Receptor which is involved in the phagocytosis of a variety of cells including apoptotic cells, severed and pruned axons, degenerating dendrites, salivary gland cells, germline cells and bacteria (PubMed:15342648, PubMed:16772168, PubMed:16772169, PubMed:18984163, PubMed:20577216, PubMed:22992958, PubMed:24412417). Binds to the ligand prtp which relocates from the endoplasmic reticulum to the cell surface during apoptosis (PubMed:19927123, PubMed:23337816). Ligand-binding may promote tyrosine phosphorylation mediated by Src42a, interaction with shark and subsequent activation of phagocytosis (PubMed:18432193). Also binds to the membrane phospholipid phosphatidylserine which is exposed on the surface of apoptotic cells (PubMed:23420848). Required for the phagocytosis of apoptotic cells by macrophages (PubMed:15342648). Also required for the phagocytosis of apoptotic neurons by glial cells in the embryonic nervous system (PubMed:12765609). Acts downstream of NimC4/simu in the glial phagocytosis of apoptotic neurons (PubMed:18455990). Plays a role in the glial engulfment of larval axons as part of programmed axon pruning during metamorphosis (PubMed:16772168, PubMed:16772170). Also mediates glial cell clearance of severed axons following axonal injury (PubMed:16772169, PubMed:27498858). Required for the engulfment of degenerating dendrites by epidermal cells (PubMed:24412417). Required in the ovary for the engulfment and subsequent processing of dying germline cells by follicular epithelial cells through activation of the JNK/bsk pathway (PubMed:22992958, PubMed:27347682). Plays a role in neuromuscular junction development by mediating the clearance of presynaptic debris and immature boutons which are shed by growing synapses (PubMed:19707574). Required for larval salivary gland cell death which occurs following a rise in steroid levels after puparium formation (PubMed:20577216). Also involved in bacterial phagocytosis (PubMed:18984163). Required for hemocyte phagocytosis of the Gram-positive bacterium S.aureus (PubMed:19890048). Lipoteichoic acid, synthesized by the S.aureus lipoteichoic acid synthase ltaS, acts as a ligand for drpr in this process (PubMed:19890048). Together with Src42a and shark, promotes the migration of macrophages to sites of wounding as part of a signaling cascade where Scr42a detects production of hydrogen peroxide at wound sites which triggers phosphorylation of drpr and subsequent recruitment and activation of shark (PubMed:26028435). Also required for macrophage priming which occurs following phagocytosis of apoptotic cells and ensures that macrophages develop a form of molecular memory that allows them to later mount an inflammatory response to tissue damage and bacterial infection (PubMed:27212238). Is also an essential factor in the regulation of muscle development and myogenesis, and as a consequence is required for normal locomotion (PubMed:12765609, PubMed:25111228, Ref.27). Likely to control the balance between skeletal muscle satellite cells proliferation and differentiation through regulation of the notch signaling pathway (PubMed:25111228, PubMed:30802937, Ref.27). Promotes engulfment of axonal debris by glial cells following axonal injury. Potently inhibits glial cell engulfment of axonal debris produced following axonal injury. Interacts (via the cytoplasmic domain) with shark; this is required for the recruitment of drpr and glial cells to severed axons and for the phagocytosis of axonal debris by glial cells following axon injury (PubMed:18432193). Interacts with ced-6 (PubMed:16772168). Interacts with csw; this results in dephosphorylation of drpr isoform A which is required for the inhibition of glial cell engulfment of axonal debris produced following axonal injury (PubMed:22426252). In olfactory receptor neurons, expressed at low levels along the axon but is up-regulated at severed axons following injury (PubMed:16772169). In follicle cells, detected at the cell membrane and in punctate speckles within the cytoplasm (PubMed:22992958). Also detected in follicle cells on the phagocytic cup and on newly internalized phagosomes (PubMed:27347682). In stage 13 macrophages, localizes to punctae around engulfed cell corpses but by stage 15, relocates to the cell cortex (PubMed:27212238). Expressed in adult head (at protein level) (PubMed:22426252). Expressed in glia, macrophages and ectoderm (at protein level) (PubMed:18455990). Detected