cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.9119942
title: A fine-tuning mechanism underlying self-control for autophagy: deSUMOylation of BECN1 by SENP3

description: The roles of SUMOylation and the related enzymes in autophagic regulation are unclear. Based on our previous studies that identified the SUMO2/3-specific peptidase SENP3 as an oxidative stress-responsive molecule, we investigated the correlation between SUMOylation and macroautophagy/autophagy. We found that <i>Senp3<sup>±</sup></i> mice showed increased autophagy in the liver under basal and fasting conditions, compared to <i>Senp3<sup>+/+</sup></i> mice. We constructed a liver-specific <i>senp3</i> knockout mouse; these <i>Senp3</i>-deficient liver tissues showed increased autophagy as well. Autophagic flux was accelerated in hepatic and other cell lines following knockdown of <i>SENP3</i>, both before and after the cells underwent starvation in the form of the serum and amino acid deprivation. We demonstrated that BECN1/beclin 1, the core molecule of the BECN1-PIK3C3 complex, could be SUMO3-conjugated by PIAS3 predominantly at K380 and deSUMOylated by SENP3. The basal SUMOylation of BECN1 was increased upon cellular starvation, which enhanced autophagosome formation by facilitating BECN1 interaction with other complex components UVRAG, PIK3C3 and ATG14, thus promoting PIK3C3 activity. In contrast, SENP3 deSUMOylated BECN1, which impaired BECN1-PIK3C3 complex formation or stability to suppress the PIK3C3 activity. DeSUMOylation of BECN1 restrained autophagy induction under basal conditions and especially upon starvation when SENP3 had accumulated in response to the increased generation of reactive oxygen species. Thus, while reversible SUMOylation regulated the degree of autophagy, SENP3 provided an intrinsic overflow valve for fine-tuning autophagy induction. AL: autolysosome; AP: autophagosome; ATG: autophagy related; ATG14: autophagy related 14; BECN1: beclin 1, autophagy related; cKO: conditional knockout; co-IP: co-immunoprecipitation; CQ: chloroquine; EBSS: Earle’s balanced salt solution; GFP: green fluorescent protein; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; NAC: N-acetyl-L-cysteine; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; PTM: post-translational modification; RFP: red fluorescent protein; ROS: reactive oxygen species; RUBCN/rubicon: RUN domain and cysteine-rich domain containing, BECN1-interacting protein; SENP3: SUMO specific peptidase 3; shRNA: small hairpin RNA; siRNA: small interfering RNA; SQSTM1: sequestosome 1; SUMO: small ubiquitin-like modifier; UVRAG: UV radiation resistance associated gene.
DOI: 10.6084/m9.figshare.9119942.v1
title: A fine-tuning mechanism underlying self-control for autophagy: deSUMOylation of BECN1 by SENP3

description: The roles of SUMOylation and the related enzymes in autophagic regulation are unclear. Based on our previous studies that identified the SUMO2/3-specific peptidase SENP3 as an oxidative stress-responsive molecule, we investigated the correlation between SUMOylation and macroautophagy/autophagy. We found that <i>Senp3<sup>±</sup></i> mice showed increased autophagy in the liver under basal and fasting conditions, compared to <i>Senp3<sup>+/+</sup></i> mice. We constructed a liver-specific <i>senp3</i> knockout mouse; these <i>Senp3</i>-deficient liver tissues showed increased autophagy as well. Autophagic flux was accelerated in hepatic and other cell lines following knockdown of <i>SENP3</i>, both before and after the cells underwent starvation in the form of the serum and amino acid deprivation. We demonstrated that BECN1/beclin 1, the core molecule of the BECN1-PIK3C3 complex, could be SUMO3-conjugated by PIAS3 predominantly at K380 and deSUMOylated by SENP3. The basal SUMOylation of BECN1 was increased upon cellular starvation, which enhanced autophagosome formation by facilitating BECN1 interaction with other complex components UVRAG, PIK3C3 and ATG14, thus promoting PIK3C3 activity. In contrast, SENP3 deSUMOylated BECN1, which impaired BECN1-PIK3C3 complex formation or stability to suppress the PIK3C3 activity. DeSUMOylation of BECN1 restrained autophagy induction under basal conditions and especially upon starvation when SENP3 had accumulated in response to the increased generation of reactive oxygen species. Thus, while reversible SUMOylation regulated the degree of autophagy, SENP3 provided an intrinsic overflow valve for fine-tuning autophagy induction. AL: autolysosome; AP: autophagosome; ATG: autophagy related; ATG14: autophagy related 14; BECN1: beclin 1, autophagy related; cKO: conditional knockout; co-IP: co-immunoprecipitation; CQ: chloroquine; EBSS: Earle’s balanced salt solution; GFP: green fluorescent protein; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; NAC: N-acetyl-L-cysteine; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; PTM: post-translational modification; RFP: red fluorescent protein; ROS: reactive oxygen species; RUBCN/rubicon: RUN domain and cysteine-rich domain containing, BECN1-interacting protein; SENP3: SUMO specific peptidase 3; shRNA: small hairpin RNA; siRNA: small interfering RNA; SQSTM1: sequestosome 1; SUMO: small ubiquitin-like modifier; UVRAG: UV radiation resistance associated gene.
DOI: 10.6084/m9.figshare.9746135
title: Modulating EGFR-MTORC1-autophagy as a potential therapy for persistent fetal vasculature (PFV) disease

