cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1483490.v2
title: Molecular chaperons and co-chaperons, Hsp90, RAR1, and SGT1 negatively regulate bacterial wilt disease caused by <i>Ralstonia solanacearum</i> in <i>Nicotiana benthamiana</i>

description: <i>Ralstonia solanacearum</i> is the causal agent of bacterial wilt disease. To better understand the molecular mechanisms involved in interaction between <i>Nicotiana benthamiana</i> and <i>R. solanacearum</i>, we focused on Hsp90, RAR1 and SGT1. Appearances of wilt symptom were significantly suppressed in <i>Hsp90</i>, <i>RAR1</i> and <i>SGT1</i>-silenced plants compared with control plants. In <i>RAR1</i>-silenced plants, population of <i>R. solanacearum</i> increased in a similar manner to control plants. In contrast, multiplication of <i>R. solanacearum</i> was significantly suppressed in <i>Hsp90</i> and <i>SGT1</i>-silenced plants. In addition, expression of PR genes were increased in <i>Hsp90</i> and <i>SGT1</i>-silenced plants challenged with <i>R. solanacearum.</i> Therefore, RAR1 might be required for disease development or suppression of disease tolerance. These results also suggested that Hsp90 and/or SGT1 might play an important role in suppression of plant defenses leading to disease susceptibility and disease development.
DOI: 10.6084/m9.figshare.1483488
title: Dates

description: A table of dates for a period of interest, usually a month, expressed in two different formats: mm/dd/yyyy and mm-dd-yyyy Start date: 12/01/2014 End date: 12/31/2014
DOI: 10.6084/m9.figshare.1483490.v1
title: Molecular chaperons and co-chaperons, Hsp90, RAR1, and SGT1 negatively regulate bacterial wilt disease caused by <i>Ralstonia solanacearum</i> in <i>Nicotiana benthamiana</i>

description: <i>Ralstonia solanacearum</i> is the causal agent of bacterial wilt disease. To better understand the molecular mechanisms involved in interaction between <i>Nicotiana benthamiana</i> and <i>R. solanacearum</i>, we focused on Hsp90, RAR1 and SGT1. Appearances of wilt symptom were significantly suppressed in <i>Hsp90</i>, <i>RAR1</i> and <i>SGT1</i>-silenced plants compared with control plants. In <i>RAR1</i>-silenced plants, population of <i>R. solanacearum</i> increased in a similar manner to control plants. In contrast, multiplication of <i>R. solanacearum</i> was significantly suppressed in <i>Hsp90</i> and <i>SGT1</i>-silenced plants. In addition, expression of PR genes were increased in <i>Hsp90</i> and <i>SGT1</i>-silenced plants challenged with <i>R. solanacearum.</i> Therefore, RAR1 might be required for disease development or suppression of disease tolerance. These results also suggested that Hsp90 and/or SGT1 might play an important role in suppression of plant defenses leading to disease susceptibility and disease development.
DOI: 10.6084/m9.figshare.1483485
title: Weather data at CIMIS station 105

description: Daily time series of solar radiation, air temperature, vapor pressure, wind speed, precipitation, relative humidity, and dew point at CIMIS station 105 near the San Joaquin River in California, USA Start date: 03/01/2010 End date: 12/31/2014
DOI: 10.6084/m9.figshare.1483487
title: Weather data at KFAT station

description: Subdaily (mostly hourly) time series of temperature, relative humidity, wind speed, wind direction, sea level barometric pressure, and altitude-corrected site barometric pressure for stations SJB, SMN, and GRF in the San Joaquin River, USA. Data was downloaded using the MesoWest interface and modified by the author. Start date: 03/01/2010 End date: 12/31/2014
DOI: 10.6084/m9.figshare.1483485.v2
title: Weather data at CIMIS station 105

description: Daily time series of solar radiation, air temperature, vapor pressure, wind speed, precipitation, relative humidity, and dew point at CIMIS station 105 near the San Joaquin River in California, USA Start date: 03/01/2010 End date: 12/31/2014
DOI: 10.6084/m9.figshare.1483487.v1
title: Weather data at KFAT station

description: Subdaily (mostly hourly) time series of temperature, relative humidity, wind speed, wind direction, sea level barometric pressure, and altitude-corrected site barometric pressure for stations SJB, SMN, and GRF in the San Joaquin River, USA. Data was downloaded using the MesoWest interface and modified by the author. Start date: 03/01/2010 End date: 12/31/2014
DOI: 10.6084/m9.figshare.1483484
title: Straightforward Approach Toward Dihydrothiazoles via Intramolecular Bromocyclization

