cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.3439253
title: The autophagy pathway participates in resistance to <i>tomato yellow leaf curl virus</i> infection in whiteflies

description: Macroautophagy/autophagy plays an important role against pathogen infection in mammals and plants. However, little has been known about the role of autophagy in the interactions of insect vectors with the plant viruses, which they transmit. Begomoviruses are a group of single-stranded DNA viruses and are exclusively transmitted by the whitefly <i>Bemisia tabaci</i> in a circulative manner. In this study, we found that the infection of a begomovirus, <i>tomato yellow leaf curl virus</i> (TYLCV) could activate the autophagy pathway in the Middle East Asia Minor 1 (MEAM1) species of the <i>B. tabaci</i> complex as evidenced by the formation of autophagosomes and ATG8-II. Interestingly, the activation of autophagy led to the subsequent degradation of TYLCV coat protein (CP) and genomic DNA. While feeding the whitefly with 2 autophagy inhibitors (3-methyladenine and bafilomycin A<sub>1</sub>) and silencing the expression of <i>Atg3</i> and <i>Atg9</i> increased the viral load; autophagy activation via feeding of rapamycin notably decreased the amount of viral CP and DNA in the whitefly. Furthermore, we found that activation of whitefly autophagy could inhibit the efficiency of virus transmission; whereas inhibiting autophagy facilitated virus transmission. Taken together, these results indicate that TYLCV infection can activate the whitefly autophagy pathway, which leads to the subsequent degradation of virus. Furthermore, our report proves that an insect vector uses autophagy as an intrinsic antiviral program to repress the infection of a circulative-transmitted plant virus. Our data also demonstrate that TYLCV may replicate and trigger complex interactions with the insect vector.
DOI: 10.6084/m9.figshare.3439253.v1
title: The autophagy pathway participates in resistance to <i>tomato yellow leaf curl virus</i> infection in whiteflies

description: Macroautophagy/autophagy plays an important role against pathogen infection in mammals and plants. However, little has been known about the role of autophagy in the interactions of insect vectors with the plant viruses, which they transmit. Begomoviruses are a group of single-stranded DNA viruses and are exclusively transmitted by the whitefly <i>Bemisia tabaci</i> in a circulative manner. In this study, we found that the infection of a begomovirus, <i>tomato yellow leaf curl virus</i> (TYLCV) could activate the autophagy pathway in the Middle East Asia Minor 1 (MEAM1) species of the <i>B. tabaci</i> complex as evidenced by the formation of autophagosomes and ATG8-II. Interestingly, the activation of autophagy led to the subsequent degradation of TYLCV coat protein (CP) and genomic DNA. While feeding the whitefly with 2 autophagy inhibitors (3-methyladenine and bafilomycin A<sub>1</sub>) and silencing the expression of <i>Atg3</i> and <i>Atg9</i> increased the viral load; autophagy activation via feeding of rapamycin notably decreased the amount of viral CP and DNA in the whitefly. Furthermore, we found that activation of whitefly autophagy could inhibit the efficiency of virus transmission; whereas inhibiting autophagy facilitated virus transmission. Taken together, these results indicate that TYLCV infection can activate the whitefly autophagy pathway, which leads to the subsequent degradation of virus. Furthermore, our report proves that an insect vector uses autophagy as an intrinsic antiviral program to repress the infection of a circulative-transmitted plant virus. Our data also demonstrate that TYLCV may replicate and trigger complex interactions with the insect vector.
DOI: 10.6084/m9.figshare.3439247
title: Global assessment of imprinted gene expression in the bovine conceptus by next generation sequencing

