Actin dependent astrocytic infiltration is a key step for axon defasciculation during remodeling
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ABSTRACT:
PROVIDER: PRJNA788369 | ENA |
REPOSITORIES: ENA
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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
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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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