cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1476253.v3
title: Global analysis of biogenesis, stability and sub-cellular localization of lncRNAs mapping to intragenic regions of the human genome

description: Long noncoding RNAs (lncRNAs) that map to intragenic regions of the human genome with the same (intronic lncRNAs) or opposite orientation (antisense lncRNAs) relative to protein-coding mRNAs have been largely dismissed from biochemical and functional characterization due to the belief that they are mRNA precursors, byproducts of RNA splicing or simply transcriptional noise. In this work, we used a custom microarray to investigate aspects of the biogenesis, processing, stability, evolutionary conservation, and cellular localization of ∼6,000 intronic lncRNAs and ∼10,000 antisense lncRNAs. Most intronic (2,903 of 3,427, 85%) and antisense lncRNAs (4,945 of 5,214, 95%) expressed in HeLa cells showed evidence of 5′ cap modification, compatible with their transcription by RNAP II. Antisense lncRNAs (median t<sub>1/2</sub> = 3.9 h) were significantly (<i>p</i> &lt; 0.0001) more stable than mRNAs (median t<sub>1/2</sub> = 3.2 h), whereas intronic lncRNAs (median t<sub>1/2</sub> = 2.1 h) comprised a more heterogeneous class that included both stable (t<sub>1/2</sub> &gt; 3 h) and unstable (t<sub>1/2</sub> &lt; 1 h) transcripts. Intragenic lncRNAs display evidence of evolutionary conservation, have little/no coding potential and were ubiquitously detected in the cytoplasm. Notably, a fraction of the intronic and antisense lncRNAs (13 and 15%, respectively) were expressed from loci at which the corresponding host mRNA was not detected. The abundances of a subset of intronic/antisense lncRNAs were correlated (r ≥ |0.8|) with those of genes encoding proteins involved in cell division and DNA replication. Taken together, the findings of this study contribute novel biochemical and genomic information regarding intronic and antisense lncRNAs, supporting the notion that these classes include independently transcribed RNAs with potentials for exerting regulatory functions in the cell.
DOI: 10.6084/m9.figshare.1476248.v1
title: Temperature dependence of NDR effect

description: Temperature dependence of NDR effect, this is a trial run looking at meeting the open data requirements
DOI: 10.6084/m9.figshare.1476244
title: Data from Ingested plastic as a vector for trace metals in Laysan Albatross (Phoebastria immutabilis) and Bonin Petrel (Pterodroma hypoleuca) from Midway Atoll

description: Data to accompany Lavers, J.L., and A.L. Bond. Ingested plastic as a vector for trace metals in Laysan Albatross (<em>Phoebastria immutabilis</em>) and Bonin Petrel (<em>Pterodroma hypoleuca</em>) from Midway Atoll. Marine Pollution Bulletin
DOI: 10.6084/m9.figshare.1476246
title: The novel function of JADE1S in cytokinesis of epithelial cells

description: JADE1 belongs to a small family of PHD zinc finger proteins that interacts with histone acetyl transferase (HAT) HBO1 and is associated with chromatin. We recently reported JADE1 chromatin shuttling and phosphorylation during G2/M to G1 transition, which was sensitive to Aurora A inhibition. In the current study we examined mechanisms of the cell cycle regulation by the small isoform of JADE1 protein, JADE1S, and report data showing that JADE1S has a novel function in the regulation of cytokinesis. Using FACS assays, we show that, JADE1S depletion facilitated rates of G1-cells accumulation in synchronously dividing HeLa cell cultures. Depletion of JADE1S protein in asynchronously dividing cells decreased the proportion of cytokinetic cells, and increased the proportion of multi-nuclear cells, indicative of premature and failed cytokinesis. In contrast, moderate overexpression of JADE1S increased the number of cytokinetic cells in time- and dose- dependent manner, indicating cytokinetic delay. Pharmacological inhibition of Aurora B kinase resulted in the release of JADE1S-mediated cytokinetic delay and allowed progression of abscission in cells over-expressing JADE1S. Finally, we show that JADE1S protein localized to centrosomes in interphase and mitotic cells, while during cytokinesis JADE1S localized to the midbody. Neither JADE1L nor partner of JADE1, HAT HBO1 was localized to the centrosomes or midbodies. Our study identifies the novel role for JADE1S in regulation of cytokinesis and suggests function in Aurora B kinase-mediated cytokinesis checkpoint.
DOI: 10.6084/m9.figshare.1476244.v1
title: Data from Ingested plastic as a vector for trace metals in Laysan Albatross (Phoebastria immutabilis) and Bonin Petrel (Pterodroma hypoleuca) from Midway Atoll

