cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.7950581
title: 3D meshes of wood samples (KUR project)

description: The repository contains 3D meshes of 83 wood samples from the LEIZA reference collection documented as part of the project „Mass Finds in Archaeological Collections“ funded by the Federal Cultural Foundation, from 15.04.2008 to 31.12.2011 within the framework of the "Programme for the Conservation and Restoration of Mobile Cultural Property" (KUR, see www.rgzm.de/kur). Each wood sample has two 3D meshes, one before conservation (KUR_3D_Vorzustand.zip) and one after conservation (KUR_3D_Endzustand.zip). A 3D fringe light projector (GOM ATOS III Rev.01) with a resolution of 0.25 mm was used to digitize the samples. Additional information can be found in the stored metafiles (*.json, *.ttl). The acquisition of 3D data was done during July 2009 - August 2014.
DOI: 10.5281/zenodo.7950582
title: 3D meshes of wood samples (KUR project)

description: The repository contains 3D meshes of 83 wood samples from the LEIZA reference collection documented as part of the project „Mass Finds in Archaeological Collections“ funded by the Federal Cultural Foundation, from 15.04.2008 to 31.12.2011 within the framework of the "Programme for the Conservation and Restoration of Mobile Cultural Property" (KUR, see www.rgzm.de/kur). Each wood sample has two 3D meshes, one before conservation (KUR_3D_Vorzustand.zip) and one after conservation (KUR_3D_Endzustand.zip). A 3D fringe light projector (GOM ATOS III Rev.01) with a resolution of 0.25 mm was used to digitize the samples. Additional information can be found in the stored metafiles (*.json, *.ttl). The acquisition of 3D data was done during July 2009 - August 2014.
DOI: 10.6084/m9.figshare.4868972.v2
title: Heparan sulfate proteoglycans regulate autophagy in <i>Drosophila</i>

description: Heparan sulfate-modified proteoglycans (HSPGs) are important regulators of signaling and molecular recognition at the cell surface and in the extracellular space. Disruption of HSPG core proteins, HS-synthesis, or HS-degradation can have profound effects on growth, patterning, and cell survival. The <i>Drosophila</i> neuromuscular junction provides a tractable model for understanding the activities of HSPGs at a synapse that displays developmental and activity-dependent plasticity. Muscle cell-specific knockdown of HS biosynthesis disrupted the organization of a specialized postsynaptic membrane, the subsynaptic reticulum (SSR), and affected the number and morphology of mitochondria. We provide evidence that these changes result from a dysregulation of macroautophagy (hereafter referred to as autophagy). Cellular and molecular markers of autophagy are all consistent with an increase in the levels of autophagy in the absence of normal HS-chain biosynthesis and modification. HS production is also required for normal levels of autophagy in the fat body, the central energy storage and nutritional sensing organ in <i>Drosophila</i>. Genetic mosaic analysis indicates that HS-dependent regulation of autophagy occurs non-cell autonomously, consistent with HSPGs influencing this cellular process via signaling in the extracellular space. These findings demonstrate that HS biosynthesis has important regulatory effects on autophagy and that autophagy is critical for normal assembly of postsynaptic membrane specializations.
DOI: 10.5281/zenodo.10725491
title: Alignment and Tree file from: Two novel species of tropical Morchella (Ascomycota, Pezizales, Morchellaceae) discovered in the UNESCO Rinjani Lombok Biosphere Reserve, Indonesia

description: Alignment and Tree file from: Two novel species of tropical Morchella (Ascomycota, Pezizales, Morchellaceae) discovered in the UNESCO Rinjani Lombok Biosphere Reserve, Indonesia
DOI: 10.5281/zenodo.10725492
title: Alignment and Tree file from: Two novel species of tropical Morchella (Ascomycota, Pezizales, Morchellaceae) discovered in the UNESCO Rinjani Lombok Biosphere Reserve, Indonesia

description: Alignment and Tree file from: Two novel species of tropical Morchella (Ascomycota, Pezizales, Morchellaceae) discovered in the UNESCO Rinjani Lombok Biosphere Reserve, Indonesia
DOI: 10.6084/m9.figshare.4868972
title: Heparan sulfate proteoglycans regulate autophagy in <i>Drosophila</i>