description: Genomic imprinting is an epigenetic mechanism that leads to parental-allele-specific gene expression. Approximately 150 imprinted genes have been identified in humans and mice but less than 30 have been described as imprinted in cattle. For the purpose of <i>de novo</i> identification of imprinted genes in bovine, we determined global monoallelic gene expression in brain, skeletal muscle, liver, kidney and placenta of day ∼105 <i>Bos taurus indicus</i> × <i>Bos taurus taurus</i> F<sub>1</sub> conceptuses using RNA sequencing. To accomplish this, we developed a bioinformatics pipeline to identify parent-specific single nucleotide polymorphism alleles after filtering adenosine to inosine (A-to-I) RNA editing sites. We identified 53 genes subject to monoallelic expression. Twenty three are genes known to be imprinted in the cow and an additional 7 have previously been characterized as imprinted in human and/or mouse that have not been reported as imprinted in cattle. Of the remaining 23 genes, we found that 10 are uncharacterized or unannotated transcripts located in known imprinted clusters, whereas the other 13 genes are distributed throughout the bovine genome and are not close to any known imprinted clusters. To exclude potential <i>cis</i>-eQTL effects on allele expression, we corroborated the parental specificity of monoallelic expression in day 86 <i>Bos taurus taurus</i> × <i>Bos taurus taurus</i> conceptuses and identified 8 novel bovine imprinted genes. Further, we identified 671 candidate A-to-I RNA editing sites and describe random X-inactivation in day 15 bovine extraembryonic membranes. Our results expand the imprinted gene list in bovine and demonstrate that monoallelic gene expression can be the result of <i>cis</i>-eQTL effects.
DOI: 10.6084/m9.figshare.3439247.v1
title: Global assessment of imprinted gene expression in the bovine conceptus by next generation sequencing

description: Genomic imprinting is an epigenetic mechanism that leads to parental-allele-specific gene expression. Approximately 150 imprinted genes have been identified in humans and mice but less than 30 have been described as imprinted in cattle. For the purpose of <i>de novo</i> identification of imprinted genes in bovine, we determined global monoallelic gene expression in brain, skeletal muscle, liver, kidney and placenta of day ∼105 <i>Bos taurus indicus</i> × <i>Bos taurus taurus</i> F<sub>1</sub> conceptuses using RNA sequencing. To accomplish this, we developed a bioinformatics pipeline to identify parent-specific single nucleotide polymorphism alleles after filtering adenosine to inosine (A-to-I) RNA editing sites. We identified 53 genes subject to monoallelic expression. Twenty three are genes known to be imprinted in the cow and an additional 7 have previously been characterized as imprinted in human and/or mouse that have not been reported as imprinted in cattle. Of the remaining 23 genes, we found that 10 are uncharacterized or unannotated transcripts located in known imprinted clusters, whereas the other 13 genes are distributed throughout the bovine genome and are not close to any known imprinted clusters. To exclude potential <i>cis</i>-eQTL effects on allele expression, we corroborated the parental specificity of monoallelic expression in day 86 <i>Bos taurus taurus</i> × <i>Bos taurus taurus</i> conceptuses and identified 8 novel bovine imprinted genes. Further, we identified 671 candidate A-to-I RNA editing sites and describe random X-inactivation in day 15 bovine extraembryonic membranes. Our results expand the imprinted gene list in bovine and demonstrate that monoallelic gene expression can be the result of <i>cis</i>-eQTL effects.
DOI: 10.6084/m9.figshare.3439241
title: Detection of differential DNA methylation in repetitive DNA of mice and humans perinatally exposed to bisphenol A

description: Developmental exposure to bisphenol A (BPA) has been shown to induce changes in DNA methylation in both mouse and human genic regions; however, the response in repetitive elements and transposons has not been explored. Here we present novel methodology to combine genomic DNA enrichment with RepeatMasker analysis on next-generation sequencing data to determine the effect of perinatal BPA exposure on repetitive DNA at the class, family, subfamily, and individual insertion level in both mouse and human samples. Mice were treated during gestation and lactation to BPA in chow at 0, 50, or 50,000 ng/g levels and total BPA was measured in stratified human fetal liver tissue samples as low (non-detect to 0.83 ng/g), medium (3.5 to 5.79 ng/g), or high (35.44 to 96.76 ng/g). Transposon methylation changes were evident in human classes, families, and subfamilies, with the medium group exhibiting hypomethylation compared to both high and low BPA groups. Mouse repeat classes, families, and subfamilies did not respond to BPA with significantly detectable differential DNA methylation. In human samples, 1251 individual transposon loci were detected as differentially methylated by BPA exposure, but only 19 were detected in mice. Of note, this approach recapitulated the discovery of a previously known mouse environmentally labile metastable epiallele, <i>Cabp</i><sup><i>IAP</i></sup>. Thus, by querying repetitive DNA in both mouse and humans, we report the first known transposons in humans that respond to perinatal BPA exposure.
DOI: 10.6084/m9.figshare.3439241.v1
title: Detection of differential DNA methylation in repetitive DNA of mice and humans perinatally exposed to bisphenol A