description: An intramolecular bromonium ion–assisted cyclization with sulfur as an internal nucleophile is described. Starting from benzoyl chlorides, this method provides an easy procedure for the synthesis of dihydrothiazole derivatives in moderate to good yields.
DOI: 10.6084/m9.figshare.1483485.v1
title: Weather data at CIMIS station 105

description: Daily time series of solar radiation, air temperature, vapor pressure, wind speed, precipitation, relative humidity, and dew point at CIMIS station 105 near the San Joaquin River in California, USA Start date: 03/01/2010 End date: 12/31/2014
DOI: 10.6084/m9.figshare.1483482.v1
title: Disruption of the ribosomal P complex leads to stress-induced autophagy

description: The human ribosomal P complex, which consists of the acidic ribosomal P proteins RPLP0, RPLP1, and RPLP2 (RPLP proteins), recruits translational factors, facilitating protein synthesis. Recently, we showed that overexpression of RPLP1 immortalizes primary cells and contributes to transformation. Moreover, RPLP proteins are overexpressed in human cancer, with the highest incidence in breast carcinomas. It is thought that disruption of the P complex would directly affect protein synthesis, causing cell growth arrest and eventually apoptosis. Here, we report a distinct mechanism by which cancer cells undergo cell cycle arrest and induced autophagy when RPLP proteins are downregulated. We found that absence of RPLP0, RPLP1, or RPLP2 resulted in reactive oxygen species (ROS) accumulation and MAPK1/ERK2 signaling pathway activation. Moreover, ROS generation led to endoplasmic reticulum (ER) stress that involved the EIF2AK3/PERK-EIF2S1/eIF2α-EIF2S2-EIF2S3-ATF4/ATF-4- and ATF6/ATF-6-dependent arms of the unfolded protein response (UPR). RPLP protein-deficient cells treated with autophagy inhibitors experienced apoptotic cell death as an alternative to autophagy. Strikingly, antioxidant treatment prevented UPR activation and autophagy while restoring the proliferative capacity of these cells. Our results indicate that ROS are a critical signal generated by disruption of the P complex that causes a cellular response that follows a sequential order: first ROS, then ER stress/UPR activation, and finally autophagy. Importantly, inhibition of the first step alone is able to restore the proliferative capacity of the cells, preventing UPR activation and autophagy. Overall, our results support a role for autophagy as a survival mechanism in response to stress due to RPLP protein deficiency.
DOI: 10.6084/m9.figshare.1483479
title: The multicopy sRNA LhrC controls expression of the oligopeptide-binding protein OppA in <i>Listeria monocytogenes</i>

description: <i>Listeria monocytogenes</i> is the causative agent of the foodborne disease listeriosis. During infection, <i>L. monocytogenes</i> produces an array of non-coding RNAs, including the multicopy sRNA LhrC. These five, nearly identical sRNAs are highly induced in response to cell envelope stress and target the virulence adhesin <i>lapB</i> at the post-transcriptional level. Here, we demonstrate that LhrC controls expression of additional genes encoding cell envelope-associated proteins with virulence function. Using transcriptomics and proteomics, we identified a set of genes affected by LhrC in response to cell envelope stress. Three targets were significantly down-regulated by LhrC at both the RNA and protein level: <i>lmo2349, tcsA</i> and <i>oppA</i>. All three genes encode membrane-associated proteins: A putative substrate binding protein of an amino acid ABC transporter (Lmo2349); the CD4+ T cell-stimulating antigen TcsA, and the oligopeptide binding protein OppA, of which the latter 2 are required for full virulence of <i>L. monocytogenes</i>. For OppA, we show that LhrC acts by direct base paring to the ribosome binding site of the <i>oppA</i> mRNA, leading to an impediment of its translation and a decreased mRNA level. The sRNA-mRNA interaction depends on 2 of 3 CU-rich regions in LhrC allowing binding of 2 <i>oppA</i> mRNAs to a single LhrC molecule. Finally, we found that LhrC contributes to infection in macrophage-like cells. These findings demonstrate a central role for LhrC in controlling the level of OppA and other virulence-associated cell envelope proteins in response to cell envelope stress.
DOI: 10.6084/m9.figshare.1483484.v4
title: Straightforward Approach Toward Dihydrothiazoles via Intramolecular Bromocyclization