description: Heparan sulfate-modified proteoglycans (HSPGs) are important regulators of signaling and molecular recognition at the cell surface and in the extracellular space. Disruption of HSPG core proteins, HS-synthesis, or HS-degradation can have profound effects on growth, patterning, and cell survival. The <i>Drosophila</i> neuromuscular junction provides a tractable model for understanding the activities of HSPGs at a synapse that displays developmental and activity-dependent plasticity. Muscle cell-specific knockdown of HS biosynthesis disrupted the organization of a specialized postsynaptic membrane, the subsynaptic reticulum (SSR), and affected the number and morphology of mitochondria. We provide evidence that these changes result from a dysregulation of macroautophagy (hereafter referred to as autophagy). Cellular and molecular markers of autophagy are all consistent with an increase in the levels of autophagy in the absence of normal HS-chain biosynthesis and modification. HS production is also required for normal levels of autophagy in the fat body, the central energy storage and nutritional sensing organ in <i>Drosophila</i>. Genetic mosaic analysis indicates that HS-dependent regulation of autophagy occurs non-cell autonomously, consistent with HSPGs influencing this cellular process via signaling in the extracellular space. These findings demonstrate that HS biosynthesis has important regulatory effects on autophagy and that autophagy is critical for normal assembly of postsynaptic membrane specializations.
DOI: 10.6084/m9.figshare.5092249.v2
title: Phototrophy and starvation-based induction of autophagy upon removal of Gcn5-catalyzed acetylation of Atg7 in <i>Magnaporthe oryzae</i>

description: <i>Magnaporthe oryzae</i>, the ascomycete fungus that causes rice blast disease, initiates conidiation in response to light when grown on Prune-Agar medium containing both carbon and nitrogen sources. Macroautophagy/autophagy was shown to be essential for <i>M. oryzae</i> conidiation and induced specifically upon exposure to light but is undetectable in the dark. Therefore, it is inferred that autophagy is naturally induced by light, rather than by starvation during <i>M. oryzae</i> conidiation. However, the signaling pathway(s) involved in such phototropic induction of autophagy remains unknown. We identified an <i>M. oryzae</i> ortholog of <i>GCN5</i> (<i>MGG_03677</i>), encoding a histone acetyltransferase (HAT) that negatively regulates light- and nitrogen-starvation-induced autophagy, by acetylating the autophagy protein Atg7. Furthermore, we unveiled novel regulatory mechanisms on Gcn5 at both transcriptional and post-translational levels, governing its function associated with the unique phototropic response of autophagy in this pathogenic fungus. Thus, our study depicts a signaling network and regulatory mechanism underlying the autophagy induction by important environmental clues such as light and nutrients.
DOI: 10.6084/m9.figshare.4868972.v1
title: Heparan sulfate proteoglycans regulate autophagy in <i>Drosophila</i>

description: Heparan sulfate-modified proteoglycans (HSPGs) are important regulators of signaling and molecular recognition at the cell surface and in the extracellular space. Disruption of HSPG core proteins, HS-synthesis, or HS-degradation can have profound effects on growth, patterning, and cell survival. The <i>Drosophila</i> neuromuscular junction provides a tractable model for understanding the activities of HSPGs at a synapse that displays developmental and activity-dependent plasticity. Muscle cell-specific knockdown of HS biosynthesis disrupted the organization of a specialized postsynaptic membrane, the subsynaptic reticulum (SSR), and affected the number and morphology of mitochondria. We provide evidence that these changes result from a dysregulation of macroautophagy (hereafter referred to as autophagy). Cellular and molecular markers of autophagy are all consistent with an increase in the levels of autophagy in the absence of normal HS-chain biosynthesis and modification. HS production is also required for normal levels of autophagy in the fat body, the central energy storage and nutritional sensing organ in <i>Drosophila</i>. Genetic mosaic analysis indicates that HS-dependent regulation of autophagy occurs non-cell autonomously, consistent with HSPGs influencing this cellular process via signaling in the extracellular space. These findings demonstrate that HS biosynthesis has important regulatory effects on autophagy and that autophagy is critical for normal assembly of postsynaptic membrane specializations.
DOI: 10.6084/m9.figshare.5092249
title: Phototrophy and starvation-based induction of autophagy upon removal of Gcn5-catalyzed acetylation of Atg7 in <i>Magnaporthe oryzae</i>