description: Developmental exposure to bisphenol A (BPA) has been shown to induce changes in DNA methylation in both mouse and human genic regions; however, the response in repetitive elements and transposons has not been explored. Here we present novel methodology to combine genomic DNA enrichment with RepeatMasker analysis on next-generation sequencing data to determine the effect of perinatal BPA exposure on repetitive DNA at the class, family, subfamily, and individual insertion level in both mouse and human samples. Mice were treated during gestation and lactation to BPA in chow at 0, 50, or 50,000 ng/g levels and total BPA was measured in stratified human fetal liver tissue samples as low (non-detect to 0.83 ng/g), medium (3.5 to 5.79 ng/g), or high (35.44 to 96.76 ng/g). Transposon methylation changes were evident in human classes, families, and subfamilies, with the medium group exhibiting hypomethylation compared to both high and low BPA groups. Mouse repeat classes, families, and subfamilies did not respond to BPA with significantly detectable differential DNA methylation. In human samples, 1251 individual transposon loci were detected as differentially methylated by BPA exposure, but only 19 were detected in mice. Of note, this approach recapitulated the discovery of a previously known mouse environmentally labile metastable epiallele, <i>Cabp</i><sup><i>IAP</i></sup>. Thus, by querying repetitive DNA in both mouse and humans, we report the first known transposons in humans that respond to perinatal BPA exposure.
DOI: 10.6084/m9.figshare.3439187
title: A new leptonectid ichthyosaur from the Lower Jurassic (Hettangian) of Nottinghamshire, England, UK, and the taxonomic usefulness of the ichthyosaurian coracoid

description: Thousands of ichthyosaurs have been discovered from the rich Lower Jurassic deposits of the UK, with the majority collected from along the Lyme Regis-Charmouth area of the Dorset coast. Here, I describe a new leptonectid ichthyosaur, <i>Wahlisaurus massarae</i> gen. et sp. nov., based on a partial skull and an incomplete skeleton collected from the Lower Jurassic (Hettangian) of Nottinghamshire, England. <i>Wahlisaurus</i> can be referred to the Leptonectidae through the possession of an extremely slender and delicate snout, and a mandible shorter than the snout which produces an overbite. This referral is supported by a phylogenetic analysis. The new taxon is distinguished from other ichthyosaurs through a unique combination of characters and autapomorphies of the pectoral girdle including the presence of both a scapular-coracoid foramen and a large and roughly ovoid coracoid foramen. A coracoid foramen has only previously been reported in the Triassic ichthyosaur <i>Cymbospondylus</i>. The peculiar coracoid morphology further highlights the taxonomic utility of coracoids in ichthyosaurs. The aforementioned features demonstrate that <i>W. massarae</i> cannot be referred to any currently recognized leptonectid. <i>Wahlisaurus</i> is the ninth Lower Jurassic ichthyosaur genus to be recognized worldwide, and the fifth documented in the Lower Lias Group. http://zoobank.org/urn:lsid:zoobank.org:pub:EE500E11-66AB-43C8-BB59-F21654763241
DOI: 10.6084/m9.figshare.3439187.v1
title: A new leptonectid ichthyosaur from the Lower Jurassic (Hettangian) of Nottinghamshire, England, UK, and the taxonomic usefulness of the ichthyosaurian coracoid

description: Thousands of ichthyosaurs have been discovered from the rich Lower Jurassic deposits of the UK, with the majority collected from along the Lyme Regis-Charmouth area of the Dorset coast. Here, I describe a new leptonectid ichthyosaur, <i>Wahlisaurus massarae</i> gen. et sp. nov., based on a partial skull and an incomplete skeleton collected from the Lower Jurassic (Hettangian) of Nottinghamshire, England. <i>Wahlisaurus</i> can be referred to the Leptonectidae through the possession of an extremely slender and delicate snout, and a mandible shorter than the snout which produces an overbite. This referral is supported by a phylogenetic analysis. The new taxon is distinguished from other ichthyosaurs through a unique combination of characters and autapomorphies of the pectoral girdle including the presence of both a scapular-coracoid foramen and a large and roughly ovoid coracoid foramen. A coracoid foramen has only previously been reported in the Triassic ichthyosaur <i>Cymbospondylus</i>. The peculiar coracoid morphology further highlights the taxonomic utility of coracoids in ichthyosaurs. The aforementioned features demonstrate that <i>W. massarae</i> cannot be referred to any currently recognized leptonectid. <i>Wahlisaurus</i> is the ninth Lower Jurassic ichthyosaur genus to be recognized worldwide, and the fifth documented in the Lower Lias Group. http://zoobank.org/urn:lsid:zoobank.org:pub:EE500E11-66AB-43C8-BB59-F21654763241
DOI: 10.6084/m9.figshare.3439148
title: PRKAA/AMPK restricts HBV replication through promotion of autophagic degradation

