare.8319209.v1
title: Additional file 6: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S6. MAML3 translocation-positive PPGL master regulators (dpiâ =â 0.00). (CSV 19 kb)
DOI: 10.6084/m9.figshare.8319197
title: Additional file 4: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S4. SDHB-loss PPGL master regulators (dpiâ =â 0.00). (CSV 18 kb)
DOI: 10.6084/m9.figshare.8319203.v1
title: Additional file 5: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S5. VHL-loss PPGL master regulators (dpiâ =â 0.00). (CSV 18 kb)
DOI: 10.6084/m9.figshare.8319197.v1
title: Additional file 4: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S4. SDHB-loss PPGL master regulators (dpiâ =â 0.00). (CSV 18 kb)
DOI: 10.6084/m9.figshare.8319191
title: Additional file 2: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S2. VHL-loss PPGL differential gene expression signature. (CSV 11 kb)
DOI: 10.6084/m9.figshare.8319194
title: Additional file 3: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S3. MAML3 translocation-positive PPGL differential gene expression signature. (CSV 19 kb)
DOI: 10.6084/m9.figshare.8319194.v1
title: Additional file 3: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S3. MAML3 translocation-positive PPGL differential gene expression signature. (CSV 19 kb)
DOI: 10.6084/m9.figshare.8319185
title: Additional file 1: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S1. SDHB-loss PPGL differential gene expression signature. (CSV 14 kb)
DOI: 10.6084/m9.figshare.8319191.v1
title: Additional file 2: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S2. VHL-loss PPGL differential gene expression signature. (CSV 11 kb)
DOI: 10.6084/m9.figshare.8319185.v1
title: Additional file 1: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S1. SDHB-loss PPGL differential gene expression signature. (CSV 14 kb)
DOI: 10.6084/m9.figshare.8319140
title: Additional file 11: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S11. SDHC-loss iMEF master regulators. (CSV 19 kb)
DOI: 10.6084/m9.figshare.8319140.v1
title: Additional file 11: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S11. SDHC-loss iMEF master regulators. (CSV 19 kb)
DOI: 10.6084/m9.figshare.8319137
title: Additional file 10: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S10. PPGL regulon overlaps. (CSV 3893 kb)
DOI: 10.6084/m9.figshare.8319137.v1
title: Additional file 10: of Master regulator analysis of paragangliomas carrying SDHx, VHL, or MAML3 genetic alterations

description: Dataset S10. PPGL regulon overlaps. (CSV 3893 kb)
DOI: 10.6084/m9.figshare.8319110
title: Additional file 8: of RNA-Seq in 296 phased trios provides a high-resolution map of genomic imprinting

description: Results of clonality analysis in LCLs. Reanalysis of unique gene fragments with FDR qâ
DOI: 10.6084/m9.figshare.8319110.v1
title: Additional file 8: of RNA-Seq in 296 phased trios provides a high-resolution map of genomic imprinting

description: Results of clonality analysis in LCLs. Reanalysis of unique gene fragments with FDR qâ
DOI: 10.6084/m9.figshare.8319101
title: Additional file 6: of RNA-Seq in 296 phased trios provides a high-resolution map of genomic imprinting

description: Comparison of LCL/WB imprinting results with previous studies. We list all genes identified as imprinted either in our dataset, as well as those reported as imprinted in recent studies that used RNAseq data in either the GTEx cohort or the Icelandic population. (XLSX 41 kb)
DOI: 10.6084/m9.figshare.8319095
title: Additional file 4: of RNA-Seq in 296 phased trios provides a high-resolution map of genomic imprinting

description: All unique gene fragments tested in this analysis. Data for all UGFs in the genome. (XLSX 19820 kb)
DOI: 10.6084/m9.figshare.8319101.v1
title: Additional file 6: of RNA-Seq in 296 phased trios provides a high-resolution map of genomic imprinting

description: Comparison of LCL/WB imprinting results with previous studies. We list all genes identified as imprinted either in our dataset, as well as those reported as imprinted in recent studies that used RNAseq data in either the GTEx cohort or the Icelandic population. (XLSX 41 kb)
DOI: 10.6084/m9.figshare.8319092
title: Additional file 3: of RNA-Seq in 296 phased trios provides a high-resolution map of genomic imprinting

description: 78 significant unique gene fragments. All UGFs with FDR qâ
DOI: 10.6084/m9.figshare.8319095.v1
title: Additional file 4: of RNA-Seq in 296 phased trios provides a high-resolution map of genomic imprinting

description: All unique gene fragments tested in this analysis. Data for all UGFs in the genome. (XLSX 19820 kb)
DOI: 10.6084/m9.figshare.8319092.v1
title: Additional file 3: of RNA-Seq in 296 phased trios provides a high-resolution map of genomic imprinting

description: 78 significant unique gene fragments. All UGFs with FDR qâ