description: <i>Magnaporthe oryzae</i>, the ascomycete fungus that causes rice blast disease, initiates conidiation in response to light when grown on Prune-Agar medium containing both carbon and nitrogen sources. Macroautophagy/autophagy was shown to be essential for <i>M. oryzae</i> conidiation and induced specifically upon exposure to light but is undetectable in the dark. Therefore, it is inferred that autophagy is naturally induced by light, rather than by starvation during <i>M. oryzae</i> conidiation. However, the signaling pathway(s) involved in such phototropic induction of autophagy remains unknown. We identified an <i>M. oryzae</i> ortholog of <i>GCN5</i> (<i>MGG_03677</i>), encoding a histone acetyltransferase (HAT) that negatively regulates light- and nitrogen-starvation-induced autophagy, by acetylating the autophagy protein Atg7. Furthermore, we unveiled novel regulatory mechanisms on Gcn5 at both transcriptional and post-translational levels, governing its function associated with the unique phototropic response of autophagy in this pathogenic fungus. Thus, our study depicts a signaling network and regulatory mechanism underlying the autophagy induction by important environmental clues such as light and nutrients.
DOI: 10.6084/m9.figshare.5097574
title: MTOR controls genesis and autophagy of GABAergic interneurons during brain development

description: Interneuron progenitors in the ganglionic eminence of the ventral telencephalon generate most cortical interneurons during brain development. However, the regulatory mechanism of interneuron progenitors remains poorly understood. Here, we show that MTOR (mechanistic target of rapamycin [serine/threonine kinase]) regulates proliferation and macroautophagy/autophagy of interneuron progenitors in the developing ventral telencephalon. To investigate the role of MTOR in interneuron progenitors, we conditionally deleted the <i>Mtor</i> gene in mouse interneuron progenitors and their progeny by using <i>Tg(mI56i-cre,EGFP)1Kc/Dlx5/6-Cre-IRES-EGFP</i> and <i>Nkx2–1-Cre</i> drivers. We found that <i>Mtor</i> deletion markedly reduced the number of interneurons in the cerebral cortex. However, relative positioning of cortical interneurons was normal, suggesting that disruption of progenitor self-renewal caused the decreased number of cortical interneurons in the <i>Mtor</i>-deleted brain. Indeed, <i>Mtor</i>-deleted interneuron progenitors showed abnormal proliferation and cell cycle progression. Additionally, we detected a significant activation of autophagy in <i>Mtor</i>-deleted brain. Our findings suggest that MTOR plays a critical role in the regulation of cortical interneuron number and autophagy in the developing brain.
DOI: 10.6084/m9.figshare.5195698
title: ADIPOQ/adiponectin induces cytotoxic autophagy in breast cancer cells through STK11/LKB1-mediated activation of the AMPK-ULK1 axis

description: ADIPOQ/adiponectin, an adipocytokine secreted by adipocytes in the breast tumor microenvironment, negatively regulates cancer cell growth hence increased levels of ADIPOQ/adiponectin are associated with decreased breast cancer growth. However, its mechanisms of action remain largely elusive. We report that ADIPOQ/adiponectin induces a robust accumulation of autophagosomes, increases MAP1LC3B-II/LC3B-II and decreases SQSTM1/p62 in breast cancer cells. ADIPOQ/adiponectin-treated cells and xenografts exhibit increased expression of autophagy-related proteins. LysoTracker Red-staining and tandem-mCherry-GFP-LC3B assay show that fusion of autophagosomes and lysosomes is augmented upon ADIPOQ/adiponectin treatment. ADIPOQ/adiponectin significantly inhibits breast cancer growth and induces apoptosis both in vitro and in vivo, and these events are preceded by macroautophagy/autophagy, which is integral for ADIPOQ/adiponectin-mediated cell death. Accordingly, blunting autophagosome formation, blocking autophagosome-lysosome fusion or genetic-knockout of <i>BECN1/Beclin1</i> and <i>ATG7</i> effectively impedes ADIPOQ/adiponectin induced growth-inhibition and apoptosis-induction. Mechanistic studies show that ADIPOQ/adiponectin reduces intracellular ATP levels and increases PRKAA1 phosphorylation leading to ULK1 activation. AMPK-inhibition abrogates ADIPOQ/adiponectin-induced ULK1-activation, LC3B-turnover and SQSTM1/p62-degradation while AMPK-activation potentiates ADIPOQ/adiponectin's effects. Further, ADIPOQ/adiponectin-mediated AMPK-activation and autophagy-induction are regulated by upstream master-kinase STK11/LKB1, which is a key node in antitumor function of ADIPOQ/adiponectin as <i>STK11/LKB1</i>-knockout abrogates ADIPOQ/adiponectin-mediated inhibition of breast tumorigenesis and molecular analyses of tumors corroborate in vitro mechanistic findings. ADIPOQ/adiponectin increases the efficacy of chemotherapeutic agents. Notably, high expression of ADIPOQ receptor <i>ADIPOR2, ADIPOQ</i>/adiponectin and <i>BECN1</i> significantly correlates with increased overall survival in chemotherapy-treated breast cancer patients. Collectively, these data uncover that ADIPOQ/adiponectin induces autophagic cell death in breast cancer and provide in vitro and in vivo evidence for the integral role of STK11/LKB1-AMPK-ULK1 axis in ADIPOQ/adiponectin-mediated cytotoxic autophagy.
DOI: 10.6084/m9.figshare.5195698.v2
title: ADIPOQ/adiponectin induces cytotoxic autophagy in breast cancer cells through STK11/LKB1-mediated activation of the AMPK-ULK1 axis