description: Adenosine monophosphate-activated protein kinase (AMPK) is a crucial energy sensor that maintains cellular energy homeostasis. AMPK plays a critical role in macroautophagy/autophagy, and autophagy facilitates hepatitis B virus (HBV) replication. To date, the intrinsic link among AMPK, autophagy and HBV production remains to be elucidated. Here, we demonstrate that PRKAA (a catalytic subunit of AMPK) is activated in response to HBV-induced oxidative stress, which in turn decreases the production of HBV. Mechanistic studies reveal that the autophagy machinery is associated with the inhibitory effect of PRKAA/AMPK on HBV production. Activation of PRKAA/AMPK promotes autolysosome-dependent degradation through stimulation of cellular ATP levels, which then leads to the depletion of autophagic vacuoles. Taken together, our data suggest that the activation of AMPK might be a stress response of host cells to restrict virus production through promotion of autophagic degradation. These findings therefore indicate that AMPK could provide a potential therapeutic target for HBV infection.
DOI: 10.6084/m9.figshare.3439148.v1
title: PRKAA/AMPK restricts HBV replication through promotion of autophagic degradation

description: Adenosine monophosphate-activated protein kinase (AMPK) is a crucial energy sensor that maintains cellular energy homeostasis. AMPK plays a critical role in macroautophagy/autophagy, and autophagy facilitates hepatitis B virus (HBV) replication. To date, the intrinsic link among AMPK, autophagy and HBV production remains to be elucidated. Here, we demonstrate that PRKAA (a catalytic subunit of AMPK) is activated in response to HBV-induced oxidative stress, which in turn decreases the production of HBV. Mechanistic studies reveal that the autophagy machinery is associated with the inhibitory effect of PRKAA/AMPK on HBV production. Activation of PRKAA/AMPK promotes autolysosome-dependent degradation through stimulation of cellular ATP levels, which then leads to the depletion of autophagic vacuoles. Taken together, our data suggest that the activation of AMPK might be a stress response of host cells to restrict virus production through promotion of autophagic degradation. These findings therefore indicate that AMPK could provide a potential therapeutic target for HBV infection.
DOI: 10.6084/m9.figshare.3439133
title: Flash-Beep

description: This is the data for the flash-beep stimuli
DOI: 10.6084/m9.figshare.3439133.v1
title: Flash-Beep

description: This is the data for the flash-beep stimuli
DOI: 10.6084/m9.figshare.3439127
title: Speech

description: This data is for the speech condition
DOI: 10.6084/m9.figshare.3439127.v1
title: Speech

description: This data is for the speech condition
DOI: 10.6084/m9.figshare.3439103
title: Mass of seed removal

description: This data set is a result of an observational study conducted in a southern California, semi-arid shrubland (Rancho Jamul Ecological Reserve, Jamul, CA). As a master's student in Biology/Ecology, I was interested in whether seed predators preferentially removed non-native over native seeds. Additionally (and most importantly), I evaluated whether field equipment intended to parse out relative patterns of seed removal between different taxa (birds, rodents, ants) were inhibiting the taxon of interest. More specifically, does the exclusion cage/PVC tube intended to permit access to rodents, but not rabbits and birds, inhibit visitation by rodents?<br><br>I deployed seed predation stations across 28 stations and three seasons (spring, fall, winter). Each seed station consisted of a dish open to all visitors ("open") and a dish accessible only to rodents and insects ("tube"). The latter dish was located inside a 1cm wire mesh cage with a PVC tube (bent at a 90-degree angle) as the only entrance. Each seed dish had a partition, separating a mixture of non-native and native seeds found across the site. In this data set, we measured the mass of seed removed from each side (native vs. non-native) of each dish (open vs. "tube"). Additionally, we deployed field cameras at all seed stations, observing the genus of visitor; this data set shows presence (1) and absence (0) of common genera observed for each 2-night trial at each station. <br><br>A separate data set contains data from the direct observation portion of this study. In that data set, you will find behavioral observations of all visitors to the seed stations.
DOI: 10.6084/m9.figshare.3439103.v1
title: Mass of seed removal

