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Actin dependent astrocytic infiltration is a key step for axon defasciculation during remodeling

ABSTRACT: Actin dependent astrocytic infiltration is a key step for axon defasciculation during remodeling

PROVIDER: PRJNA788369 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17212434.fastq.gz	Fastqsanger.gz
	SRR17212435.fastq.gz	Fastqsanger.gz
	SRR17212436.fastq.gz	Fastqsanger.gz
	SRR17212437.fastq.gz	Fastqsanger.gz
	SRR17212438.fastq.gz	Fastqsanger.gz

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Actin dependent astrocytic infiltration is a key step for axon defasciculation during remodeling

Project description:A strocytes are essential for synapse formation, maturation and plasticity, yet their function during developmental neuronal remodeling is largely unknown To identify astrocytic molecules required for axon pruning of mushroom body ( γ neurons in Drosophi la we profile d the expression of astrocytes before ( and after ( remodeling. F ocus ing on genes enriched in larval astrocytes we identified 12 genes that are required in astrocytes, for axon pruning including the F actin regulat ors Arpc1 and form3 Interestingly, perturbing astrocytic actin dynamics did not affect their gross morphology migration or TGF β secretion In contrast, actin dynamics was required for astrocyte infiltration into the axon bundle at the onset of pruning. Remarkably, decreasing axonal adhesion facilitated the infiltration of Arpc1 KD astrocytes, and suppressed the pruning defect driven by the astrocytic perturbation Together, our findings suggest that actin dependent astrocytic infiltration is a key step in axon pruning thus promoting our understanding of neuron glia interactions during remodeling

2023-02-12 | GSE190743 | GEO

Actin-dependent astrocytic infiltration is a key step for axon defasciculation during remodeling.

Project description:Astrocytes are essential for synapse formation, maturation, and plasticity; however, their function during developmental neuronal remodeling is largely unknown. To identify astrocytic molecules required for axon pruning of mushroom body (MB) γ neurons in Drosophila, we profiled astrocytes before (larva) and after (adult) remodeling. Focusing on genes enriched in larval astrocytes, we identified 12 astrocytic genes that are required for axon pruning, including the F-actin regulators Actin-related protein 2/3 complex, subunit 1 (Arpc1) and formin3 (form3). Interestingly, perturbing astrocytic actin dynamics does not affect their gross morphology, migration, or transforming growth factor β (TGF-β) secretion. In contrast, actin dynamics is required for astrocyte infiltration into the axon bundle at the onset of pruning. Remarkably, decreasing axonal adhesion facilitates infiltration by Arpc1 knockdown (KD) astrocytes and promotes axon pruning. Conversely, increased axonal adhesion reduces lobe infiltration by wild-type (WT) astrocytes. Together, our findings suggest that actin-dependent astrocytic infiltration is a key step in axon pruning, thus promoting our understanding of neuron-glia interactions during remodeling.

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Structural plasticity of actin-spectrin membrane skeleton and functional role of actin and spectrin in axon degeneration

Project description:Axon degeneration sculpts precise patterns of connectivity in the developing nervous system and is an early pathological hallmark of several adult-onset neurodegenerative disorders. Substantial progress has been made in identifying effector mechanisms that drive axon fragmentation, but far less is known about the upstream signaling pathways that initiate this process. Here we describe a role for the newly discovered axonal Membrane-associated Periodic Skeleton (MPS) –a quasi-1D periodic ultrastructure composed of actin, spectrin and associated molecules– during sensory axon degeneration. We find that trophic deprivation (TD) of sensory axons causes a rapid breakdown in the periodicity of the MPS in distal axons. These structural changes occur prior to and independently of caspase-driven axon fragmentation. We further show that acute actin destabilization to break down the MPS can initiate TD-related retrograde signaling. Actin stabilization prevents MPS breakdown during TD and blocks this signal. Moreover, deletion of βII-spectrin (Sptbn1), an obligate component of the MPS, suppresses this retrograde signaling and protects axons against degeneration. Together our data suggest that ultrastructural plasticity of the MPS underlies the earliest steps of axon degeneration.

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