description: An intramolecular bromonium ion–assisted cyclization with sulfur as an internal nucleophile is described. Starting from benzoyl chlorides, this method provides an easy procedure for the synthesis of dihydrothiazole derivatives in moderate to good yields.
DOI: 10.6084/m9.figshare.1483482.v2
title: Disruption of the ribosomal P complex leads to stress-induced autophagy

description: The human ribosomal P complex, which consists of the acidic ribosomal P proteins RPLP0, RPLP1, and RPLP2 (RPLP proteins), recruits translational factors, facilitating protein synthesis. Recently, we showed that overexpression of RPLP1 immortalizes primary cells and contributes to transformation. Moreover, RPLP proteins are overexpressed in human cancer, with the highest incidence in breast carcinomas. It is thought that disruption of the P complex would directly affect protein synthesis, causing cell growth arrest and eventually apoptosis. Here, we report a distinct mechanism by which cancer cells undergo cell cycle arrest and induced autophagy when RPLP proteins are downregulated. We found that absence of RPLP0, RPLP1, or RPLP2 resulted in reactive oxygen species (ROS) accumulation and MAPK1/ERK2 signaling pathway activation. Moreover, ROS generation led to endoplasmic reticulum (ER) stress that involved the EIF2AK3/PERK-EIF2S1/eIF2α-EIF2S2-EIF2S3-ATF4/ATF-4- and ATF6/ATF-6-dependent arms of the unfolded protein response (UPR). RPLP protein-deficient cells treated with autophagy inhibitors experienced apoptotic cell death as an alternative to autophagy. Strikingly, antioxidant treatment prevented UPR activation and autophagy while restoring the proliferative capacity of these cells. Our results indicate that ROS are a critical signal generated by disruption of the P complex that causes a cellular response that follows a sequential order: first ROS, then ER stress/UPR activation, and finally autophagy. Importantly, inhibition of the first step alone is able to restore the proliferative capacity of the cells, preventing UPR activation and autophagy. Overall, our results support a role for autophagy as a survival mechanism in response to stress due to RPLP protein deficiency.
DOI: 10.6084/m9.figshare.1483484.v3
title: Straightforward Approach Toward Dihydrothiazoles via Intramolecular Bromocyclization

description: An intramolecular bromonium ion–assisted cyclization with sulfur as an internal nucleophile is described. Starting from benzoyl chlorides, this method provides an easy procedure for the synthesis of dihydrothiazole derivatives in moderate to good yields.
DOI: 10.6084/m9.figshare.1483477
title: Rationally designed, heterologous <i>S. cerevisiae</i> transcripts expose novel expression determinants

description: Deducing generic causal relations between RNA transcript features and protein expression profiles from endogenous gene expression data remains a major unsolved problem in biology. The analysis of gene expression from heterologous genes contributes significantly to solving this problem, but has been heavily biased toward the study of the effect of 5′ transcript regions and to prokaryotes. Here, we employ a synthetic biology driven approach that systematically differentiates the effect of different regions of the transcript on gene expression up to 240 nucleotides into the ORF. This enabled us to discover new causal effects between features in previously unexplored regions of transcripts, and gene expression in natural regimes. We rationally designed, constructed, and analyzed 383 gene variants of the viral <i>HRSVgp04</i> gene ORF, with multiple synonymous mutations at key positions along the transcript in the eukaryote <i>S. cerevisiae</i>. Our results show that a few silent mutations at the 5′UTR can have a dramatic effect of up to 15 fold change on protein levels, and that even synonymous mutations in positions more than 120 nucleotides downstream from the ORF 5′end can modulate protein levels up to 160%–300%. We demonstrate that the correlation between protein levels and folding energy increases with the significance of the level of selection of the latter in endogenous genes, reinforcing the notion that selection for folding strength in different parts of the ORF is related to translation regulation. Our measured protein abundance correlates notably(correlation up to r = 0.62 (p=0.0013)) with mean relative codon decoding times, based on ribosomal densities (Ribo-Seq) in endogenous genes, supporting the conjecture that translation elongation and adaptation to the tRNA pool can modify protein levels in a causal/direct manner. This report provides an improved understanding of transcript evolution, design principles of gene expression regulation, and suggests simple rules for engineering synthetic gene expression in eukaryotes.
DOI: 10.6084/m9.figshare.1483482.v3
title: Disruption of the ribosomal P complex leads to stress-induced autophagy

