7/31/2023 0 Comments Neurite dendrite axon![]() Furthermore, several known pathways that contribute to neurite pruning have been revealed: ubiquitin proteasomal degradation ( Kuo et al., 2005 Watts et al., 2003 Wong et al., 2013), caspase activity ( Kuo et al., 2006 Williams et al., 2006), microtubule disassembly ( Bu et al., 2021 Herzmann et al., 2017 Lee et al., 2009) and polarity ( Herzmann et al., 2018 Rui et al., 2020b Tang et al., 2020 Wang et al., 2019), glia engulf ( Awasaki et al., 2011 Awasaki and Ito, 2004 Tasdemir-Yilmaz and Freeman, 2014 Watts et al., 2004), epithelial engulf ( Han et al., 2014), nitric oxide ( Rabinovich et al., 2016), secretory pathway ( Rui et al., 2020a Wang et al., 2017), endocytic pathway ( Issman-Zecharya and Schuldiner, 2014 Zhang et al., 2014), cell adhesion ( Bornstein et al., 2015) and energy metabolism ( Marzano et al., 2021). ![]() Extensive studies have suggested that ecdysone signaling is the main gatekeeper of axon/dendrite remodeling ( Kirilly et al., 2009, 2011 Lee et al., 2000 Zheng et al., 2003). Similarly, in the peripheral nervous system (PNS), a subset of dendritic arborization (da) sensory neurons, class I (ddaD/ddaE) and class IV (ddaC) neurons, remove almost all of the dendrites without losing their axons and somas, whereas class II (ddaB) and class III (ddaA/ddaF) da neurons are eliminated through apoptosis ( Kuo et al., 2005 Williams and Truman, 2005). In the central nervous system (CNS), mushroom body (MB) γ neurons eliminate the dorsal and medial axon branches as well as all dendrites and subsequently regrow the medial branches to form the adult-specific nervous system ( Lee et al., 1999). During the metamorphosis of the holometabolous insect Drosophila, early-stage neurons undergo stereotyped pruning to reconstruct adult-specific neural circuits ( Consoulas et al., 2000 Kanamori et al., 2015 Truman, 1990). This article has an associated First Person interview with the first author of the paper.ĭuring animal development, neurons generate excessive or exuberant connections at an early stage, and subsequently remodel their dendritic arbors and axon projections to wire functional circuits ( Luo and O'Leary, 2005 Williams and Truman, 2005). Finally, our findings establish an unprecedented axon pruning mode that will serve to systematically screen and identify undiscovered axon pruning regulators. Consistently, the classical axon pruning regulators in the Drosophila MB γ neuron, including TGF-β signaling, ecdysone signaling, JNK signaling, and the ubiquitin-proteasome system are also involved in governing motor axon pruning. Strikingly, the pruning process of the motor axon bundle is straightforward to investigate via live imaging and it occurs approximately at 22 h after pupal formation (APF), when axon bundles are completely cleared. Interestingly, we uncover that long-range projecting axon bundle from soma at ventral nerve cord (VNC), undergoes degeneration rather than retraction during metamorphosis. Here, we report that the Drosophila motor neuron offers a unique advantage for studying axon pruning. Thus, an excellent model system to assess axon specific pruning directly via live-cell imaging remains elusive. Alternatively, dendrite pruning of ddaC neurons is usually investigated via live-cell imaging, while dissection and fixation are currently used for evaluating MB γ neuron axon pruning. In the peripheral nervous system (PNS), class IV dendritic arborization (da) sensory neurons of Drosophila, selectively remove the dendrites without losing their somas and axons, while the dendrites and axons of mushroom body (MB) γ neuron in the central nervous system (CNS) are eliminated by localized fragmentation during metamorphosis. Importantly, this process is widely used for the refinement of neural circuits in both vertebrates and invertebrates, and may also contribute to the pathogenesis of neuropsychiatric disorders, such as autism and schizophrenia. Developmental neuronal pruning is a process by which neurons selectively remove excessive or unnecessary neurite without causing neuronal death.
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