description: ADIPOQ/adiponectin, an adipocytokine secreted by adipocytes in the breast tumor microenvironment, negatively regulates cancer cell growth hence increased levels of ADIPOQ/adiponectin are associated with decreased breast cancer growth. However, its mechanisms of action remain largely elusive. We report that ADIPOQ/adiponectin induces a robust accumulation of autophagosomes, increases MAP1LC3B-II/LC3B-II and decreases SQSTM1/p62 in breast cancer cells. ADIPOQ/adiponectin-treated cells and xenografts exhibit increased expression of autophagy-related proteins. LysoTracker Red-staining and tandem-mCherry-GFP-LC3B assay show that fusion of autophagosomes and lysosomes is augmented upon ADIPOQ/adiponectin treatment. ADIPOQ/adiponectin significantly inhibits breast cancer growth and induces apoptosis both in vitro and in vivo, and these events are preceded by macroautophagy/autophagy, which is integral for ADIPOQ/adiponectin-mediated cell death. Accordingly, blunting autophagosome formation, blocking autophagosome-lysosome fusion or genetic-knockout of <i>BECN1/Beclin1</i> and <i>ATG7</i> effectively impedes ADIPOQ/adiponectin induced growth-inhibition and apoptosis-induction. Mechanistic studies show that ADIPOQ/adiponectin reduces intracellular ATP levels and increases PRKAA1 phosphorylation leading to ULK1 activation. AMPK-inhibition abrogates ADIPOQ/adiponectin-induced ULK1-activation, LC3B-turnover and SQSTM1/p62-degradation while AMPK-activation potentiates ADIPOQ/adiponectin's effects. Further, ADIPOQ/adiponectin-mediated AMPK-activation and autophagy-induction are regulated by upstream master-kinase STK11/LKB1, which is a key node in antitumor function of ADIPOQ/adiponectin as <i>STK11/LKB1</i>-knockout abrogates ADIPOQ/adiponectin-mediated inhibition of breast tumorigenesis and molecular analyses of tumors corroborate in vitro mechanistic findings. ADIPOQ/adiponectin increases the efficacy of chemotherapeutic agents. Notably, high expression of ADIPOQ receptor <i>ADIPOR2, ADIPOQ</i>/adiponectin and <i>BECN1</i> significantly correlates with increased overall survival in chemotherapy-treated breast cancer patients. Collectively, these data uncover that ADIPOQ/adiponectin induces autophagic cell death in breast cancer and provide in vitro and in vivo evidence for the integral role of STK11/LKB1-AMPK-ULK1 axis in ADIPOQ/adiponectin-mediated cytotoxic autophagy.
DOI: 10.6084/m9.figshare.5092249.v1
title: Phototrophy and starvation-based induction of autophagy upon removal of Gcn5-catalyzed acetylation of Atg7 in <i>Magnaporthe oryzae</i>

description: <i>Magnaporthe oryzae</i>, the ascomycete fungus that causes rice blast disease, initiates conidiation in response to light when grown on Prune-Agar medium containing both carbon and nitrogen sources. Macroautophagy/autophagy was shown to be essential for <i>M. oryzae</i> conidiation and induced specifically upon exposure to light but is undetectable in the dark. Therefore, it is inferred that autophagy is naturally induced by light, rather than by starvation during <i>M. oryzae</i> conidiation. However, the signaling pathway(s) involved in such phototropic induction of autophagy remains unknown. We identified an <i>M. oryzae</i> ortholog of <i>GCN5</i> (<i>MGG_03677</i>), encoding a histone acetyltransferase (HAT) that negatively regulates light- and nitrogen-starvation-induced autophagy, by acetylating the autophagy protein Atg7. Furthermore, we unveiled novel regulatory mechanisms on Gcn5 at both transcriptional and post-translational levels, governing its function associated with the unique phototropic response of autophagy in this pathogenic fungus. Thus, our study depicts a signaling network and regulatory mechanism underlying the autophagy induction by important environmental clues such as light and nutrients.
DOI: 10.6084/m9.figshare.5097574.v1
title: MTOR controls genesis and autophagy of GABAergic interneurons during brain development

