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Microtubule-RAB5 mutual-influential system screening based on gene-regulatory networks map in Rab5 RNAi eye-degeneration model

ABSTRACT: Rabs are involved in neuronal development and protrusion formation. Existing studies support the notion that manipulation or mutation of Rab genes could lead to functional changes in neurons. However, whether Rabs gene-manipulation induced Drosophila eye-degeneration remains unknown. By down-regulating Rab5, but not Rab7, we first constructed a compound eye injury model in Drosophila. As the distribution, content, and even maturation of RAB5-positive endosomes are influenced by cytoskeletal proteins, like actin or tubulin-related proteins, the existence of a bidirectional regulatory relationship between RAB5 and the cytoskeleton is unclear and worth researching. Through complete transcriptome sequencing combined immunofluorescence testing, we confirmed that down-regulation of Rab5 affected the expression of α-Tub84B (alternatively named TubA84B) but not γ-tubulin. Based on Weighted Gene Co-Expression Network Analysis (WGCNA) and multi-tissue screening verification, this study proposes that the apoptosis-related factors–Rab5–TubA84B have conserved regulatory functions with cooperative expression. Gene-manipulation confirmed that apoptotic factors, especially rpr, strongly regulated RAB5, and may ultimately influence microtubule structure through extremely complicated routes, including the RAB5 variance and the intracellular configuration ratio of α-tubulin to Glyceraldehyde-3-phosphate dehydrogenase.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE273282 | GEO | 2026/07/28

REPOSITORIES: GEO

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Microtubule-RAB5 mutual-influential system screening based on gene-regulatory networks map in Rab5 RNAi eye-degeneration model

Project description:Microtubule-RAB5 mutual-influential system screening based on gene-regulatory networks map in Rab5 RNAi eye-degeneration model

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PFF induce LRRK2-Mediated Rab5 Phosphorylation Triggering Lysosomal Dysfunction and Neuronal Senescence [ATAC-seq]

Project description:While there is significant progress in characterizing the pathogenesis of Parkinson's disease (PD), underlying cell biological events are less well-defined. Increasing evidence suggests that endolysosomal dysfunction is a critical driver of PD pathogenesis. In this study, we explored the impact of preformed α-synuclein fibrils (PFF) on endolysosomal function and downstream events, including activation of cellular senescence pathways. We found that PFF treatment of primary cultures of mouse cortical neurons caused widespread endolysosomal dysfunction. PFF treatment also induced changes in transcriptional reprogramming and chromatin accessibility. To define underlying mechanisms we explored the status of LRRK2, finding that PFF treatment activated LRRK2 on early endosomes where it phosphorylated Rab5. PFF also induced phosphorylation of Rab7. LRRK2 activation was necessary for endolysosomal dysfunction and transcriptional changes as these changes were prevented by pharmacological inhibition of LRRK2 with MLi-2. In addition, Rab5 changes mediated by PFF treatment contributed to changes in chromatin remodeling. These cell biological insights point to a critical role in PD pathogenesis for LRRK2 activation and its engagement of the endolysosomal network and to a novel role for the LRRK2-Rab5 axis in mediating its manifestations.

2026-05-13 | GSE294156 | GEO

Fat body-derived cytokine Upd2 regulates the polarity of Drosophila tracheal stem cells [RNA-seq]

Project description:Adult stem cells are essential for maintaining tissue homeostasis. We employ Drosophila tracheal progenitors to understand the mechanism controlling the polarity of stem cell migration. Here, we show that polarity of tracheal progenitors depends on the function of fat body. Cytokine, Upd2, produced by fat body, signals to tracheal progenitors and activation JAK/STAT signal transduction. Perturbation of Upd2 production or loss-of-function of JAK/STAT signaling in the trachea cause aberrant bidirectional migration of tracheal progenitors. JAK/STAT signaling promotes the expression of a series of genes involved in planar cell polarity, which generates asymmetric localization of Fat and Pod1. Furthermore, the transport of Upd2 requires Rab5-, Rab7-mediated endocytic sorting and Lbm-dependent vesicle trafficking, where vesicular Upd2 functionally interacts with Rabs, Tetraspanin and Grasp65. These results reveal an inter-organ communication in which cytokines from fat body direct the polarity of ectodermal origin tracheal progenitors and suggest that Upd2-dependent JAK/STAT signaling regulates anterior-posterior polarity of tracheal progenitor movement.

