When a neuron is injured or undergoes remodeling, the resulting debris from degenerating processes must be cleared away efficiently by phagocytes. Debris removal is important for preventing inflammation and promoting recovery. In both vertebrates and invertebrates, epithelial cells are the primary phagocytes responsible for clearing the debris of peripheral sensory neurites that innervate the epidermis. Epithelial cells recognize degenerating neurites but ignore intact ones. The goal of my dissertation work was to understand how eat-me signals contribute to the recognition and engulfment of degenerating neurites by phagocytes. Most apoptotic cells externalize a highly conserved eat-me signal – a negatively charged phospholipid called phosphatidylserine (PS). Together with colleagues, I found that degenerating dendrites of Drosophila sensory neurons expose PS on their plasma membrane, suggesting that PS plays a role during degeneration. We investigated the functional consequences of PS exposure by flippase knockout and/or scramblase overexpression. Ectopically induced PS exposure on the surface of undamaged neurites is sufficient to cause neurite degeneration in both the central nervous system (CNS) and the peripheral nervous system (PNS). In the PNS, this degeneration requires phagocytosis of dendrites by epidermal cells. Therefore, PS exposure is sufficient to induce recognition and engulfment of dendrites by the epidermal cells. Next, we asked how is PS exposure regulated during degeneration and how does PS exposure contribute to the process of degeneration? Neurite fragmentation after injury is controlled by an “axon-death” pathway which involves a catastrophic depletion of nicotinamide adenine dinucleotide (NAD+). We found that perturbing NAD+ synthesis in uninjured sensory neurites induces not only spontaneous dendrite fragmentation but also PS exposure prior to fragmentation. Interestingly, dendrite fragmentation is suppressed when epidermal phagocytosis is blocked. Conversely, maintaining neuronal NAD+ levels by overexpressing Wlds suppresses PS exposure and neurite fragmentation after dendrite injury. However, when PS exposure is induced on these dendrites, Wlds mediated neuroprotection is reversed and neurite fragmentation occurs. These data demonstrate that the axon-death pathway promotes neurite degeneration largely through inducing neurite PS exposure and the subsequent attack by phagocytes on PS-exposing neurites. In summary, I demonstrate that PS exposure results from and causes neurite degeneration in Drosophila and provide further evidence that phagocytes play an active role during neurite degeneration.