description: Persistent fetal vasculature (PFV) is a human disease that results from failure of the fetal vasculature to regress normally. The regulatory mechanisms responsible for fetal vascular regression remain obscure, as does the underlying cause of regression failure. However, there are a few animal models that mimic the clinical manifestations of human PFV, which can be used to study different aspects of the disease. One such model is the Nuc1 rat model that arose from a spontaneous mutation in the <i>Cryba1</i> (crystallin, beta 1) gene and exhibits complete failure of the hyaloid vasculature to regress. Our studies with the Nuc1 rat indicate that macroautophagy/autophagy, a process in eukaryotic cells for degrading dysfunctional components to ensure cellular homeostasis, is severely impaired in Nuc1 ocular astrocytes. Further, we show that CRYBA1 interacts with EGFR (epidermal growth factor receptor) and that loss of this interaction in Nuc1 astrocytes increases EGFR levels. Moreover, our data also show a reduction in EGFR degradation in Nuc1 astrocytes compared to control cells that leads to over-activation of the mechanistic target of rapamycin kinase complex 1 (MTORC1) pathway. The impaired EGFR-MTORC1-autophagy signaling in Nuc1 astrocytes triggers abnormal proliferation and migration. The abnormally migrating astrocytes ensheath the hyaloid artery, contributing to the pathogenesis of PFV in Nuc1, by adversely affecting the vascular remodeling processes essential to regression of the fetal vasculature. Herein, we demonstrate <i>in vivo</i> that gefitinib (EGFR inhibitor) can rescue the PFV phenotype in Nuc1 and may serve as a novel therapy for PFV disease by modulating the EGFR-MTORC1-autophagy pathway. ACTB: actin, beta; CCND3: cyclin 3; CDK6: cyclin-dependent kinase 6; CHQ: chloroquine; COL4A1: collagen, type IV, alpha 1; CRYBA1: crystallin, beta A1; DAPI: 4ʹ6-diamino-2-phenylindole; EGFR: epidermal growth factor receptor; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFAP: glial fibrillary growth factor; KDR: kinase insert domain protein receptor; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MKI67: antigen identified by monoclonal antibody Ki 67; MTORC1: mechanistic target of rapamycin kinase complex 1; PARP: poly (ADP-ribose) polymerase family; PCNA: proliferating cell nuclear antigen; PFV: persistent fetal vasculature; PHPV: persistent hyperplastic primary vitreous; RPE: retinal pigmented epithelium; RPS6: ribosomal protein S6; RPS6KB1: ribosomal protein S6 kinase, polypeptide 1; SQSTM1/p62: sequestome 1; TUBB: tubulin, beta; VCL: vinculin; VEGFA: vascular endothelial growth factor A; WT: wild type.
DOI: 10.6084/m9.figshare.9746135.v1
title: Modulating EGFR-MTORC1-Autophagy as a potential therapy for Persistent Fetal Vasculature (PFV) disease