2024-10-28 | GSE256177 | GEO

Fat body-derived cytokine Upd2 regulates the polarity of Drosophila tracheal stem cells [ChIP-seq]

2025-05-01 | GSE256176 | GEO

Gene Expression in mice liver after knockdown of Rab5

2015-05-03 | GSE67227 | GEO

RNA-seq analysis of human CD19 CAR T cells overexpressing RAB5

Project description:Chimeric antigen receptor (CAR) T cells (CARTs) are engineered T cells designed to target specific molecules on the surface of cancer cells. Using a continuous antigen exposure (CAE) assay to model this interaction, we observed that tumors can capture CAR molecules, leaving the CARTs devoid of surface-expressed CARs and unable to kill tumors after repeated challenges. Overexpression of Rab5, a key regulator of endocytosis, prevents the loss of CARs and enhances CARTs activity. Rab5 significantly increased the endocytic recycling of T cells without causing other perturbations to CART function. Interestingly, we observed membrane protrusions on the CART cell surface, which disappeared after multiple tumor challenges. Rab5 overexpression maintained these protrusions after multiple tumor engagements, and the presence of membrane protrusions correlated with tumor clearance. In vivo, Rab5-expressing CARTs demonstrated improved activity and were able to clear an otherwise recalcitrant mesothelin-expressing solid cancer. These findings suggest that engineering CARTs with Rab5 overexpression could enhance the clinical efficacy of CAR T cell therapy.

2026-04-10 | GSE269885 | GEO

The PripA-TbcrA complex-centered Rab GAP cascade facilitates macropinosome maturation in Dictyostelium

Project description:Macropinocytosis, an evolutionarily conserved mechanism mediating nonspecific bulk uptake of extracellular fluid, has been ascribed diverse functions. How nascent macropinosomes mature after internalization remains largely unknown. By searching for proteins that localize on macropinosomes during the Rab5-to-Rab7 transition stage in Dictyostelium, we uncover a complex composed of two proteins, which we name PripA and TbcrA. We show that the Rab5-to-Rab7 conversion involves fusion of Rab5-marked early macropinosomes with Rab7-marked late macropinosomes. PripA links the two membrane compartments by interacting with PI(3,4)P2 and Rab7. In addition, PripA recruits TbcrA, which acts as a GAP, to turn off Rab5. Thus, the conversion to Rab7 is linked to inactivation of the upstream Rab5. Consistently, disruption of either pripA or tbcrA impairs Rab5 inactivation and macropinocytic cargo processing. Therefore, the PripA-TbcrA complex is the central component of a Rab GAP cascade that facilitates programmed Rab switch and efficient cargo trafficking during macropinosome maturation.

2022-03-14 | PXD032072 | Pride

Gene Expression in mice liver after knockdown of Rab5

Project description:RNAi-mediated silencing of Rab5 and the consequent loss of endosomes in the mouse liver caused severe metabolic defects such as hypoglycemia, hepatomegaly, hypercholesterolemia, hyperlipidemia and glycogen accumulation. Gene expression in mice liver after knockdown of Rab5 has been performed the Mouse Genome 430 2.0 microarrays to identify biological processes and pathways affected by Rab5. The mice received either PBS or lipid nanoparticles (LNPs) loaded with siRNAs agains Rab5all or Luciferase control at 1.5 mg/kg via tail vein injection. At 5 day post injection mice were sacrificed using cervical dislocation and liver tissue was harvested, snap frozen in liquid nitrogen for RNA isolation; Gene expression studies were performed applying the Mouse Genome 430 2.0 microarrays.

