cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5325364
title: <i>Mir505–3p</i> regulates axonal development via inhibiting the autophagy pathway by targeting <i>Atg12</i>

description: In addition to the canonical role in protein homeostasis, autophagy has recently been found to be involved in axonal dystrophy and neurodegeneration. Whether autophagy may also be involved in neural development remains largely unclear. Here we report that <i>Mir505–3p</i> is a crucial regulator for axonal elongation and branching in vitro and in vivo, through modulating autophagy in neurons. We identify that the key target gene of <i>Mir505–3p</i> in neurons is <i>Atg12</i>, encoding ATG12 (autophagy-related 12) which is an essential component of the autophagy machinery during the initiation and expansion steps of autophagosome formation. Importantly, axonal development is compromised in brains of <i>mir505</i> knockout mice, in which autophagy signaling and formation of autophagosomes are consistently enhanced. These results define <i>Mir505–3p</i>-ATG12 as a vital signaling cascade for axonal development via the autophagy pathway, further suggesting the critical role of autophagy in neural development.
DOI: 10.6084/m9.figshare.5325364.v2
title: <i>Mir505–3p</i> regulates axonal development via inhibiting the autophagy pathway by targeting <i>Atg12</i>

description: In addition to the canonical role in protein homeostasis, autophagy has recently been found to be involved in axonal dystrophy and neurodegeneration. Whether autophagy may also be involved in neural development remains largely unclear. Here we report that <i>Mir505–3p</i> is a crucial regulator for axonal elongation and branching in vitro and in vivo, through modulating autophagy in neurons. We identify that the key target gene of <i>Mir505–3p</i> in neurons is <i>Atg12</i>, encoding ATG12 (autophagy-related 12) which is an essential component of the autophagy machinery during the initiation and expansion steps of autophagosome formation. Importantly, axonal development is compromised in brains of <i>mir505</i> knockout mice, in which autophagy signaling and formation of autophagosomes are consistently enhanced. These results define <i>Mir505–3p</i>-ATG12 as a vital signaling cascade for axonal development via the autophagy pathway, further suggesting the critical role of autophagy in neural development.
DOI: 10.6084/m9.figshare.5325364.v1
title: <i>Mir505-3p</i> regulates axonal development via inhibiting the autophagy pathway by targeting <i>Atg12</i>

description: In addition to the canonical role in protein homeostasis, autophagy has recently been found to be involved in axonal dystrophy and neurodegeneration. Whether autophagy may also be involved in neural development remains largely unclear. Here we report that <i>Mir505-3p</i> is a crucial regulator for axonal elongation and branching <i>in vitro</i> and <i>in vivo</i>, through modulating autophagy in neurons. We identify that the key target gene of <i>Mir505-3p</i> in neurons is <i>Atg12</i>, encoding ATG12 (autophagy related 12) which is an essential component of the autophagy machinery during the initiation and expansion steps of autophagosome formation. Importantly, axonal development is compromised in brains of <i>mir505</i> knockout mice, in which autophagy signaling and formation of autophagosomes are consistently enhanced. These results define <i>Mir505-3p</i>-ATG12 as a vital signaling cascade for axonal development via the autophagy pathway, further suggesting the critical role of autophagy in neural development.
DOI: 10.6084/m9.figshare.5327515
title: High-quality Neurospora tetrasperma genome assemblies