description: Persistent fetal vasculature (PFV) is a human disease that results from failure of the fetal vasculature to regress normally. The regulatory mechanisms responsible for fetal vascular regression remain obscure, as does the underlying cause of regression failure. However, there are a few animal models that mimic the clinical manifestations of human PFV, which can be used to study different aspects of the disease. One such model is the Nuc1 rat model that arose from a spontaneous mutation in the <i>Cryba1</i> (crystallin, beta 1) gene and exhibits complete failure of the hyaloid vasculature to regress. Our studies with the Nuc1 rat indicate that macroautophagy/autophagy, a process in eukaryotic cells for degrading dysfunctional components to ensure cellular homeostasis, is severely impaired in Nuc1 ocular astrocytes. Further, we show that CRYBA1 interacts with EGFR (epidermal growth factor receptor) and that loss of this interaction in Nuc1 astrocytes increases EGFR levels. Moreover, our data also show a reduction in EGFR degradation in Nuc1 astrocytes compared to control cells that leads to over-activation of the mechanistic target of rapamycin kinase complex 1 (MTORC1) pathway. The impaired EGFR-MTORC1-autophagy signaling in Nuc1 astrocytes triggers abnormal proliferation and migration. The abnormally migrating astrocytes ensheath the hyaloid artery, contributing to the pathogenesis of PFV in Nuc1, by adversely affecting the vascular remodeling processes essential to regression of the fetal vasculature. Herein, we demonstrate <i>in vivo</i> that gefitinib (EGFR inhibitor) can rescue the PFV phenotype in Nuc1 and may serve as a novel therapy for PFV disease by modulating the EGFR-MTORC1-autophagy pathway.​
DOI: 10.6084/m9.figshare.9746135.v2
title: Modulating EGFR-MTORC1-autophagy as a potential therapy for persistent fetal vasculature (PFV) disease

description: Persistent fetal vasculature (PFV) is a human disease that results from failure of the fetal vasculature to regress normally. The regulatory mechanisms responsible for fetal vascular regression remain obscure, as does the underlying cause of regression failure. However, there are a few animal models that mimic the clinical manifestations of human PFV, which can be used to study different aspects of the disease. One such model is the Nuc1 rat model that arose from a spontaneous mutation in the <i>Cryba1</i> (crystallin, beta 1) gene and exhibits complete failure of the hyaloid vasculature to regress. Our studies with the Nuc1 rat indicate that macroautophagy/autophagy, a process in eukaryotic cells for degrading dysfunctional components to ensure cellular homeostasis, is severely impaired in Nuc1 ocular astrocytes. Further, we show that CRYBA1 interacts with EGFR (epidermal growth factor receptor) and that loss of this interaction in Nuc1 astrocytes increases EGFR levels. Moreover, our data also show a reduction in EGFR degradation in Nuc1 astrocytes compared to control cells that leads to over-activation of the mechanistic target of rapamycin kinase complex 1 (MTORC1) pathway. The impaired EGFR-MTORC1-autophagy signaling in Nuc1 astrocytes triggers abnormal proliferation and migration. The abnormally migrating astrocytes ensheath the hyaloid artery, contributing to the pathogenesis of PFV in Nuc1, by adversely affecting the vascular remodeling processes essential to regression of the fetal vasculature. Herein, we demonstrate <i>in vivo</i> that gefitinib (EGFR inhibitor) can rescue the PFV phenotype in Nuc1 and may serve as a novel therapy for PFV disease by modulating the EGFR-MTORC1-autophagy pathway. ACTB: actin, beta; CCND3: cyclin 3; CDK6: cyclin-dependent kinase 6; CHQ: chloroquine; COL4A1: collagen, type IV, alpha 1; CRYBA1: crystallin, beta A1; DAPI: 4ʹ6-diamino-2-phenylindole; EGFR: epidermal growth factor receptor; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFAP: glial fibrillary growth factor; KDR: kinase insert domain protein receptor; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MKI67: antigen identified by monoclonal antibody Ki 67; MTORC1: mechanistic target of rapamycin kinase complex 1; PARP: poly (ADP-ribose) polymerase family; PCNA: proliferating cell nuclear antigen; PFV: persistent fetal vasculature; PHPV: persistent hyperplastic primary vitreous; RPE: retinal pigmented epithelium; RPS6: ribosomal protein S6; RPS6KB1: ribosomal protein S6 kinase, polypeptide 1; SQSTM1/p62: sequestome 1; TUBB: tubulin, beta; VCL: vinculin; VEGFA: vascular endothelial growth factor A; WT: wild type.
DOI: 10.6084/m9.figshare.9746129
title: Induction of autophagy through CLEC4E in combination with TLR4: an innovative strategy to restrict the survival of <i>Mycobacterium tuberculosis</i>