description: Interneuron progenitors in the ganglionic eminence of the ventral telencephalon generate most cortical interneurons during brain development. However, the regulatory mechanism of interneuron progenitors remains poorly understood. Here, we show that MTOR (mechanistic target of rapamycin [serine/threonine kinase]) regulates proliferation and macroautophagy/autophagy of interneuron progenitors in the developing ventral telencephalon. To investigate the role of MTOR in interneuron progenitors, we conditionally deleted the <i>Mtor</i> gene in mouse interneuron progenitors and their progeny by using <i>Tg(mI56i-cre,EGFP)1Kc/Dlx5/6-Cre-IRES-EGFP</i> and <i>Nkx2–1-Cre</i> drivers. We found that <i>Mtor</i> deletion markedly reduced the number of interneurons in the cerebral cortex. However, relative positioning of cortical interneurons was normal, suggesting that disruption of progenitor self-renewal caused the decreased number of cortical interneurons in the <i>Mtor</i>-deleted brain. Indeed, <i>Mtor</i>-deleted interneuron progenitors showed abnormal proliferation and cell cycle progression. Additionally, we detected a significant activation of autophagy in <i>Mtor</i>-deleted brain. Our findings suggest that MTOR plays a critical role in the regulation of cortical interneuron number and autophagy in the developing brain.
DOI: 10.6084/m9.figshare.5097574.v2
title: MTOR controls genesis and autophagy of GABAergic interneurons during brain development

description: Interneuron progenitors in the ganglionic eminence of the ventral telencephalon generate most cortical interneurons during brain development. However, the regulatory mechanism of interneuron progenitors remains poorly understood. Here, we show that MTOR (mechanistic target of rapamycin [serine/threonine kinase]) regulates proliferation and macroautophagy/autophagy of interneuron progenitors in the developing ventral telencephalon. To investigate the role of MTOR in interneuron progenitors, we conditionally deleted the <i>Mtor</i> gene in mouse interneuron progenitors and their progeny by using <i>Tg(mI56i-cre,EGFP)1Kc/Dlx5/6-Cre-IRES-EGFP</i> and <i>Nkx2–1-Cre</i> drivers. We found that <i>Mtor</i> deletion markedly reduced the number of interneurons in the cerebral cortex. However, relative positioning of cortical interneurons was normal, suggesting that disruption of progenitor self-renewal caused the decreased number of cortical interneurons in the <i>Mtor</i>-deleted brain. Indeed, <i>Mtor</i>-deleted interneuron progenitors showed abnormal proliferation and cell cycle progression. Additionally, we detected a significant activation of autophagy in <i>Mtor</i>-deleted brain. Our findings suggest that MTOR plays a critical role in the regulation of cortical interneuron number and autophagy in the developing brain.
DOI: 10.6084/m9.figshare.5097583.v1
title: Classical autophagy proteins LC3B and ATG4B facilitate melanosome movement on cytoskeletal tracks

description: Macroautophagy/autophagy is a dynamic and inducible catabolic process that responds to a variety of hormonal and environmental cues. Recent studies highlight the interplay of this central pathway in a variety of pathophysiological diseases. Although defective autophagy is implicated in melanocyte proliferation and pigmentary disorders, the mechanistic relationship between the 2 pathways has not been elucidated. In this study, we show that autophagic proteins LC3B and ATG4B mediate melanosome trafficking on cytoskeletal tracks. While studying melanogenesis, we observed spatial segregation of LC3B-labeled melanosomes with preferential absence at the dendritic ends of melanocytes. This LC3B labeling of melanosomes did not impact the steady-state levels of these organelles but instead facilitated their intracellular positioning. Melanosomes primarily traverse on microtubule and actin cytoskeletal tracks and our studies reveal that LC3B enables the assembly of microtubule translocon complex. At the microtubule-actin crossover junction, ATG4B detaches LC3B from melanosomal membranes by enzymatic delipidation. Further, by live-imaging we show that melanosomes transferred to keratinocytes lack melanocyte-specific LC3B. Our study thus elucidates a new role for autophagy proteins in directing melanosome movement and reveal the unconventional use of these proteins in cellular trafficking pathways. Such crosstalk between the central cellular function and housekeeping pathway may be a crucial mechanism to balance melanocyte bioenergetics and homeostasis.