cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29083122.v1
title: Experimental assessment of 3D-printed traps and chemical attractants for the collection of wild <i>Drosophila melanogaster</i>

description: <i>Drosophila melanogaster</i>, the common fruit fly, has been instrumental to our understanding of evolution, genetics and disease. There are benefits to studying these flies in the wild, including assessment of their naturally occurring microbiota. To facilitate efforts to catch wild <i>D. melanogaster</i>, we designed two fly traps and evaluated several candidate attractants. The first trap utilized a stable food substrate that can be used to catch live flies to establish new lab colonies. The second trap was designed to be reusable and easy to ship to enable the collection of flies over time from diverse locations. We evaluated several chemical attractants derived from banana and from marula fruit, which is the proposed ancestral food host of <i>D. melanogaster</i>. We found that wild flies were preferentially attracted to banana-based odorants over marula-derived ones. Overall, these traps and attractants represent an inexpensive and simple option for the collection of wild <i>D. melanogaster</i> and related species for sampling or colony establishment.
DOI: 10.6084/m9.figshare.30616122
title: UCH-L1 regulates eye differentiation-related genes and modulates EGFR signalling in <i>Drosophila melanogaster</i>

description: UCH-L1 (Ubiquitin Carboxyl-terminal Hydrolase – L1) is a protein that plays a critical role in the ubiquitin-proteasome system. Previous studies have demonstrated a link between UCH-L1 and various diseases, including neurodegenerative disorders, diabetes, and cancer. However, the role of UCH-L1 in development remains unclear. To investigate the functions of UCH-L1 in a living organism, taking advantage of the <i>Drosophila</i> model, and to explore the correlation between Drosophila UCH (dUCH) and human UCH-L1, we established a GAL4/UAS-targeted expression system to examine the effect of dUCH on <i>Drosophila</i> eye development. We found that knockdown of dUCH resulted in a rough eye phenotype associated with the MAPK pathway. In this study, for the first time, we revealed that loss of dUCH function leads to a reduction in EGFR protein levels. Additionally, dUCH knockdown downregulated Spitz (spi), a ligand of EGFR, as well as <i>Draf</i>, a key component of the MAPK pathway. Furthermore, under dUCH knockdown conditions, several genes known to play critical roles in eye cell differentiation were affected, including the downregulation of sens, salm, lz, barth1/2, and salm, which are essential for the differentiation of R2/5, R3/4, and R1/6 photoreceptor cells. Interestingly, dUCH was found to be involved not only in the MAPK pathway but also in the regulation of <i>pros, lz, barth1/2, and sev</i> gene expression, suggesting its role in R7 photoreceptor differentiation. Taken together, these findings highlight the important role of dUCH in regulating genes associated with eye cell differentiation and its involvement in EGFR signalling in <i>Drosophila melanogaster</i>.
DOI: 10.6084/m9.figshare.28937395
title: 25 years of <i>Drosophila</i> “Sleep genes”

description: The field of <i>Drosophila</i> sleep research, which began 25 years ago, has identified more than 200 genes influencing sleep. In this review, I summarize the foundation of the field and the growing list of genes implicated in sleep regulation. I compare the genetic methods used to identify genes governing sleep and circadian rhythms and the distinct outcomes of screens for genes regulating these two highly related processes. Finally, I discuss the ~ 200 sleep-regulating genes of <i>Drosophila</i> in the context of recent developments in the field and voice reasons for scepticism regarding the relevance of these genes to the homoeostatic regulation of sleep. Finally, I speculate on the future promise of the fly model system for revealing conserved molecular mechanisms of sleep homoeostasis.
DOI: 10.6084/m9.figshare.28937395.v1
title: 25 years of <i>Drosophila</i> “Sleep genes”

description: The field of <i>Drosophila</i> sleep research, which began 25 years ago, has identified more than 200 genes influencing sleep. In this review, I summarize the foundation of the field and the growing list of genes implicated in sleep regulation. I compare the genetic methods used to identify genes governing sleep and circadian rhythms and the distinct outcomes of screens for genes regulating these two highly related processes. Finally, I discuss the ~ 200 sleep-regulating genes of <i>Drosophila</i> in the context of recent developments in the field and voice reasons for scepticism regarding the relevance of these genes to the homoeostatic regulation of sleep. Finally, I speculate on the future promise of the fly model system for revealing conserved molecular mechanisms of sleep homoeostasis.
DOI: 10.6084/m9.figshare.30616122.v1
title: UCH-L1 regulates eye differentiation-related genes and modulates EGFR signalling in <i>Drosophila melanogaster</i>