description: Data to accompany Lavers, J.L., and A.L. Bond. Ingested plastic as a vector for trace metals in Laysan Albatross (<em>Phoebastria immutabilis</em>) and Bonin Petrel (<em>Pterodroma hypoleuca</em>) from Midway Atoll. Marine Pollution Bulletin
DOI: 10.6084/m9.figshare.1476247.v1
title: Chromosomal instability, tolerance of mitotic errors and multidrug resistance are promoted by tetraploidization in human cells

description: Up to 80 % of human cancers, in particular solid tumors, contain cells with abnormal chromosomal numbers, or aneuploidy, which is often linked with marked chromosomal instability. Whereas in some tumor the aneuploidy occurs by missegregation of one or a few chromosomes, aneuploidy can also arise by proliferation of inherently unstable tetraploid cells generated by whole genome doubling from diploid cells. Recent findings from cancer genome sequencing projects suggest that nearly 40 % of tumors underwent whole genome doubling at some point of tumorigenesis, yet its contribution to cancer phenotypes and benefits for malignant growth remain unclear. Here, we investigated the consequences of a whole genome doubling in both cancerous and non-transformed p53 positive human cells. SNP array analysis and multicolor karyotyping revealed that induced whole-genome doubling led to variable aneuploidy. We found that chromosomal instability (CIN) is a frequent, but not a default outcome of whole genome doubling. The CIN phenotypes were accompanied by increased tolerance to mitotic errors that was mediated by suppression of the p53 signaling. Additionally, the expression of pro-apoptotic factors, such as iASPP and cIAP2, was downregulated. Furthermore, we found that whole genome doubling promotes marked resistance to a broad spectrum of chemotherapeutic drugs and stimulates anchorage-independent growth even in non-transformed p53-positive human cells. Taken together, whole genome doubling provides multifaceted benefits for malignant growth. Our findings provide new insight why genome-doubling promotes tumorigenesis and correlates with poor survival in cancer.
DOI: 10.6084/m9.figshare.1476247
title: Chromosomal instability, tolerance of mitotic errors and multidrug resistance are promoted by tetraploidization in human cells

description: Up to 80% of human cancers, in particular solid tumors, contain cells with abnormal chromosomal numbers, or aneuploidy, which is often linked with marked chromosomal instability. Whereas in some tumors the aneuploidy occurs by missegregation of one or a few chromosomes, aneuploidy can also arise during proliferation of inherently unstable tetraploid cells generated by whole genome doubling from diploid cells. Recent findings from cancer genome sequencing projects suggest that nearly 40% of tumors underwent whole genome doubling at some point of tumorigenesis, yet its contribution to cancer phenotypes and benefits for malignant growth remain unclear. Here, we investigated the consequences of a whole genome doubling in both cancerous and non-transformed p53 positive human cells. SNP array analysis and multicolor karyotyping revealed that induced whole-genome doubling led to variable aneuploidy. We found that chromosomal instability (CIN) is a frequent, but not a default outcome of whole genome doubling. The CIN phenotypes were accompanied by increased tolerance to mitotic errors that was mediated by suppression of the p53 signaling. Additionally, the expression of pro-apoptotic factors, such as iASPP and cIAP2, was downregulated. Furthermore, we found that whole genome doubling promotes resistance to a broad spectrum of chemotherapeutic drugs and stimulates anchorage-independent growth even in non-transformed p53-positive human cells. Taken together, whole genome doubling provides multifaceted benefits for malignant growth. Our findings provide new insight why genome-doubling promotes tumorigenesis and correlates with poor survival in cancer.
DOI: 10.6084/m9.figshare.1476247.v2
title: Chromosomal instability, tolerance of mitotic errors and multidrug resistance are promoted by tetraploidization in human cells