description: Host-directed therapies are gaining considerable impetus because of the emergence of drug-resistant strains of pathogens due to antibiotic therapy. Therefore, there is an urgent need to exploit alternative and novel strategies directed at host molecules to successfully restrict infections. The C-type lectin receptor CLEC4E and Toll-like receptor TLR4 expressed by host cells are among the first line of defense in encountering pathogens. Therefore, we exploited signaling of macrophages through CLEC4E in association with TLR4 agonists (C<sub>4</sub>.T<sub>4</sub>) to control the growth of <i>Mycobacterium tuberculosis</i> (<i>Mtb</i>). We observed significant improvement in host immunity and reduced bacterial load in the lungs of <i>Mtb-</i>infected mice and guinea pigs treated with C<sub>4</sub>.T<sub>4</sub> agonists. Further, intracellular killing of <i>Mtb</i> was achieved with a 10-fold lower dose of isoniazid or rifampicin in conjunction with C<sub>4</sub>.T<sub>4</sub> than the drugs alone. C<sub>4</sub>.T<sub>4</sub> activated MYD88, PtdIns3K, STAT1 and RELA/NFKB, increased lysosome biogenesis, decreased <i>Il10</i> and <i>Il4</i> gene expression and enhanced macroautophagy/autophagy. Macrophages from autophagy-deficient (<i>atg5</i> knockout or <i>Becn1</i> knockdown) mice showed elevated survival of <i>Mtb</i>. The present findings also unveiled the novel role of CLEC4E in inducing autophagy through MYD88, which is required for control of <i>Mtb</i> growth. This study suggests a unique immunotherapeutic approach involving CLEC4E in conjunction with TLR4 to restrict the survival of <i>Mtb</i> through autophagy. 3MA: 3 methyladenine; AO: acridine orange; Atg5: autophagy related 5; AVOs: acidic vesicular organelles; BECN1: beclin 1, autophagy related; BMDMs: bone marrow derived macrophages; bw: body weight; C<sub>4</sub>.T<sub>4</sub>: agonists of CLEC4E (C<sub>4</sub>/TDB) and TLR4 (T<sub>4</sub>/ultra-pure-LPS); CFU: colony forming unit; CLEC4E/Mincle: C-type lectin domain family 4, member e; CLR: c-type lectin receptor; INH: isoniazid; LAMP1: lysosomal-associated membrane protein 1; Mφ<sup>C4.T4</sup>: <i>Mtb-</i>infected C<sub>4</sub>.T<sub>4</sub> stimulated macrophages; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MDC: monodansylcadaverine; MTOR: mechanistic target of rapamycin kinase; MYD88: myeloid differentiation primary response 88; NFKB: nuclear factor of kappa light polypeptide gene enhance in B cells; NLR: NOD (nucleotide-binding oligomerization domain)-like receptors; PFA: paraformaldehyde; PPD: purified protein derivative; PtdIns3K: class III phosphatidylinositol 3-kinase; RELA: v-rel reticuloendotheliosis viral oncogene homolog A (avian); RIF: rifampicin; RLR: retinoic acid-inducible gene-I-like receptors; TDB: trehalose-6,6´-dibehenate; TLR4: toll-like receptor 4; Ultra-pure-LPS: ultra-pure lipopolysaccharide-EK; V-ATPase: vacuolar-type H<sup>+</sup> ATPase.
DOI: 10.6084/m9.figshare.9746129.v1
title: Induction of autophagy through CLEC4E in combination with TLR4: an innovative strategy to restrict the survival of <i>Mycobacterium tuberculosis</i>