description: The human ribosomal P complex, which consists of the acidic ribosomal P proteins RPLP0, RPLP1, and RPLP2 (RPLP proteins), recruits translational factors, facilitating protein synthesis. Recently, we showed that overexpression of RPLP1 immortalizes primary cells and contributes to transformation. Moreover, RPLP proteins are overexpressed in human cancer, with the highest incidence in breast carcinomas. It is thought that disruption of the P complex would directly affect protein synthesis, causing cell growth arrest and eventually apoptosis. Here, we report a distinct mechanism by which cancer cells undergo cell cycle arrest and induced autophagy when RPLP proteins are downregulated. We found that absence of RPLP0, RPLP1, or RPLP2 resulted in reactive oxygen species (ROS) accumulation and MAPK1/ERK2 signaling pathway activation. Moreover, ROS generation led to endoplasmic reticulum (ER) stress that involved the EIF2AK3/PERK-EIF2S1/eIF2α-EIF2S2-EIF2S3-ATF4/ATF-4- and ATF6/ATF-6-dependent arms of the unfolded protein response (UPR). RPLP protein-deficient cells treated with autophagy inhibitors experienced apoptotic cell death as an alternative to autophagy. Strikingly, antioxidant treatment prevented UPR activation and autophagy while restoring the proliferative capacity of these cells. Our results indicate that ROS are a critical signal generated by disruption of the P complex that causes a cellular response that follows a sequential order: first ROS, then ER stress/UPR activation, and finally autophagy. Importantly, inhibition of the first step alone is able to restore the proliferative capacity of the cells, preventing UPR activation and autophagy. Overall, our results support a role for autophagy as a survival mechanism in response to stress due to RPLP protein deficiency.
DOI: 10.6084/m9.figshare.1483476
title: Intra-individual variation in wood traits from 20 tropical tree species

description: This dataset contains wood traits measured on wood segments from near pith (sapling) and near bark (adult) for 20 tree species (three adults each) from Barro Colorado Island, Panama. In the dataset, unique IDs are provided for species, species and individual tree combined, and wood segment. Also provided in the dataset are the radial position for each segment (i.e., inner or near pith vs. outer or near bark), and the distance from pith from which the wood segment was obtained. Wood traits measured on each wood segment include wood density, and anatomical traits including fiber lumen area, fiber wall thickness, vessel density, vessel area, and fractions of area occupied each tissue type (vessel, fiber, fiber wall, fiber lumen, and parenchyma). The attached text file provides further description of the variable names in the dataset and unit of measurement. However, details of the methods used in measuring these wood traits can be found in Osazuwa-Peters, Oyomoare L., S. Joseph Wright, and Amy E. Zanne (2017). Linking wood traits to vitatl rates in tropical rainforest trees: insights from comparing sapling and adult wood. American Journal of Botany; in press.<br>
DOI: 10.6084/m9.figshare.1483479.v1
title: The multicopy sRNA LhrC controls expression of the oligopeptide-binding protein OppA in <i>Listeria monocytogenes</i>

description: <i>Listeria monocytogenes</i> is the causative agent of the foodborne disease listeriosis. During infection, <i>L. monocytogenes</i> produces an array of non-coding RNAs, including the multicopy sRNA LhrC. These five, nearly identical sRNAs are highly induced in response to cell envelope stress and target the virulence adhesin <i>lapB</i> at the post-transcriptional level. Here, we demonstrate that LhrC controls expression of additional genes encoding cell envelope-associated proteins with virulence function. Using transcriptomics and proteomics, we identified a set of genes affected by LhrC in response to cell envelope stress. Three targets were significantly down-regulated by LhrC at both the RNA and protein level: <i>lmo2349, tcsA</i> and <i>oppA</i>. All three genes encode membrane-associated proteins: A putative substrate binding protein of an amino acid ABC transporter (Lmo2349); the CD4+ T cell-stimulating antigen TcsA, and the oligopeptide binding protein OppA, of which the latter two are required for full virulence of <i>L. monocytogenes</i>. For OppA, we show that LhrC acts by direct base paring to the ribosome binding site of the <i>oppA</i> mRNA, leading to an impediment of its translation and a decreased mRNA level. The sRNA-mRNA interaction depends on two of three CU-rich regions in LhrC allowing binding of two <i>oppA</i> mRNAs to a single LhrC molecule. Finally, we found that LhrC contributes to infection in macrophage-like cells. These findings demonstrate a central role for LhrC in controlling the level of OppA and other virulence-associated cell envelope proteins in response to cell envelope stress.
DOI: 10.6084/m9.figshare.1483475
title: A bacterial homolog YciH of eukaryotic translation initiation factor eIF1 regulates stress-related gene expression and is unlikely to be involved in translation initiation fidelity