description: Up to 80% of human cancers, in particular solid tumors, contain cells with abnormal chromosomal numbers, or aneuploidy, which is often linked with marked chromosomal instability. Whereas in some tumors the aneuploidy occurs by missegregation of one or a few chromosomes, aneuploidy can also arise during proliferation of inherently unstable tetraploid cells generated by whole genome doubling from diploid cells. Recent findings from cancer genome sequencing projects suggest that nearly 40% of tumors underwent whole genome doubling at some point of tumorigenesis, yet its contribution to cancer phenotypes and benefits for malignant growth remain unclear. Here, we investigated the consequences of a whole genome doubling in both cancerous and non-transformed p53 positive human cells. SNP array analysis and multicolor karyotyping revealed that induced whole-genome doubling led to variable aneuploidy. We found that chromosomal instability (CIN) is a frequent, but not a default outcome of whole genome doubling. The CIN phenotypes were accompanied by increased tolerance to mitotic errors that was mediated by suppression of the p53 signaling. Additionally, the expression of pro-apoptotic factors, such as iASPP and cIAP2, was downregulated. Furthermore, we found that whole genome doubling promotes resistance to a broad spectrum of chemotherapeutic drugs and stimulates anchorage-independent growth even in non-transformed p53-positive human cells. Taken together, whole genome doubling provides multifaceted benefits for malignant growth. Our findings provide new insight why genome-doubling promotes tumorigenesis and correlates with poor survival in cancer.
DOI: 10.6084/m9.figshare.1476246.v2
title: The novel function of JADE1S in cytokinesis of epithelial cells

description: JADE1 belongs to a small family of PHD zinc finger proteins that interacts with histone acetyl transferase (HAT) HBO1 and is associated with chromatin. We recently reported JADE1 chromatin shuttling and phosphorylation during G2/M to G1 transition, which was sensitive to Aurora A inhibition. In the current study we examined mechanisms of the cell cycle regulation by the small isoform of JADE1 protein, JADE1S, and report data showing that JADE1S has a novel function in the regulation of cytokinesis. Using FACS assays, we show that, JADE1S depletion facilitated rates of G1-cells accumulation in synchronously dividing HeLa cell cultures. Depletion of JADE1S protein in asynchronously dividing cells decreased the proportion of cytokinetic cells, and increased the proportion of multi-nuclear cells, indicative of premature and failed cytokinesis. In contrast, moderate overexpression of JADE1S increased the number of cytokinetic cells in time- and dose- dependent manner, indicating cytokinetic delay. Pharmacological inhibition of Aurora B kinase resulted in the release of JADE1S-mediated cytokinetic delay and allowed progression of abscission in cells over-expressing JADE1S. Finally, we show that JADE1S protein localized to centrosomes in interphase and mitotic cells, while during cytokinesis JADE1S localized to the midbody. Neither JADE1L nor partner of JADE1, HAT HBO1 was localized to the centrosomes or midbodies. Our study identifies the novel role for JADE1S in regulation of cytokinesis and suggests function in Aurora B kinase-mediated cytokinesis checkpoint.
DOI: 10.6084/m9.figshare.1476247.v4
title: Chromosomal instability, tolerance of mitotic errors and multidrug resistance are promoted by tetraploidization in human cells

description: Up to 80% of human cancers, in particular solid tumors, contain cells with abnormal chromosomal numbers, or aneuploidy, which is often linked with marked chromosomal instability. Whereas in some tumors the aneuploidy occurs by missegregation of one or a few chromosomes, aneuploidy can also arise during proliferation of inherently unstable tetraploid cells generated by whole genome doubling from diploid cells. Recent findings from cancer genome sequencing projects suggest that nearly 40% of tumors underwent whole genome doubling at some point of tumorigenesis, yet its contribution to cancer phenotypes and benefits for malignant growth remain unclear. Here, we investigated the consequences of a whole genome doubling in both cancerous and non-transformed p53 positive human cells. SNP array analysis and multicolor karyotyping revealed that induced whole-genome doubling led to variable aneuploidy. We found that chromosomal instability (CIN) is a frequent, but not a default outcome of whole genome doubling. The CIN phenotypes were accompanied by increased tolerance to mitotic errors that was mediated by suppression of the p53 signaling. Additionally, the expression of pro-apoptotic factors, such as iASPP and cIAP2, was downregulated. Furthermore, we found that whole genome doubling promotes resistance to a broad spectrum of chemotherapeutic drugs and stimulates anchorage-independent growth even in non-transformed p53-positive human cells. Taken together, whole genome doubling provides multifaceted benefits for malignant growth. Our findings provide new insight why genome-doubling promotes tumorigenesis and correlates with poor survival in cancer.
DOI: 10.6084/m9.figshare.1476246.v3
title: The novel function of JADE1S in cytokinesis of epithelial cells