description: UCH-L1 (Ubiquitin Carboxyl-terminal Hydrolase – L1) is a protein that plays a critical role in the ubiquitin-proteasome system. Previous studies have demonstrated a link between UCH-L1 and various diseases, including neurodegenerative disorders, diabetes, and cancer. However, the role of UCH-L1 in development remains unclear. To investigate the functions of UCH-L1 in a living organism, taking advantage of the <i>Drosophila</i> model, and to explore the correlation between Drosophila UCH (dUCH) and human UCH-L1, we established a GAL4/UAS-targeted expression system to examine the effect of dUCH on <i>Drosophila</i> eye development. We found that knockdown of dUCH resulted in a rough eye phenotype associated with the MAPK pathway. In this study, for the first time, we revealed that loss of dUCH function leads to a reduction in EGFR protein levels. Additionally, dUCH knockdown downregulated Spitz (spi), a ligand of EGFR, as well as <i>Draf</i>, a key component of the MAPK pathway. Furthermore, under dUCH knockdown conditions, several genes known to play critical roles in eye cell differentiation were affected, including the downregulation of sens, salm, lz, barth1/2, and salm, which are essential for the differentiation of R2/5, R3/4, and R1/6 photoreceptor cells. Interestingly, dUCH was found to be involved not only in the MAPK pathway but also in the regulation of <i>pros, lz, barth1/2, and sev</i> gene expression, suggesting its role in R7 photoreceptor differentiation. Taken together, these findings highlight the important role of dUCH in regulating genes associated with eye cell differentiation and its involvement in EGFR signalling in <i>Drosophila melanogaster</i>.
DOI: 10.6084/m9.figshare.30620790
title: Innate immunity pathways activate cell proliferation after penetrating traumatic brain injury in adult <i>Drosophila</i>

description: We are utilizing an adult penetrating traumatic brain injury (PTBI) model in Drosophila to investigate regenerative mechanisms after damage to the central brain. Here, we focus on cell proliferation as an early event in the regenerative process. To identify pathways that could trigger cell proliferation following PTBI, we utilized bulk RNA-Seq. We find that transcript levels for components of both Toll and Immune Deficiency (Imd) innate immunity pathways are rapidly and highly upregulated post-PTBI. We then tested mutants for the NF-κB transcription factors of the Toll and Imd pathways, Dorsal-related immunity factor (Dif) and Relish (Rel), respectively. We find that loss of either Dif or Rel results in loss of cell proliferation after injury and identify tissue-specific requirements for Dif and Rel. In addition, while the canonical downstream targets of <i>Drosophila</i> innate immune signalling, the antimicrobial peptides (AMPs), are upregulated following PTBI, their levels revert to near baseline within 24 hr. Taken together, these results indicate that the innate immunity pathways play an integral role in the regenerative response and that this response may not require the antimicrobial peptides. Innate immunity previously has been implicated as both a potentiator and an inhibitor of regenerative processes. Our work suggests that modulation of innate immunity may be essential to prevent adverse outcomes. Thus, this work is likely to inform future experiments to dissect regenerative mechanisms in higher organisms as well as in <i>Drosophila</i>.
DOI: 10.6084/m9.figshare.30620790.v2
title: Innate immunity pathways activate cell proliferation after penetrating traumatic brain injury in adult <i>Drosophila</i>