description: Host-directed therapies are gaining considerable impetus because of the emergence of drug-resistant strains of pathogens due to antibiotic therapy. Therefore, there is an urgent need to exploit alternative and novel strategies directed at host molecules to successfully restrict infections. The C-type lectin receptor CLEC4E and Toll-like receptor TLR4 expressed by host cells are among the first line of defense in encountering pathogens. Therefore, we exploited signaling of macrophages through CLEC4E in association with TLR4 agonists (C<sub>4</sub>.T<sub>4</sub>) to control the growth of <i>Mycobacterium tuberculosis</i> (<i>Mtb</i>). We observed significant improvement in host immunity and reduced bacterial load in the lungs of <i>Mtb-</i>infected mice and guinea pigs treated with C<sub>4</sub>.T<sub>4</sub> agonists. Further, intracellular killing of <i>Mtb</i> was achieved with a 10-fold lower dose of isoniazid or rifampicin in conjunction with C<sub>4</sub>.T<sub>4</sub> than the drugs alone. C<sub>4</sub>.T<sub>4</sub> activated MYD88, PtdIns3K, STAT1 and RELA/NFKB, increased lysosome biogenesis, decreased <i>Il10</i> and <i>Il4</i> gene expression and enhanced macroautophagy/autophagy. Macrophages from autophagy-deficient (<i>atg5</i> knockout or <i>Becn1</i> knockdown) mice showed elevated survival of <i>Mtb</i>. The present findings also unveiled the novel role of CLEC4E in inducing autophagy through MYD88, which is required for control of <i>Mtb</i> growth. This study suggests a unique immunotherapeutic approach involving CLEC4E in conjunction with TLR4 to restrict the survival of <i>Mtb</i> through autophagy. 3MA: 3 methyladenine; AO: acridine orange; Atg5: autophagy related 5; AVOs: acidic vesicular organelles; BECN1: beclin 1, autophagy related; BMDMs: bone marrow derived macrophages; bw: body weight; C<sub>4</sub>.T<sub>4</sub>: agonists of CLEC4E (C<sub>4</sub>/TDB) and TLR4 (T<sub>4</sub>/ultra-pure-LPS); CFU: colony forming unit; CLEC4E/Mincle: C-type lectin domain family 4, member e; CLR: c-type lectin receptor; INH: isoniazid; LAMP1: lysosomal-associated membrane protein 1; Mφ<sup>C4.T4</sup>: <i>Mtb-</i>infected C<sub>4</sub>.T<sub>4</sub> stimulated macrophages; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MDC: monodansylcadaverine; MTOR: mechanistic target of rapamycin kinase; MYD88: myeloid differentiation primary response 88; NFKB: nuclear factor of kappa light polypeptide gene enhance in B cells; NLR: NOD (nucleotide-binding oligomerization domain)-like receptors; PFA: paraformaldehyde; PPD: purified protein derivative; PtdIns3K: class III phosphatidylinositol 3-kinase; RELA: v-rel reticuloendotheliosis viral oncogene homolog A (avian); RIF: rifampicin; RLR: retinoic acid-inducible gene-I-like receptors; TDB: trehalose-6,6´-dibehenate; TLR4: toll-like receptor 4; Ultra-pure-LPS: ultra-pure lipopolysaccharide-EK; V-ATPase: vacuolar-type H<sup>+</sup> ATPase.
DOI: 10.15468/dl.8xczpk
title: Occurrence Download