description: JADE1 belongs to a small family of PHD zinc finger proteins that interacts with histone acetyl transferase (HAT) HBO1 and is associated with chromatin. We recently reported JADE1 chromatin shuttling and phosphorylation during G2/M to G1 transition, which was sensitive to Aurora A inhibition. In the current study we examined mechanisms of the cell cycle regulation by the small isoform of JADE1 protein, JADE1S, and report data showing that JADE1S has a novel function in the regulation of cytokinesis. Using FACS assays, we show that, JADE1S depletion facilitated rates of G1-cells accumulation in synchronously dividing HeLa cell cultures. Depletion of JADE1S protein in asynchronously dividing cells decreased the proportion of cytokinetic cells, and increased the proportion of multi-nuclear cells, indicative of premature and failed cytokinesis. In contrast, moderate overexpression of JADE1S increased the number of cytokinetic cells in time- and dose- dependent manner, indicating cytokinetic delay. Pharmacological inhibition of Aurora B kinase resulted in the release of JADE1S-mediated cytokinetic delay and allowed progression of abscission in cells over-expressing JADE1S. Finally, we show that JADE1S protein localized to centrosomes in interphase and mitotic cells, while during cytokinesis JADE1S localized to the midbody. Neither JADE1L nor partner of JADE1, HAT HBO1 was localized to the centrosomes or midbodies. Our study identifies the novel role for JADE1S in regulation of cytokinesis and suggests function in Aurora B kinase-mediated cytokinesis checkpoint.
DOI: 10.6084/m9.figshare.1476209
title: Behave_BMPS_Uncertainty_All Data Points

description: Data of post-movement beta synchronisation recorded through EEG during sensorimotor control in 15 subjects, with 31 data points for each subject in each experimental condition. There are two experimental conditions: stable-world priming and random-world priming.
DOI: 10.6084/m9.figshare.1476209.v1
title: Behave_BMPS_Uncertainty_All Data Points

description: Data of post-movement beta synchronisation recorded through EEG during sensorimotor control in 15 subjects, with 31 data points for each subject in each experimental condition. There are two experimental conditions: stable-world priming and random-world priming.
DOI: 10.6084/m9.figshare.1476210
title: Analysis of Norway spruce dieback phenomenon in Latvia – a belowground perspective

description: In 2010, dieback of Norway spruce (<i>Picea abies</i>) was observed in Latvia. As mostly stands on seasonally or permanently water-saturated soils were damaged, we hypothesized that the recorded foliar damage might be associated with belowground factors. We established 48 sample plots in stands with damage symptoms for soil parameter evaluation and fine root sampling to determine the number of fine roots in different growth stages and to describe the associated fungal community. Among sample plots on organic soils, there were fewer viable older fine roots and greater number of dead fine roots in more damaged sites than in less damaged. These root parameters were significantly correlated with higher groundwater level and soil pH. The fungal community was dominated by ectomycorrhizal (ECM) species (the most common was <i>Tylospora asterophora</i>), the endophyte <i>Oidiodendron maius</i> and saprotrophic species <i>Cryptococcus magnus</i>. Saprotrophic species had higher abundance in more damaged sites, suggesting a shift in fungal communities from ECM fungi. In conclusion, the results of this work suggest Norway spruce root system response to short-term climatic stress, which should be considered when planning spruce forest management, especially on organic soils with a high groundwater level.
DOI: 10.6084/m9.figshare.1476208
title: PMBS_DifTrial_DifCondition

description: Average post-movement beta synchronisation at different trial number during sensorimotor adaptation with different priming condition.
DOI: 10.6084/m9.figshare.1476208.v1
title: PMBS_DifTrial_DifCondition