description: We are utilizing an adult penetrating traumatic brain injury (PTBI) model in Drosophila to investigate regenerative mechanisms after damage to the central brain. Here, we focus on cell proliferation as an early event in the regenerative process. To identify pathways that could trigger cell proliferation following PTBI, we utilized bulk RNA-Seq. We find that transcript levels for components of both Toll and Immune Deficiency (Imd) innate immunity pathways are rapidly and highly upregulated post-PTBI. We then tested mutants for the NF-κB transcription factors of the Toll and Imd pathways, Dorsal-related immunity factor (Dif) and Relish (Rel), respectively. We find that loss of either Dif or Rel results in loss of cell proliferation after injury and identify tissue-specific requirements for Dif and Rel. In addition, while the canonical downstream targets of <i>Drosophila</i> innate immune signalling, the antimicrobial peptides (AMPs), are upregulated following PTBI, their levels revert to near baseline within 24 hr. Taken together, these results indicate that the innate immunity pathways play an integral role in the regenerative response and that this response may not require the antimicrobial peptides. Innate immunity previously has been implicated as both a potentiator and an inhibitor of regenerative processes. Our work suggests that modulation of innate immunity may be essential to prevent adverse outcomes. Thus, this work is likely to inform future experiments to dissect regenerative mechanisms in higher organisms as well as in <i>Drosophila</i>.
DOI: 10.6084/m9.figshare.30175848
title: 3D imaging and quantitative analysis of adipocytes in situ and ex situ

description: Different adipose tissues (AT) have been described, including subcutaneous and visceral tissues (SCAT and VAT). They display different morphological structures, physiological and metabolic functions. Imaging adipocytes in the whole AT was not feasible because of the large adipocyte sizes and the lipid-full content of the droplets that increased the refractive index. Tissue clearing is then required mainly through a delipidation step, which induces also a tissue shrinkage. Our aim was to image in 3D freshly extracted adipocytes and compare them to those within their tissues. Trout ATs were stained with 5DTAF (extracellular matrix) and Nile Red (lipids). After clearing with Histodenz, 3D images were obtained using a confocal microscope, and adipocytes were segmented and measured. In situ, major differences in adipocyte size and shape were observed between the VAT and SCAT. Ex situ, only the size mattered because all cells were round outside their tissues. This method can be applied to other species, such as mice. In situ, adipocyte sphericity was even higher in the SCAT from a Swiss and a C57Bl6. This approach demonstrates that 3D adipocyte imaging with lipid labeling enables accurate morphological characterization, provides insights into depot-specific structural features, and supports optimization of cell isolation protocols
DOI: 10.6084/m9.figshare.30175848.v1
title: 3D imaging and quantitative analysis of adipocytes in situ and ex situ

description: Different adipose tissues (AT) have been described, including subcutaneous and visceral tissues (SCAT and VAT). They display different morphological structures, physiological and metabolic functions. Imaging adipocytes in the whole AT was not feasible because of the large adipocyte sizes and the lipid-full content of the droplets that increased the refractive index. Tissue clearing is then required mainly through a delipidation step, which induces also a tissue shrinkage. Our aim was to image in 3D freshly extracted adipocytes and compare them to those within their tissues. Trout ATs were stained with 5DTAF (extracellular matrix) and Nile Red (lipids). After clearing with Histodenz, 3D images were obtained using a confocal microscope, and adipocytes were segmented and measured. In situ, major differences in adipocyte size and shape were observed between the VAT and SCAT. Ex situ, only the size mattered because all cells were round outside their tissues. This method can be applied to other species, such as mice. In situ, adipocyte sphericity was even higher in the SCAT from a Swiss and a C57Bl6. This approach demonstrates that 3D adipocyte imaging with lipid labeling enables accurate morphological characterization, provides insights into depot-specific structural features, and supports optimization of cell isolation protocols
DOI: 10.6084/m9.figshare.24591914
title: Adipogenic characterization of immortalized CD55<sup>+</sup> progenitor cells from human white adipose tissue

description: Mature adipocytes are difficult to study ex vivo, prompting the use of human adipose progenitor cells (hAPCs). However, hAPCs undergo replicative senescence, limiting their utility in long-term studies. We inserted human telomerase reverse transcriptase (TERT) into the AAVS1 locus of CD55+ hAPCs derived from abdominal subcutaneous adipose tissue, and characterized the cells before and after adipogenic differentiation. TERT-hAPCs retained proliferative and adipogenic capacities for over 80 passages, comparable to early-passage wild type hAPCs. Transcriptomic and proteomic analyses confirmed strong adipocyte gene expression. Functionally, TERT-hAPCs responded to insulin and lipolytic stimuli (isoprenaline, dibutyryl cAMP, TNF-α). They adapted well to both 2D and 3D cultures, with improved adipogenesis under spheroid conditions. Immortalization of CD55+ hAPCs yields cells with stable proliferative and adipogenic capacity across passages. Being cryopreservable and suitable for both 2D and 3D cultures, TERT-hAPCs offer a reliable, reusable model system for adipocyte studies using cells with a consistent genetic background.
DOI: 10.6084/m9.figshare.24591914.v1
title: Adipogenic characterization of immortalized CD55<sup>+</sup> progenitor cells from human white adipose tissue

