Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Sensory neurons display cell-type specific vulnerability to loss of axon-glia interactions

ABSTRACT: Sensory neurons display cell-type specific vulnerability to loss of axon-glia interactions

PROVIDER: PRJNA845777 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19539264_1.fastq.gz	Fastqsanger.gz
	SRR19539264_2.fastq.gz	Fastqsanger.gz
	SRR19539265_1.fastq.gz	Fastqsanger.gz
	SRR19539265_2.fastq.gz	Fastqsanger.gz
	SRR19539266_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

Sensory neurons display cell-type specific vulnerability to loss of neuron-glia interactions

Project description:Sensory neurons display cell-type specific vulnerability to loss of neuron-glia interactions

| PRJNA846329 | ENA

Sensory neurons display cell-type specific vulnerability to loss of axon-glia interactions

Project description:In this study we characterized the transcriptional response of sensory neurons to PNS demyelination caused by genetic ablation of glial cells

2022-06-06 | GSE205461 | GEO

Sensory neurons display cell-type specific vulnerability to loss of neuron-glia interactions

Project description:PNS injuries initiate transcriptional changes in glial cells and sensory neurons that promote axonal regeneration. While the factors that initiate the transcriptional changes in glial cells are well characterized, the full range of stimuli that initiate the response of sensory neurons remain elusive. Here, using a genetic model of glial cell ablation, we find that glial cell loss results in transient PNS demyelination without overt axonal loss. By profiling sensory ganglia at single-cell resolution we show that glial cell loss induces a transcriptional injury response preferentially in proprioceptive and Aβ RA-LTMR neurons. The transcriptional response of sensory neurons to mechanical injury has been assumed to be a cell autonomous response. By identifying a similar response in non-injured, demyelinated neurons, our study suggests that this represents a non-cell autonomous transcriptional response of sensory neurons to the loss of axon-glial cell interactions.

2022-06-11 | GSE205561 | GEO

SEMA3B switches axon-axon to axon-glia interactions required for unmyelinated axon envelopment and integrity

Project description:SEMA3B switches axon-axon to axon-glia interactions required for unmyelinated axon envelopment and integrity

| PRJNA1248491 | ENA

SEMA3B switches axon-axon to axon-glia interactions required for unmyelinated axon envelopment and integrity

Project description:During peripheral nerve (PN) development, unmyelinated axons (nmAs) initially form tight fascicles before being separated and enveloped by non-myelinating Schwann cells (nmSCs), which are essential for maintaining nmA integrity. The mechanism underlying this transition from axon-axon to axon-glia interactions remains unclear. Here, we found that inactivating nmSC-derived SEMA3B or its axonal receptor components in mice led to incomplete nmA separation and envelopment by nmSCs, leading to nmA dysfunction and inducing hyperalgesia and allodynia. Conversely, increasing SEMA3B levels in nmSCs accelerated nmA separation and envelopment. SEMA3B transiently promoted nmA defasciculation accompanied by cell adhesion molecule (CAM) endocytosis, thus facilitating subsequent CAM-mediated nmA-mSC association. Restoring SEMA3B expression post-PN injury promoted nmA-nmSC re-association and alleviated hyperalgesia and allodynia. We propose that SEMA3B-induced CAM turnover facilitates the switch from axon-axon to axon-glia interactions, promoting nmA envelopment by nmSCs, which may be exploited to alleviate PN injury-induced pain by accelerating the restoration of nmA integrity.

2025-04-09 | GSE294160 | GEO

Diversity of satellite glia in sympathetic and sensory ganglia

Project description:Satellite glia are the major glial type found in ganglia of the peripheral nervous system that wrap around cell bodies of sympathetic and sensory neurons that are very diverse. Other than their close physical association with peripheral neurons, little is known about this glial population. Here, we performed single cell RNA sequencing analysis and identified five different populations of satellite glia from sympathetic and sensory ganglia. We identify three shared populations of satellite glia enriched in immune-response genes, immediate-early genes and ion channels/ECM-interactors, respectively. Sensory- and sympathetic-specific satellite glia are differentially enriched for modulators of lipid metabolism. Sensory glia are also specifically enriched for genes involved in glutamate turnover. Further, satellite glia and Schwann cells can be distinguished by unique transcriptional signatures. This study reveals remarkable heterogeneity of satellite glia in the peripheral nervous system.

2021-06-01 | GSE175421 | GEO

Glia detect and transiently protect against dendrite substructure disruption

Project description:Glia assess axon structure to modulate myelination and axon repair. Whether glia similarly detect dendrites and their substructures is not well understood. Here, we show that glia monitor the integrity of dendrite substructures and transiently protect their perturbation. We demonstrate that disruption of C. elegans sensory neuron dendrite cilia elicits acute glial responses, including increased accumulation of glia-derived extracellular matrix around cilia, changes in gene expression, and alteration of secreted protein repertoire. DGS-1, a 7-transmembrane domain neuronal protein, and FIG-1, a multifunctional thrombospondin-domain glial protein, are required for glial detection of cilia integrity, physically interact, and exhibit mutually-dependent localization to and around cilia, respectively. Glial responses to dendrite cilia disruption transiently protect against damage. Thus, our studies uncover a homeostatic, protective, dendrite glia signaling interaction regulating dendrite substructure integrity.

2024-12-06 | GSE282640 | GEO

Sensory neurons display cell-type-specific vulnerability to loss of neuron-glia interactions.

Project description:Peripheral nervous system (PNS) injuries initiate transcriptional changes in glial cells and sensory neurons that promote axonal regeneration. While the factors that initiate the transcriptional changes in glial cells are well characterized, the full range of stimuli that initiate the response of sensory neurons remain elusive. Here, using a genetic model of glial cell ablation, we find that glial cell loss results in transient PNS demyelination without overt axonal loss. By profiling sensory ganglia at single-cell resolution, we show that glial cell loss induces a transcriptional injury response preferentially in proprioceptive and Aβ RA-LTMR neurons. The transcriptional response of sensory neurons to mechanical injury has been assumed to be a cell-autonomous response. By identifying a similar response in non-injured, demyelinated neurons, our study suggests that this represents a non-cell-autonomous transcriptional response of sensory neurons to glial cell loss and demyelination.

| S-EPMC9354470 | biostudies-literature

Macrophages protect against sensory axon degeneration in diabetic neuropathy

Project description:Macrophages protect against sensory axon degeneration in diabetic neuropathy

| PRJNA1075431 | ENA

Diversity of satellite glia in sympathetic and sensory ganglia

Project description:Diversity of satellite glia in sympathetic and sensory ganglia

| PRJNA732372 | ENA