description: This dataset contains ten high-quality genome assemblies from ten strains of the fungal genus <i>Neurospora</i>. The genomes are released together with the paper "Large-scale suppression of recombination predates genomic rearrangements in Neurospora tetrasperma" by Sun et al., which is published in Nature Communications (2017).<br><br>Three of the genomes have been assembled using Illumina paired-end and matepair data, which have been scaffolded using optical mapping. The other seven have been assembled using only PacBio data, but have also been error-corrected using Illumina paired-end reads. Raw PacBio reads have been deposited in the Sequence Read Archive (SRA) as part of BioProject PRJNA398702. Raw Illumina reads have also been deposited at SRA in the BioProject PRJNA239947 (matepair reads) and PRJNA239947 (paired-end reads). See Sun et al. for further details.<br><br>Most strains can be ordered from the Fungal Genetics Stock Center at http://www.fgsc.net. Use the FGSC numbers provided below.<br><br>Genomes:<br><br>965A (<i>Neurospora tetrasperma</i>)<br>Technique: Optical mapping + Illumina<br>FGSC number: 10751<br><br>965a (<i>N. tetrasperma</i>)<br>Technique: PacBio<br>FGSC number: 10752<br><br>9033 (<i>N. tetrasperma</i>)<br>Technique: Optical mapping + Illumina<br>FGSC number: 9033<br><br>9034 (<i>N. tetrasperma</i>)<br>Technique: Optical mapping + Illumina<br>FGSC number: 9034<br><br>CJ73 (<i>N. tetrasperma</i>)<br>Technique: PacBio<br>FGSC number: 9045<br><br>CJ74 (<i>N. tetrasperma</i>)<br>Technique: PacBio<br>FGSC number: 9046<br><br>CJ85 (<i>N. tetrasperma</i>)<br>Technique: PacBio<br>FGSC number: 2503<br><br>CJ86 (<i>N. tetrasperma</i>)<br>Technique: PacBio<br>FGSC number: 2504<br><br>8807 (<i>N. intermedia</i>)<br>Technique: PacBio<br>FGSC number: 8807<br><br>W1434 (<i>N. sitophila</i>)<br>Technique: PacBio<br>FGSC number: -
DOI: 10.6084/m9.figshare.5327515.v1
title: High-quality Neurospora tetrasperma genome assemblies

description: This dataset contains ten high-quality genome assemblies from ten strains of the fungal genus <i>Neurospora</i>. The genomes are released together with the paper "Large-scale suppression of recombination predates genomic rearrangements in Neurospora tetrasperma" by Sun et al., which is published in Nature Communications (2017).<br><br>Three of the genomes have been assembled using Illumina paired-end and matepair data, which have been scaffolded using optical mapping. The other seven have been assembled using only PacBio data, but have also been error-corrected using Illumina paired-end reads. Raw PacBio reads have been deposited in the Sequence Read Archive (SRA) as part of BioProject PRJNA398702. Raw Illumina reads have also been deposited at SRA in the BioProject PRJNA239947 (matepair reads) and PRJNA239947 (paired-end reads). See Sun et al. for further details.<br><br>Most strains can be ordered from the Fungal Genetics Stock Center at http://www.fgsc.net. Use the FGSC numbers provided below.<br><br>Genomes:<br><br>965A (<i>Neurospora tetrasperma</i>)<br>Technique: Optical mapping + Illumina<br>FGSC number: 10751<br><br>965a (<i>N. tetrasperma</i>)<br>Technique: PacBio<br>FGSC number: 10752<br><br>9033 (<i>N. tetrasperma</i>)<br>Technique: Optical mapping + Illumina<br>FGSC number: 9033<br><br>9034 (<i>N. tetrasperma</i>)<br>Technique: Optical mapping + Illumina<br>FGSC number: 9034<br><br>CJ73 (<i>N. tetrasperma</i>)<br>Technique: PacBio<br>FGSC number: 9045<br><br>CJ74 (<i>N. tetrasperma</i>)<br>Technique: PacBio<br>FGSC number: 9046<br><br>CJ85 (<i>N. tetrasperma</i>)<br>Technique: PacBio<br>FGSC number: 2503<br><br>CJ86 (<i>N. tetrasperma</i>)<br>Technique: PacBio<br>FGSC number: 2504<br><br>8807 (<i>N. intermedia</i>)<br>Technique: PacBio<br>FGSC number: 8807<br><br>W1434 (<i>N. sitophila</i>)<br>Technique: PacBio<br>FGSC number: -
DOI: 10.6084/m9.figshare.5327809
title: De novo genome assemblies of Neurospora tetrasperma based on Illumina HiSeq reads