description: Mature adipocytes are difficult to study ex vivo, prompting the use of human adipose progenitor cells (hAPCs). However, hAPCs undergo replicative senescence, limiting their utility in long-term studies. We inserted human telomerase reverse transcriptase (TERT) into the AAVS1 locus of CD55+ hAPCs derived from abdominal subcutaneous adipose tissue, and characterized the cells before and after adipogenic differentiation. TERT-hAPCs retained proliferative and adipogenic capacities for over 80 passages, comparable to early-passage wild type hAPCs. Transcriptomic and proteomic analyses confirmed strong adipocyte gene expression. Functionally, TERT-hAPCs responded to insulin and lipolytic stimuli (isoprenaline, dibutyryl cAMP, TNF-α). They adapted well to both 2D and 3D cultures, with improved adipogenesis under spheroid conditions. Immortalization of CD55+ hAPCs yields cells with stable proliferative and adipogenic capacity across passages. Being cryopreservable and suitable for both 2D and 3D cultures, TERT-hAPCs offer a reliable, reusable model system for adipocyte studies using cells with a consistent genetic background.
DOI: 10.6084/m9.figshare.24533139
title: Bioactive peptide PDBSN improves mitochondrial function and suppresses oxidative stress in human adipose cells

description: Mitochondria are essential for generating cellular energy and are significant in the pathogenesis of obesity. Human visceral and subcutaneous preadipocytes (HPA-v and HPA-s) were cultured into mature adipocytes. Intracellular triglyceride (TG) content was assessed using oil-red O staining and tissue triglyceride determination. Mitochondrial membrane potential (MMP) and reactive
oxygen species (ROS) levels were measured with fluorescent indicators. Gene and protein expression related to mitochondrial biogenesis were analyzed by real-time quantitative PCR and Western blotting. Morphological changes were observed via electron microscopy. Results show that PDBSN significantly increased MMP while decreasing TG and ROS levels. The transcription and protein levels
of PGC1-α and MTFA were upregulated, and mitochondrial fusion and fission markers (MFN1, MFN2, NRF1, DRP1) were elevated. Additionally, PDBSN enhanced maximum
respiratory capacity and reduced ROS. These findings suggest that PDBSN improves mitochondrial function, providing insights for obesity treatment and metabolic disease management.
DOI: 10.6084/m9.figshare.24533139.v2
title: Bioactive peptide PDBSN improves mitochondrial function and suppresses oxidative stress in human adipose cells

description: Mitochondria are essential for generating cellular energy and are significant in the pathogenesis of obesity. Human visceral and subcutaneous preadipocytes (HPA-v and HPA-s) were cultured into mature adipocytes. Intracellular triglyceride (TG) content was assessed using oil-red O staining and tissue triglyceride determination. Mitochondrial membrane potential (MMP) and reactive
oxygen species (ROS) levels were measured with fluorescent indicators. Gene and protein expression related to mitochondrial biogenesis were analyzed by real-time quantitative PCR and Western blotting. Morphological changes were observed via electron microscopy. Results show that PDBSN significantly increased MMP while decreasing TG and ROS levels. The transcription and protein levels
of PGC1-α and MTFA were upregulated, and mitochondrial fusion and fission markers (MFN1, MFN2, NRF1, DRP1) were elevated. Additionally, PDBSN enhanced maximum
respiratory capacity and reduced ROS. These findings suggest that PDBSN improves mitochondrial function, providing insights for obesity treatment and metabolic disease management.
DOI: 10.6084/m9.figshare.28524221
title: miR-6402 targets <i>Bmpr2</i> and negatively regulates mouse adipogenesis