description: Average post-movement beta synchronisation at different trial number during sensorimotor adaptation with different priming condition.
DOI: 10.6084/m9.figshare.1476210.v2
title: Analysis of Norway spruce dieback phenomenon in Latvia – a belowground perspective

description: In 2010, dieback of Norway spruce (<i>Picea abies</i>) was observed in Latvia. As mostly stands on seasonally or permanently water-saturated soils were damaged, we hypothesized that the recorded foliar damage might be associated with belowground factors. We established 48 sample plots in stands with damage symptoms for soil parameter evaluation and fine root sampling to determine the number of fine roots in different growth stages and to describe the associated fungal community. Among sample plots on organic soils, there were fewer viable older fine roots and greater number of dead fine roots in more damaged sites than in less damaged. These root parameters were significantly correlated with higher groundwater level and soil pH. The fungal community was dominated by ectomycorrhizal (ECM) species (the most common was <i>Tylospora asterophora</i>), the endophyte <i>Oidiodendron maius</i> and saprotrophic species <i>Cryptococcus magnus</i>. Saprotrophic species had higher abundance in more damaged sites, suggesting a shift in fungal communities from ECM fungi. In conclusion, the results of this work suggest Norway spruce root system response to short-term climatic stress, which should be considered when planning spruce forest management, especially on organic soils with a high groundwater level.
DOI: 10.6084/m9.figshare.1476246.v4
title: The novel function of JADE1S in cytokinesis of epithelial cells

description: JADE1 belongs to a small family of PHD zinc finger proteins that interacts with histone acetyl transferase (HAT) HBO1 and is associated with chromatin. We recently reported JADE1 chromatin shuttling and phosphorylation during G2/M to G1 transition, which was sensitive to Aurora A inhibition. In the current study we examined mechanisms of the cell cycle regulation by the small isoform of JADE1 protein, JADE1S, and report data showing that JADE1S has a novel function in the regulation of cytokinesis. Using FACS assays, we show that, JADE1S depletion facilitated rates of G1-cells accumulation in synchronously dividing HeLa cell cultures. Depletion of JADE1S protein in asynchronously dividing cells decreased the proportion of cytokinetic cells, and increased the proportion of multi-nuclear cells, indicative of premature and failed cytokinesis. In contrast, moderate overexpression of JADE1S increased the number of cytokinetic cells in time- and dose- dependent manner, indicating cytokinetic delay. Pharmacological inhibition of Aurora B kinase resulted in the release of JADE1S-mediated cytokinetic delay and allowed progression of abscission in cells over-expressing JADE1S. Finally, we show that JADE1S protein localized to centrosomes in interphase and mitotic cells, while during cytokinesis JADE1S localized to the midbody. Neither JADE1L nor partner of JADE1, HAT HBO1 was localized to the centrosomes or midbodies. Our study identifies the novel role for JADE1S in regulation of cytokinesis and suggests function in Aurora B kinase-mediated cytokinesis checkpoint.
DOI: 10.6084/m9.figshare.1476210.v1
title: Analysis of Norway Spruce Dieback Phenomenon in Latvia – a Below-Ground Perspective

description: In 2010, dieback of Norway spruce (<i>Picea abies</i>) was observed in Latvia. As mostly stands on seasonally or permanently water-saturated soils were damaged, we hypothesized that the recorded foliar damage might be associated with below-ground factors.We established 48 sample plots in stands with damage symptoms for soil parameter evaluation and fine root sampling to determine the number of fine roots in different growth stages and to describe the associated fungal community.Among sample plots on organic soils, there were fewer viable older fine roots and greater number of dead fine roots in more damaged sites than in less damaged. These root parameters were significantly correlated with higher groundwater level and soil pH. The fungal community was dominated by ectomycorrhizal (ECM) species (the most common was <i>Tylospora asterophora</i>), the endophyte <i>Oidiodendron maius</i> and saprotrophic species <i>Cryptococcus magnus</i>. Saprotrophic species had higher abundance in more damaged sites, suggesting a shift in fungal communities from ECM fungi.In conclusion, the results of this work suggest Norway spruce root system response to short-term climatic stress, which should be considered when planning spruce forest management, especially on organic soils with a high groundwater level.