in glia around the mushroom body dorsal lobe and in glial processes infiltrating the medial lobe (at protein level) (PubMed:16772168). Expressed in adult brain glia including antennal lobe glia (at protein level) (PubMed:16772169). Expressed in the larval fat body (at protein level) (PubMed:20577216). Expressed in the ovary (at protein level) (PubMed:22992958). Isoform B: Predominant isoform in adult glia (PubMed:22426252). In glial cells around the mushroom body dorsal lobe, expression is weak in wandering larvae and pupae at 12 hours after puparium formation (APF) and is elevated in pupae at 6 hours APF (PubMed:16772168). In naive stage 11 macrophages, expressed at low levels with increased levels seen following apoptotic cell corpse uptake and a further increase observed by stage 15 (PubMed:27212238). Isoform A: Selectively expressed in adults (PubMed:22426252). By axon injury which results in up-regulation on severed axons with levels reaching a peak between 12 and 24 hours after injury (at protein level) (PubMed:16772169). By ecdysone (PubMed:16772168). Isoform B: The intracellular domain is required for glial engulfment activity. Isoform A: The intracellular domain contains an 11-residue insertion compared to isoform B and is incapable of promoting glial engulfment. Phosphorylated on tyrosine residues (PubMed:18432193, PubMed:19927123, PubMed:23337816, PubMed:23420848). Phosphorylation is induced by binding to prtp (PubMed:19927123). It is also induced by binding to the membrane phospholipid phosphatidylserine (PubMed:23420848). Phosphorylation may be mediated directly or indirectly by Src42a and is required for interaction with shark (PubMed:18432193). Dephosphorylated by csw which is required for the inhibition of glial cell engulfment of axonal debris produced following axonal injury. Embryos show no defects in early central nervous system (CNS) development but display defective CNS cell corpse engulfment (PubMed:12765609). Increased number and volume of apoptotic particles in the nerve cord (PubMed:18455990). Suppression of glial engulfment of larval axons which results in defective axon pruning with most larval axons remaining in the mushroom body dorsal lobe at 18 hours after puparium formation in contrast to the wild-type where most of the larval axons are pruned by this time (PubMed:16772168, PubMed:16772170). Failure of glia to respond to axon injury, resulting in severed axons not being cleared from the CNS (PubMed:16772169). Impaired clearance of degenerating dendrites (PubMed:24412417). Highly abnormal neuromuscular junctions characterized by reduced synaptic growth, the accumulation of presynaptic debris and pruned ghost boutons, and reduced larval mobility (PubMed:19707574). Significant defects in germ cell engulfment by follicle cells (PubMed:22992958). Defective larval salivary gland death with persistance of salivary gland material in 98% of mutants 24 hours after puparium formation (PubMed:20577216). Reduced hemocyte phagocytosis of S.aureus following infection with infected flies dying earlier than controls (PubMed:19890048). Following wounding, impaired migration of macrophages to wound sites (PubMed:26028435). Reduced lifespan.(PubMed:25111228,Ref.27) Reduced climbing performance and impaired motor function with mutants displaying abnormal positioning of the legs and a rapid age-dependent decline in locomotor activity from 3 days to 7-10 days of adult life (PubMed:25111228). In 30-40 day old flies, pathological changes in thoracic skeletal muscle, such as loss of striation, variability in fiber size and vacuolization, that mainly affect the tergal depressor of the trochanter.(PubMed:25111228) Marked degeneration and vacuolization of the nervous system including brain and thoracic ventral ganglia, and degeneration of the retina and optic ganglia (PubMed:25111228). RNAi-mediated knockdown results in greatly reduced phagocytosis of apoptotic cells (PubMed:15342648). RNAi-mediated knockdown in neurons does not affect clearance of axon fragments resulting from developmental axon pruning but RNAi-mediated knockdown in glial cells results in defective clearance of axon fragments (PubMed:16772170). RNAi-mediated knockdown in the mesoderm or in adult precursor muscle cells results in impaired locomotor activity which is not seen following RNAi-mediated knockdown in neurons or glia (PubMed:25111228). Belongs to the MEGF family.