description: Obesity is characterized by macrophage infiltration into adipose tissue. White adipose tissue remodelling under inflammatory conditions involves both hypertrophy and adipogenesis and is regulated by transcription factors, which are influenced by bone morphogenetic protein (BMP) signalling. MicroRNAs (miRNAs) regulate gene expression and are involved in obesity-related processes such as adipogenesis. Therefore, we identified differentially expressed miRNAs in the epididymal white adipose tissue (eWAT) of mice fed a normal diet (ND) and those fed a high-fat diet (HFD). The expression of miR-6402 was significantly suppressed in the inflamed eWAT of HFD-fed mice than in ND-fed mice. Furthermore, <i>Bmpr2</i>, the receptor for BMP4, was identified as a target gene of miR-6402. Consistently, miR-6402 was downregulated in the inflamed eWAT of HFD-fed mice and in 3T3-L1 cells (preadipocytes) and differentiated 3T3-L1 cells (mature adipocytes) , and BMPR2 expression in these cells was upregulated. Adipogenesis was induced in WAT by BMP4 injection (<i>in vivo</i>) and in 3T3-L1 cells by BMP4 stimulation (<i>in vitro</i>), both of which were inhibited by miR-6402 transfection. Inflamed eWAT showed higher expression of BMPR2 and the adipogenesis markers C/EBPβ and PPARγ, which was suppressed by miR-6402 transfection. Our findings suggest that miR-6402 is a novel anti-adipogenic miRNA that combats obesity by inhibiting the BMP4/BMPR2 signalling pathway and subsequently reducing adipose tissue expansion.
DOI: 10.6084/m9.figshare.28524221.v1
title: miR-6402 targets <i>Bmpr2</i> and negatively regulates mouse adipogenesis

description: Obesity is characterized by macrophage infiltration into adipose tissue. White adipose tissue remodelling under inflammatory conditions involves both hypertrophy and adipogenesis and is regulated by transcription factors, which are influenced by bone morphogenetic protein (BMP) signalling. MicroRNAs (miRNAs) regulate gene expression and are involved in obesity-related processes such as adipogenesis. Therefore, we identified differentially expressed miRNAs in the epididymal white adipose tissue (eWAT) of mice fed a normal diet (ND) and those fed a high-fat diet (HFD). The expression of miR-6402 was significantly suppressed in the inflamed eWAT of HFD-fed mice than in ND-fed mice. Furthermore, <i>Bmpr2</i>, the receptor for BMP4, was identified as a target gene of miR-6402. Consistently, miR-6402 was downregulated in the inflamed eWAT of HFD-fed mice and in 3T3-L1 cells (preadipocytes) and differentiated 3T3-L1 cells (mature adipocytes) , and BMPR2 expression in these cells was upregulated. Adipogenesis was induced in WAT by BMP4 injection (<i>in vivo</i>) and in 3T3-L1 cells by BMP4 stimulation (<i>in vitro</i>), both of which were inhibited by miR-6402 transfection. Inflamed eWAT showed higher expression of BMPR2 and the adipogenesis markers C/EBPβ and PPARγ, which was suppressed by miR-6402 transfection. Our findings suggest that miR-6402 is a novel anti-adipogenic miRNA that combats obesity by inhibiting the BMP4/BMPR2 signalling pathway and subsequently reducing adipose tissue expansion.
DOI: 10.6084/m9.figshare.24533139.v1
title: Bioactive peptides PDBSN improve mitochondrial function and suppression the oxidative stress in human adiposity cells

description: Mitochondria are essential for generating cellular energy and are significant in the pathogenesis of obesity. Human visceral and subcutaneous preadipocytes (HPA-v and HPA-s) were cultured into mature adipocytes. Intracellular triglyceride (TG) content was assessed using oil-red O staining and tissue triglyceride determination. Mitochondrial membrane potential (MMP) and reactive
oxygen species (ROS) levels were measured with fluorescent indicators. Gene and protein expression related to mitochondrial biogenesis were analyzed by real-time quantitative PCR and Western blotting. Morphological changes were observed via electron microscopy. Results show that PDBSN significantly increased MMP while decreasing TG and ROS levels. The transcription and protein levels
of PGC1-α and MTFA were upregulated, and mitochondrial fusion and fission markers (MFN1, MFN2, NRF1, DRP1) were elevated. Additionally, PDBSN enhanced maximum
respiratory capacity and reduced ROS. These findings suggest that PDBSN improves mitochondrial function, providing insights for obesity treatment and metabolic disease management.