description: This dataset contains 92 de novo genome assemblies of <i>Neurospora tetrasperma</i>, together with one assembly of a <i>N. hispaniola</i> genome (8817) and one assembly of a <i>N. sitophila genome</i> (1135). The genomes were assembled using SOAPdenovo.<br><br>Raw reads have been deposited in the Sequence Read Archive (SRA, https://www.ncbi.nlm.nih.gov/sra/) in BioProjects PRJNA238188 (paired-end reads) and PRJNA239947 (matepair reads for four of the genomes).<br><br>All strains can be ordered from the Fungal Genetics Stock Center (FGSC) at http://www.fgsc.net.<br><br>For further information on the strains and the genome assemblies, please see:<br><br>
 Corcoran, P., Anderson, J.L., Jacobson, D.J., Sun, Y., Ni, P., Lascoux, M., and Johannesson, H. (2016). Introgression maintains the genetic integrity of the mating-type determining chromosome of the fungus <i>Neurospora tetrasperma</i>. Genome Res.<br>
 
 Sun, Y., Whittle, C.A., Corcoran, P., and Johannesson, H. (2015). Intron evolution in <i>Neurospora</i>: the role of mutational bias and selection. Genome Res. <i>25</i>, 100–110.<br>Sun, Y., Svedberg, J., Hiltunen, M., Corcoran, P., and Johannesson, H. (In press). Large-scale suppression of recombination predates genomic rearrangements in <i>Neurospora tetrasperma</i>.<br>
DOI: 10.6084/m9.figshare.5328988
title: Function of RAD6B and RNF8 in spermatogenesis

description: Histone ubiquitination regulates sperm formation and is important for nucleosome removal during spermatogenesis. RNF8 is an E3 ubiquitin ligase, and RAD6B is an E2 ubiquitin-conjugating enzyme. Both proteins participate in DNA damage repair processes via histone ubiquitination. Loss of RNF8 or RAD6B can lead to sterility in male mice. However, the specific mechanisms regulating these ubiquitin-mediated processes are unclear. In this study, we found that RNF8 knockout mice were either subfertile or sterile based on the numbers of offspring they produced. We explored the mechanism by which RAD6B and RNF8 knockouts cause infertility in male mice and compared the effects of their loss on spermatogenesis. Our results demonstrate that RAD6B can polyubiquitinate histones H2 A and H2B. In addition, RNF8 was shown to monoubiquitinate histones H2 A and H2B. Furthermore, we observed that absence of histone ubiquitination was not the only reason for infertility. Senescence played a role in intensifying male sterility by affecting the number of germ cells during spermatogenesis. In summary, both histone ubiquitination and senescence play important roles in spermatogenesis.
DOI: 10.6084/m9.figshare.5328988.v1
title: Function of RAD6B and RNF8 in spermatogenesis

description: Histone ubiquitination regulates sperm formation and is important for nucleosome removal during spermatogenesis. RNF8 is an E3 ubiquitin ligase, and RAD6B is an E2 ubiquitin-conjugating enzyme. Both proteins participate in DNA damage repair processes via histone ubiquitination. Loss of RNF8 or RAD6B can lead to sterility in male mice. However, the specific mechanisms regulating these ubiquitin-mediated processes are unclear. In this study, we found that RNF8 knockout mice were either subfertile or sterile based on the numbers of offspring they produced. We explored the mechanism by which RAD6B and RNF8 knockouts cause infertility in male mice and compared the effects of their loss on spermatogenesis. Our results demonstrate that RAD6B can polyubiquitinate histones H2 A and H2B. In addition, RNF8 was shown to monoubiquitinate histones H2 A and H2B. Furthermore, we observed that absence of histone ubiquitination was not the only reason for infertility. Senescence played a role in intensifying male sterility by affecting the number of germ cells during spermatogenesis. In summary, both histone ubiquitination and senescence play important roles in spermatogenesis.
DOI: 10.6084/m9.figshare.5330410
title: Restoring diabetes-induced autophagic flux arrest in ischemic/reperfused heart by ADIPOR (adiponectin receptor) activation involves both AMPK-dependent and AMPK-independent signaling

