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

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

PROVIDER: PRJNA1248491 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33050179_1.fastq.gz	Fastqsanger.gz
	SRR33050179_2.fastq.gz	Fastqsanger.gz
	SRR33050180_1.fastq.gz	Fastqsanger.gz
	SRR33050180_2.fastq.gz	Fastqsanger.gz
	SRR33050181_1.fastq.gz	Fastqsanger.gz

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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

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

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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.

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Axon-enriched lincRNA ALAE is required for axon elongation via regulating local mRNA translation

Project description:Axon-enriched lincRNA ALAE is required for axon elongation via regulating local mRNA translation

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Lmx1b is required at multiple stages to build expansive serotonergic axon architectures

Project description:Formation of long-range axons occurs over multiple stages of morphological maturation. However, the intrinsic transcriptional mechanisms that temporally control different stages of axon projection development are unknown. Here, we addressed this question by studying the formation of mouse serotonin (5-HT) axons, the exemplar of long-range profusely arborized axon architectures. We report that LIM homeodomain factor 1b (Lmx1b)-deficient 5-HT neurons fail to generate axonal projections to the forebrain and spinal cord. Stage-specific targeting demonstrates that Lmx1b is required at successive stages to control 5-HT axon primary outgrowth, selective routing, and terminal arborization. We show a Lmx1b→Pet1 regulatory cascade is temporally required for 5-HT arborization and upregulation of the 5-HT axon arborization gene, Protocadherin-alphac2, during postnatal development of forebrain 5-HT axons. Our findings identify a temporal regulatory mechanism in which a single continuously expressed transcription factor functions at successive stages to orchestrate the progressive development of long-range axon architectures enabling expansive neuromodulation.

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