2015-05-03 | E-GEOD-67227 | biostudies-arrayexpress

The Plant-Specific RAB5 GTPase ARA6 is Required for Starch and Sugar Homeostasis in Arabidopsis thaliana

Project description:Endosomal trafficking plays integral roles in various eukaryotic cell activities. In animal cells, a member of the RAB GTPase family, RAB5, is a key regulator of various endosomal functions. In addition to orthologs of animal RAB5, plants harbor the plant-specific RAB5 group, the ARA6 group, which is conserved in land plant lineages. In Arabidopsis thaliana, ARA6 and conventional RAB5 act in distinct endosomal trafficking pathways; ARA6 mediates trafficking from endosomes to the plasma membrane, whereas conventional RAB5 acts in endocytic and vacuolar trafficking pathways. ARA6 is also required for normal salt and osmotic stress tolerance, although the functional link between ARA6 and stress tolerance remains unclear. In this study, we investigated ARA6 function in stress tolerance by monitoring broad-scale changes in gene expression in the ara6 mutant. A comparison of the expression profiles between wild-type and ara6‐1 plants revealed that the expression of the Qua-Quine Starch (QQS) gene was significantly affected by the ara6‐1 mutation. QQS is involved in starch homeostasis, consistent with the starch content decreasing in the ara6 mutants to approximately 60% of that of the wild-type plant. In contrast, the free and total glucose content increased in the ara6 mutants. Moreover, the proliferation of Pseudomonas syringae pv. tomato DC3000 was repressed in ara6 mutants, which could be attributed to the elevated sugar content. These results suggest that ARA6 is responsible for starch and sugar homeostasis, most probably through the function of QQS.

2015-02-18 | GSE57013 | GEO

Mefloquine disrupts cancer stem cells by inhibiting lysosomal RAB5/7 mediated mitophagy

Project description:BACKGROUND & AIMS Cancer stem cells (CSCs) establish hierarchy in tumor tissue and a critical role for acquisition of resistance to therapy. Thus, the targeting of CSCs is important. We focused on lysosome which characteristically upregulated in colon CSCs for the aim of CSC targeting and search for new maintenance of CSCs by analyzing the function of CSC targeting drug. METHODS Correlation of lysosomal activity and CSC markers was assessed and single sphere formation and limiting dilution assay were performed, to evaluate CSCs property. Additionally, in vitro and vivo, we evaluated that anticancer drugs, antimalarial drugs, antitumor effect by combining them, and changes in cancer stem cell hierarchy. We performed microarray analyses to compare gene expression patterns from the tumors of treated patient derived xenograft mice. RESULTS LC3B+ or Lysotracker+ cells were characteristically existed in CD44V9+/ CD133+ CSC fraction as a small cell subpopulation. Single sphere formation assay and limiting dilution assay showed higher sphere formation activity and higher tumorigenic activity of LC3B+ or Lysotracker+ cells compared to LC3B－or Lysotracker－cells. Mefloquine treatment significantly decreased CD44v9+/ CD133+ cell number than representative antimalarial drugs, chloroquine and hydroxychloroquine. Mefloquine demonstrated the synergic effect on oxaliplatin and irinotecan. In Microarray analysis, we elucidated that mefloquine disrupted lysosome pathway by inhibiting Rab5 and Rab7. In patient-derived colon cancer tissue xenografted (PDX) mouse model, combined treatment of mefloquine with oxaliplatin or irinotecan drastically abrogated the tumorigenic activity of cancer cells. CONCLUSIONS Lysosomal activity in CSCs is a promising therapeutic target, and repositioning of mefloquine to colon cancer together with conventional chemotherapeutic agent will be a promising strategy for cure of colon cancer.

2018-06-20 | GSE116023 | GEO

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