description: Macroautophagy/autophagy is increasingly recognized as an important regulator of myocardial ischemia-reperfusion (MI-R) injury. However, whether and how diabetes may alter autophagy in response to MI-R remains unknown. Deficiency of ADIPOQ, a cardioprotective molecule, markedly increases MI-R injury. However, the role of diabetic hypoadiponectinemia in cardiac autophagy alteration after MI-R is unclear. Utilizing normal control (NC), high-fat-diet-induced diabetes, and <i>Adipoq</i> knockout (<i>adipoq</i><sup>−/−</sup>) mice, we demonstrated that autophagosome formation was modestly inhibited and autophagosome clearance was markedly impaired in the diabetic heart subjected to MI-R. <i>adipoq</i><sup>−/−</sup> largely reproduced the phenotypic alterations observed in the ischemic-reperfused diabetic heart. Treatment of diabetic and <i>adipoq</i><sup>−/−</sup> mice with AdipoRon, a novel ADIPOR (adiponectin receptor) agonist, stimulated autophagosome formation, markedly increased autophagosome clearance, reduced infarct size, and improved cardiac function (P &lt; 0.01 vs vehicle). Mechanistically, AdipoRon caused significant phosphorylation of AMPK-BECN1 (Ser93/Thr119)-class III PtdIns3K (Ser164) and enhanced lysosome protein LAMP2 expression both in vivo and in isolated adult cardiomyocytes. Pharmacological AMPK inhibition or genetic <i>Prkaa2</i> mutation abolished AdipoRon-induced BECN1 (Ser93/Thr119)-PtdIns3K (Ser164) phosphorylation and AdipoRon-stimulated autophagosome formation. However, AdipoRon-induced LAMP2 expression, AdipoRon-stimulated autophagosome clearance, and AdipoRon-suppressed superoxide generation were not affected by AMPK inhibition. Treatment with MnTMPyP (a superoxide scavenger) increased LAMP2 expression and stimulated autophagosome clearance in simulated ischemic-reperfused cardiomyocytes. However, no additive effect between AdipoRon and MnTMPyP was observed. Collectively, these results demonstrate that hypoadiponectinemia impairs autophagic flux, contributing to enhanced MI-R injury in the diabetic state. ADIPOR activation restores AMPK-mediated autophagosome formation and antioxidant-mediated autophagosome clearance, representing a novel intervention effective against MI-R injury in diabetic conditions.
DOI: 10.6084/m9.figshare.5330410.v1
title: Restoring diabetes-induced autophagic flux arrest in ischemic/reperfused heart by ADIPOR (adiponectin receptor) activation involves both AMPK-dependent and AMPK-independent signaling