description: This data set is a result of an observational study conducted in a southern California, semi-arid shrubland (Rancho Jamul Ecological Reserve, Jamul, CA). As a master's student in Biology/Ecology, I was interested in whether seed predators preferentially removed non-native over native seeds. Additionally (and most importantly), I evaluated whether field equipment intended to parse out relative patterns of seed removal between different taxa (birds, rodents, ants) were inhibiting the taxon of interest. More specifically, does the exclusion cage/PVC tube intended to permit access to rodents, but not rabbits and birds, inhibit visitation by rodents?<br><br>I deployed seed predation stations across 28 stations and three seasons (spring, fall, winter). Each seed station consisted of a dish open to all visitors ("open") and a dish accessible only to rodents and insects ("tube"). The latter dish was located inside a 1cm wire mesh cage with a PVC tube (bent at a 90-degree angle) as the only entrance. Each seed dish had a partition, separating a mixture of non-native and native seeds found across the site. In this data set, we measured the mass of seed removed from each side (native vs. non-native) of each dish (open vs. "tube"). Additionally, we deployed field cameras at all seed stations, observing the genus of visitor; this data set shows presence (1) and absence (0) of common genera observed for each 2-night trial at each station. <br><br>A separate data set contains data from the direct observation portion of this study. In that data set, you will find behavioral observations of all visitors to the seed stations.
DOI: 10.6084/m9.figshare.3439082
title: ARTD1 regulates cyclin E expression and consequently cell-cycle re-entry and G<sub>1</sub>/S progression in T24 bladder carcinoma cells

description: ADP-ribosylation is involved in a variety of biological processes, many of which are chromatin-dependent and linked to important functions during the cell cycle. However, any study on ADP-ribosylation and the cell cycle faces the problem that synchronization with chemical agents or by serum starvation and subsequent growth factor addition already activates ADP-ribosylation by itself. Here, we investigated the functional contribution of ARTD1 in cell cycle re-entry and G<sub>1</sub>/S cell cycle progression using T24 urinary bladder carcinoma cells, which synchronously re-enter the cell cycle after splitting without any additional stimuli. In synchronized cells, ARTD1 knockdown, but not inhibition of its enzymatic activity, caused specific down-regulation of <i>cyclin E</i> during cell cycle re-entry and G<sub>1</sub>/S progression through alterations of the chromatin composition and histone acetylation, but not of other E2F-1 target genes. Although Cdk2 formed a functional complex with the residual cyclin E, p27<sup>Kip1</sup> protein levels increased in G<sub>1</sub> upon ARTD1 knockdown most likely due to inappropriate cyclin E-Cdk2-induced phosphorylation-dependent degradation, leading to decelerated G<sub>1</sub>/S progression. These results provide evidence that ARTD1 regulates cell cycle re-entry and G<sub>1</sub>/S progression via <i>cyclin E</i> expression and p27<sup>Kip1</sup> stability independently of its enzymatic activity, uncovering a novel cell cycle regulatory mechanism.
DOI: 10.6084/m9.figshare.3439082.v1
title: ARTD1 regulates cyclin E expression and consequently cell-cycle re-entry and G<sub>1</sub>/S progression in T24 bladder carcinoma cells

description: ADP-ribosylation is involved in a variety of biological processes, many of which are chromatin-dependent and linked to important functions during the cell cycle. However, any study on ADP-ribosylation and the cell cycle faces the problem that synchronization with chemical agents or by serum starvation and subsequent growth factor addition already activates ADP-ribosylation by itself. Here, we investigated the functional contribution of ARTD1 in cell cycle re-entry and G<sub>1</sub>/S cell cycle progression using T24 urinary bladder carcinoma cells, which synchronously re-enter the cell cycle after splitting without any additional stimuli. In synchronized cells, ARTD1 knockdown, but not inhibition of its enzymatic activity, caused specific down-regulation of <i>cyclin E</i> during cell cycle re-entry and G<sub>1</sub>/S progression through alterations of the chromatin composition and histone acetylation, but not of other E2F-1 target genes. Although Cdk2 formed a functional complex with the residual cyclin E, p27<sup>Kip1</sup> protein levels increased in G<sub>1</sub> upon ARTD1 knockdown most likely due to inappropriate cyclin E-Cdk2-induced phosphorylation-dependent degradation, leading to decelerated G<sub>1</sub>/S progression. These results provide evidence that ARTD1 regulates cell cycle re-entry and G<sub>1</sub>/S progression via <i>cyclin E</i> expression and p27<sup>Kip1</sup> stability independently of its enzymatic activity, uncovering a novel cell cycle regulatory mechanism.