Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A lysosomal regulatory circuit essential for the development and function of microglia

ABSTRACT: We performed Illumina NovaSeq on macrophages isolated from zebrafish

ORGANISM(S): Danio rerio

PROVIDER: GSE197349 | GEO | 2022/07/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

A lysosomal regulatory circuit essential for the development and function of microglia

Project description:We performed Illumina NovaSeq on zebrafish larvae with or without Zymosan A injection

2022-07-15 | GSE197348 | GEO

A lysosomal regulatory circuit essential for the development and function of microglia

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-15 | GSE197350 | GEO

A lysosomal regulatory circuit essential for the development and function of microglia

Project description:A lysosomal regulatory circuit essential for the development and function of microglia

| PRJNA809952 | ENA

A lysosomal regulatory circuit essential for the development and function of microglia

Project description:A lysosomal regulatory circuit essential for the development and function of microglia

| PRJNA809950 | ENA

A lysosomal regulatory circuit essential for the development and function of microglia

Project description:A lysosomal regulatory circuit essential for the development and function of microglia

| PRJNA809951 | ENA

insomniac links the development and function of a sleep-regulatory circuit.

Project description:Although many genes are known to influence sleep, when and how they impact sleep-regulatory circuits remain ill-defined. Here, we show that insomniac (inc), a conserved adaptor for the autism-associated Cul3 ubiquitin ligase, acts in a restricted period of neuronal development to impact sleep in adult Drosophila. The loss of inc causes structural and functional alterations within the mushroom body (MB), a center for sensory integration, associative learning, and sleep regulation. In inc mutants, MB neurons are produced in excess, develop anatomical defects that impede circuit assembly, and are unable to promote sleep when activated in adulthood. Our findings link neurogenesis and postmitotic development of sleep-regulatory neurons to their adult function and suggest that developmental perturbations of circuits that couple sensory inputs and sleep may underlie sleep dysfunction in neurodevelopmental disorders.

| S-EPMC8758140 | biostudies-literature

Crohn's disease risk variant in GPR65 alters lysosomal function

Project description:Using an siRNA screen we identify a role for GPR65 in the defense against intracellular pathogens. Epithelial cells and macrophages lacking GPR65 exhibited impaired clearance of intracellular bacteria as well as an accumulation of aberrant phagosomes and lysosomes. Transcriptional profiling revealed changes in genes associated with lysosomal function. Bone marrow-derived macrophages from WT or Gpr65-/- mice were harvested for RNA analysis.

2016-06-15 | E-GEOD-69445 | biostudies-arrayexpress

Lipid-induced lysosomal damage after demyelination corrupts microglia protective function in lysosomal storage disorders.

Project description:Neuropathic lysosomal storage disorders (LSDs) present with activated pro-inflammatory microglia. However, anti-inflammatory treatment failed to improve disease pathology. We characterise the mechanisms underlying microglia activation in Niemann-Pick disease type A (NPA). We establish that an NPA patient and the acid sphingomyelinase knockout (ASMko) mouse model show amoeboid microglia in neurodegeneration-prone areas. In vivo microglia ablation worsens disease progression in ASMko mice. We demonstrate the coexistence of different microglia phenotypes in ASMko brains that produce cytokines or counteract neuronal death by clearing myelin debris. Overloading microglial lysosomes through myelin debris accumulation and sphingomyelin build-up induces lysosomal damage and cathepsin B extracellular release by lysosomal exocytosis. Inhibition of cathepsin B prevents neuronal death and behavioural anomalies in ASMko mice. Similar microglia phenotypes occur in a Niemann-Pick disease type C mouse model and patient. Our results show a protective function for microglia in LSDs and how this is corrupted by lipid lysosomal overload. Data indicate cathepsin B as a key molecule mediating neurodegeneration, opening research pathways for therapeutic targeting of LSDs and other demyelinating diseases.

| S-EPMC6331723 | biostudies-literature

Microglia development and function.

Project description:Proper development and function of the mammalian central nervous system (CNS) depend critically on the activity of parenchymal sentinels referred to as microglia. Although microglia were first described as ramified brain-resident phagocytes, research conducted over the past century has expanded considerably upon this narrow view and ascribed many functions to these dynamic CNS inhabitants. Microglia are now considered among the most versatile cells in the body, possessing the capacity to morphologically and functionally adapt to their ever-changing surroundings. Even in a resting state, the processes of microglia are highly dynamic and perpetually scan the CNS. Microglia are in fact vital participants in CNS homeostasis, and dysregulation of these sentinels can give rise to neurological disease. In this review, we discuss the exciting developments in our understanding of microglial biology, from their developmental origin to their participation in CNS homeostasis and pathophysiological states such as neuropsychiatric disorders, neurodegeneration, sterile injury responses, and infectious diseases. We also delve into the world of microglial dynamics recently uncovered using real-time imaging techniques.

| S-EPMC5001846 | biostudies-literature

Lipid induced lysosomal damage after demyelination corrupts microglia protective function in Lysosomal Storage Disorders

Project description:Neuropathic Lysosomal Storage Disorders (LSDs) present with activated pro-inflammatory microglia. However, anti-inflammatory treatment failed to improve disease pathology. We characterise the mechanisms underlying microglia activation in Niemann Pick disease type A (NPA). We establish that an NPA patient and the Acid Sphingomyelinase knockout (ASMko) mouse model show amoeboid microglia in neurodegeneration-prone areas. In vivo microglia ablation worsens disease progression in ASMko mice. We demonstrate the coexistence of different microglia phenotypes in ASMko brains that produce cytokines or counteract neuronal death by clearing myelin debris. Overloading microglial lysosomes through myelin debris accumulation and sphingomyelin build up induces lysosomal damage and Cathepsin B extracellular release by lysosomal exocytosis. Inhibition of Cathepsin B prevents neuronal death and behavioural anomalies in ASMko mice. Similar microglia phenotypes occur in a Niemann Pick disease type C mouse model and patient. Our results show a protective function for microglia in LSDs and how this is corrupted by lipid lysosomal overload. Data indicate Cathepsin B as a key molecule mediating neurodegeneration, opening research pathways for therapeutic targeting LSDs and other demyelinating diseases.

| S-SCDT-EMBOJ-2018-99553 | biostudies-other

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data