description: A dataset containing 1092882 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is one of (Agelasa nigriceps, Alloeotomus chinensis Reuter, 1903, Araniella coreana Namkung, 2002, Asiopodabrus Wittmer, 1982, Bathyphantes gracilis (Blackwall, 1841), Camponotus atrox Emery, 1925, Carbula putoni, Chaetocnema ingenua (Baly, 1876), Chrysolina aurichalcea (Mannerheim, 1825), Chrysso octomaculata (Bösenberg & Strand, 1906), Cletus schmidti Kiritshenko, 1916, Curculio distinguendus W.Roelofs, 1874, Demotina modesta Baly, 1874, Diaea subdola O.Pickard-Cambridge, 1885, Dorcus tityus Hope, 1842, Ebelingia kumadai (Ono, 1985), Ebrechtella tricuspidata (Fabricius, 1775), Enaptorrhinus granulatus Pascoe, 1881, Enoplognatha margarita Yaginuma, 1964, Eskovina clava (Zhu & Wen, 1980), Eurydema dominulus (Scopoli, 1763), Eurystylus coelestialium (Kirkaldy, 1902), Evarcha coreana Seo, 1988, Harmonia axyridis (Pallas, 1773), Helicius yaginumai Bohdanowicz & Prószyński, 1987, Hymenalia Mulsant, 1851, Lema diversa, Lysiteles coronatus (Grube, 1861), Melanotus castanipes (Paykull, 1800), Melolontha incana (Motschulsky, 1853), Menida disjecta (Uhler, 1860), Moneta caudifera (Dönitz & Strand, 1906), Myrmica kotokui Forel, 1911, Neolethaeus dallasi (Scott, 1874), Nicrophorus concolor (Kraatz, 1877), Nicrophorus maculifrons (Kraatz, 1877), Nicrophorus quadripunctatus (Kraatz, 1877), Nylanderia flavipes (Smith, 1874), Nysius plebeius Distant, 1883, Oecanthus longicauda Matsumura, 1904, Paracentrocorynus E.Voss, 1929, Pentatoma rufipes (Linnaeus, 1758), Pentatoma G.A.Olivier, 1789, Pheidole fervida Smith, 1874, Philodromus emarginatus (Schrank, 1803), Phintella cavaleriei (Schenkel, 1963), Phintella parva (Wesołowska, 1981), Phycosoma mustelinum (Simon, 1889), Pidonia puziloi (Solsky, 1872), Pisaura ancora Paik, 1969, Plebs sachalinensis (Saito, 1934), Propylea japonica (Thunberg, 1781), Psammoecus fasciatus Reitter, 1874, Rhagonycha Eschscholtz, 1830, Riptortus clavatus (Thunberg, 1783), Silesis Candèze, 1863, Sospita oblongoguttata (Linnaeus, 1758), Spilota plagiicollis Fairmaire, 1886, Strandella pargongensis (Paik, 1965), Stictopleurus crassicornis (Linnaeus, 1758), Stictopleurus minutus Blöte, 1934, Synema globosum (Fabricius, 1775), Takayus takayensis (Saito, 1939), Temnothorax Mayr, 1861, Tetragnatha pinicola L.Koch, 1870, Tetragnatha yesoensis Saito, 1934, Tibellus tenellus (L.Koch, 1876), Tmarus piger (Walckenaer, 1802), Tmarus rimosus Paik, 1973, Trichius succinctus Fabricius, 1787, Xanthochroa luteipennis, Xysticus ephippiatus Simon, 1880, Yaginumaella medvedevi Prószyński, 1979, Yaginumena castrata (Bösenberg & Strand, 1906))",
 "HasCoordinate is true",
 "HasGeospatialIssue is false"
 ]
}

 The dataset includes 1092882 records from 2463 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0072076-241126133413365/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.j4w7jn
title: Occurrence Download

description: A dataset containing 4394 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Prangos Lindl."
 ]
}

 The dataset includes 4394 records from 133 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0041874-210914110416597/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.4k886k
title: Occurrence Download

description: A dataset containing 12 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Tateomys macrocercus Musser, 1982"
 ]
}

 The dataset includes 12 records from 3 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0352600-210914110416597/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.t32l65
title: Occurrence Download

description: A dataset containing 243275 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Haloragaceae"
 ]
}

 The dataset includes 243275 records from 753 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0046039-180508205500799/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.vhbvos
title: Occurrence Download

description: A dataset containing 7069 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is Cyathodes fasciculata (G.Forst.) Allan",
 {
 "or" : [
 "BasisOfRecord is Human Observation",
 "BasisOfRecord is Observation"
 ]
 },
 "HasCoordinate is true",
 "HasGeospatialIssue is false"
 ]
}

 The dataset includes 7069 records from 3 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0032959-190918142434337/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.