description: Macroautophagy/autophagy is increasingly recognized as an important regulator of myocardial ischemia-reperfusion (MI-R) injury. However, whether and how diabetes may alter autophagy in response to MI-R remains unknown. Deficiency of ADIPOQ, a cardioprotective molecule, markedly increases MI-R injury. However, the role of diabetic hypoadiponectinemia in cardiac autophagy alteration after MI-R is unclear. Utilizing normal control (NC), high-fat-diet-induced diabetes, and <i>Adipoq</i> knockout (<i>adipoq</i><sup>−/−</sup>) mice, we demonstrated that autophagosome formation was modestly inhibited and autophagosome clearance was markedly impaired in the diabetic heart subjected to MI-R. <i>adipoq</i><sup>−/−</sup> largely reproduced the phenotypic alterations observed in the ischemic-reperfused diabetic heart. Treatment of diabetic and <i>adipoq</i><sup>−/−</sup> mice with AdipoRon, a novel ADIPOR (adiponectin receptor) agonist, stimulated autophagosome formation, markedly increased autophagosome clearance, reduced infarct size, and improved cardiac function (P &lt; 0.01 vs vehicle). Mechanistically, AdipoRon caused significant phosphorylation of AMPK-BECN1 (Ser93/Thr119)-class III PtdIns3K (Ser164) and enhanced lysosome protein LAMP2 expression both in vivo and in isolated adult cardiomyocytes. Pharmacological AMPK inhibition or genetic <i>Prkaa2</i> mutation abolished AdipoRon-induced BECN1 (Ser93/Thr119)-PtdIns3K (Ser164) phosphorylation and AdipoRon-stimulated autophagosome formation. However, AdipoRon-induced LAMP2 expression, AdipoRon-stimulated autophagosome clearance, and AdipoRon-suppressed superoxide generation were not affected by AMPK inhibition. Treatment with MnTMPyP (a superoxide scavenger) increased LAMP2 expression and stimulated autophagosome clearance in simulated ischemic-reperfused cardiomyocytes. However, no additive effect between AdipoRon and MnTMPyP was observed. Collectively, these results demonstrate that hypoadiponectinemia impairs autophagic flux, contributing to enhanced MI-R injury in the diabetic state. ADIPOR activation restores AMPK-mediated autophagosome formation and antioxidant-mediated autophagosome clearance, representing a novel intervention effective against MI-R injury in diabetic conditions.
DOI: 10.6084/m9.figshare.5332051
title: 2898059.csv

description: The result of continuous measurement
DOI: 10.6084/m9.figshare.5332051.v1
title: 2898059.csv

description: The result of continuous measurement
DOI: 10.6084/m9.figshare.5332054
title: 2898063.csv

description: The result of pressure calibration experiments
DOI: 10.6073/pasta/4a8cbfc4011ff759a0b5a3f08d7fc872
title: Environmental and behavioral sensor data to identify heat stress in dairy cows

description: Heat stress impairs the health and performance of dairy cows, yet only a few studies have investigated the diversity of cattle behavioral responses to heat waves. This research was conducted on an Italian Holstein dairy farm equipped with precision livestock farming sensors to assess potential different behavioral patterns of the animals. Three heat waves, defined as at least five consecutive days with mean daily temperature-humidity index higher than 72, were recorded in the farm area during the summer of 2021. Individual daily milk yield data of 102 cows were used to identify ‘heat-sensitive’ animals, meaning the cows that, under a given heat wave, experienced a milk yield drop that was not linked with other health events (e.g., mastitis). Milk yield drops were detected as perturbations of the lactation curve estimated by iteratively using Wood’s equation. Individual daily minutes of lying, chewing, and activity were retrieved from ear-tag-based accelerometer sensors. Semi-parametric generalized estimating equations models were used to assess behavioral deviations of heat-sensitive cows from the herd means under heat stress conditions. Heat waves were associated with an overall increase in the herd’s chewing and activity times, along with an overall decrease of lying time. Heat-sensitive cows spent approximately 15 min/d more chewing and performing activities (p &lt; 0.05). The findings of this research suggest that the information provided by high-frequency sensor data could assist farmers in identifying cows for which personalized interventions to alleviate heat stress are needed.
DOI: 10.6084/m9.figshare.5335861
title: Preprocessed IgG Fc glycomics data in four Croatian cohorts (LC-ESI-MS)

description: The file contains preprocessed IgG glycan
concentrations in four large scale Croatian cohorts. Glycan abundances were measured via LC-ESI-MS and preprocessed as described in the first sheet of the file. For confidentiality reasons, age and gender data could not be shared
publicly; glycan values corrected for those variables are therefore additionally provided. A GGM inferred on
this corrected data matrix will be substantially the same as the one presented in
the original paper.The Croatian
cohorts received ethical approval of the ethics committee of the University of
Split School of Medicine, as well as the South East Scotland Research. Written
informed consent was obtained from each participant.
DOI: 10.6084/m9.figshare.5335861.v1
title: Preprocessed IgG Fc glycomics data in four Croatian cohorts (LC-ESI-MS)