description: YciH is a bacterial protein, homologous to eukaryotic translation initiation factor eIF1. Preceding evidence obtained with the aid of <i>in vitro</i> translation initiation system suggested that it may play a role of a translation initiation factor, ensuring selection against suboptimal initiation complexes. Here we studied the effect of <i>Escherichia coli yciH</i> gene inactivation on translation of model mRNAs. Neither the translation efficiency of leaderless mRNAs, nor mRNAs with non AUG start codons, was found to be affected by YciH <i>in vivo</i>. Comparative proteome analysis revealed that <i>yciH</i> gene knockout leads to a more than fold2- increase in expression of 66 genes and a more than fold2- decrease in the expression of 20 genes. Analysis of these gene sets allowed us to suggest a role of YciH as an inhibitor of translation in a stress response rather than the role of a translation initiation factor.
DOI: 10.6084/m9.figshare.1483476.v1
title: Intra-individual variation in wood traits from 20 tropical tree species

description: This dataset contains wood traits measured on wood segments from near pith (sapling) and near bark (adult) for 20 tree species (three adults each) from Barro Colorado Island, Panama. In the dataset, unique IDs are provided for species, species and individual tree combined, and wood segment. Also provided in the dataset are the radial position for each segment (i.e., inner or near pith vs. outer or near bark), and the distance from pith from which the wood segment was obtained. Wood traits measured on each wood segment include wood density, and anatomical traits including fiber lumen area, fiber wall thickness, vessel density, vessel area, and fractions of area occupied each tissue type (vessel, fiber, fiber wall, fiber lumen, and parenchyma). The attached text file provides further description of the variable names in the dataset and unit of measurement. However, details of the methods used in measuring these wood traits can be found in Osazuwa-Peters, Oyomoare L., S. Joseph Wright, and Amy E. Zanne (2017). Linking wood traits to vitatl rates in tropical rainforest trees: insights from comparing sapling and adult wood. American Journal of Botany; in press.<br>
DOI: 10.6084/m9.figshare.1483477.v1
title: Rationally designed, heterologous <i>S. cerevisiae</i>transcripts expose novel expression determinants

description: Deducing generic causal relations between RNA transcript features and protein expression profiles from endogenous gene expression data remains a major unsolved problem in biology. The analysis of gene expression from heterologous genes contributes significantly to solving this problem, but has been heavily biased towards the study of the effect of 5′ transcript regions and to prokaryotes. Here, we employ a synthetic biology driven approach that systematically differentiates the effect of different regions of the transcript on gene expression up to 240 nucleotides into the ORF. This enabled us to discover new causal effects between features in previously unexplored regions of transcripts, and gene expression in natural regimes. We rationally designed, constructed, and analyzed 383 gene variants of the viral <i>HRSVgp04</i> gene ORF, with multiple synonymous mutations at key positions along the transcript in the eukaryote <i>S. cerevisiae</i>. Our results show that a few silent mutations at the 5′UTR can have a dramatic effect of up to 15 fold change on protein levels, and that even synonymous mutations in positions more than 120 nucleotides downstream from the ORF 5′end can modulate protein levels up to 160%–300%. We demonstrate that the correlation between protein levels and folding energy increases with the significance of the level of selection of the latter in endogenous genes, reinforcing the notion that selection for folding strength in different parts of the ORF is related to translation regulation. Our measured protein abundance correlates notably(correlation up to r = 0.62 (p=0.0013)) with mean relative codon decoding times, based on ribosomal densities (Ribo-Seq) in endogenous genes, supporting the conjecture that translation elongation and adaptation to the tRNA pool can modify protein levels in a causal/direct manner. This report provides an improved understanding of transcript evolution, design principles of gene expression regulation, and suggests simple rules for engineering synthetic gene expression in eukaryotes.