description: The file contains preprocessed IgG glycan
concentrations in four large scale Croatian cohorts. Glycan abundances were measured via LC-ESI-MS and preprocessed as described in the first sheet of the file. For confidentiality reasons, age and gender data could not be shared
publicly; glycan values corrected for those variables are therefore additionally provided. A GGM inferred on
this corrected data matrix will be substantially the same as the one presented in
the original paper.The Croatian
cohorts received ethical approval of the ethics committee of the University of
Split School of Medicine, as well as the South East Scotland Research. Written
informed consent was obtained from each participant.
DOI: 10.6084/m9.figshare.5339914
title: Chinese Xibe population genetic composition according to linkage groups of X-chromosomal STRs: population genetic variability and interpopulation comparisons

description: <b>Background:</b> The Xibe population is one of China’s officially recognised populations and is now distributed separately from west to east in the northern part of China. X-chromosomal short tandem repeats have a special inheritance pattern, and could be used as complements in forensic application, especially for complex or deficiency cases. <b>Subjects and methods:</b> This study obtained the allelic and haplotypic frequencies of 19 X-STR loci in the Xibe population from Xinjiang Uygur Autonomous Region, China, and studied the genetic differentiations between the Xibe and other populations. <b>Results:</b> The combined power of discrimination in females and males and mean exclusion chances in deficiency cases, normal trios and duo cases was at least 0.999 999 994. In the haplotypic study, the Xibe population showed a more similar pattern of haplotype distribution with Asian populations than populations from other continents, while allelic study also indicated a closer relationship between the Xibe and Asian populations. <b>Conclusions:</b> The 19 X-STR loci would be useful in forensic application in the studied population. The Xibe population showed a closer genetic relationship with Asian populations in the study, and more population data would be necessary for more detailed genetic relationship studies.
DOI: 10.6084/m9.figshare.5339962
title: PDTCM: a systems pharmacology platform of traditional Chinese medicine for psoriasis

description: <b>Introduction:</b> Psoriasis is a refractory skin disorder, and usually requires a lifetime control. Traditional Chinese medicine (TCM) is effective and safe for this disease. However, the cellular and molecular mechanisms of TCM remedies for psoriasis are still not fully understood. TCM contains numerous natural products. Natural products have historically been invaluable as a resource of therapeutic agents. Yet, there is no integrated information about active compounds of TCM for psoriasis. <b>Method:</b> We use systems pharmacology methods to develop the Psoriasis Database of Traditional Chinese Medicine (PDTCM). The database covered a number of psoriasis-related information (formulas, TCM, compounds, target proteins, diseases and biomarkers). With these data information, an online platform was constructed <b>Results:</b> PDTCM comprises 38 empirical therapeutic formulas, 34373 compounds from 1424 medicinal plants, 44 psoriasis-related proteins and 76 biomarkers from 111 related diseases. On this platform, users can screen active compounds for a psoriasis-related target and explore molecular mechanisms of TCM. Accordingly, users can also download the retrieved structures and data information with a defined value set. In addition, it helps to get a better understanding of Chinese prescriptions in disease treatment. <b>Conclusion:</b> With the systems pharmacology-based data, PDTCM would become a valuable resource for TCM in psoriasis-related research.Key messagesPDTCM platform comprises a great deal of data on TCM and psoriasis.On this platform, users can retrieve and get needed information with systems pharmacology methods, such as active compounds screening, target prediction and molecular mechanisms exploration.It is a tool for psoriasis-related research on natural drugs systematically. PDTCM platform comprises a great deal of data on TCM and psoriasis. On this platform, users can retrieve and get needed information with systems pharmacology methods, such as active compounds screening, target prediction and molecular mechanisms exploration. It is a tool for psoriasis-related research on natural drugs systematically.