The SMN complex plays an essential role in spliceosomal snRNP assembly in the cytoplasm, is required for pre-mRNA splicing in the nucleus and acts as a chaperone that discriminates target and non-target RNAs of Sm proteins. Required for normal expression of spliceosomal snRNAs and for U12 intron splicing. Required in cholinergic neurons, but not in motor neurons, to ensure correct splicing and proper levels of stas mRNA and normal neurotransmitter release by motor neurons (PubMed:23063130 and PubMed:23063131). However, Smn is required in motor neurons, but not in cholinergic neurons, for normal motor behavior but plays no role in synaptic transmission according to PubMed:23103409. In both muscle and neurons, required for the formation of a normal neuromuscular junction (NMJ) structure. Plays a neuron-specific role in long-term homeostatic compensation at the larval NMJ. In the thorax of adult flies, required for Act88F, an indirect flight muscle (IFM)-specific actin, expression and for proper IFM myofibril formation. In nurse cells, oocytes and follicle cells, required to maintain normal organization of nuclear compartments including chromosomes, nucleoli, Cajal bodies, histone locus bodies and heterochromatin. Required for the functional integrity of the cytoplasmic U snRNP body (U body) and P body. Required in dividing postembryonic neuroblasts (pNBs) for the correct basal localization of mira. The tight regulation of its expression is critical for stem cell division, proliferation and differentiation in male germline and developing central nervous system (CNS). Required for tracheal terminal cell lumen formation. Homodimer (via C-terminal region) (PubMed:11113446, PubMed:12783845, PubMed:22813737). Part of the core SMN complex, which seems to be composed of Smn and Gem2 only (PubMed:18621711, PubMed:23333303). The SMN complex associates with the entire set of spliceosomal snRNP Sm proteins, SmB, SmD1, SmD2, SmD3, SmE, SmF and SmG, and with the snRNP-specific proteins snRNP-U1-70K, U2A, snf/U1A and U5-116KD (PubMed:18621711, PubMed:23333303). Associates weakly with Gem3 (PubMed:18621711). Interacts with SmB and SmD1; the interaction is favored by methylation of the Sm proteins (PubMed:16753561, PubMed:18369183). Interacts with Actn; the interaction occurs in thoracic tissues and in adult flies (PubMed:17353360). Interacts with Rpp20 (PubMed:14715275). Interacts with msk and Snup; these interactions are RNA-dependent (PubMed:23885126). Component of U bodies. High expression detected in the cytoplasm of female germline stem cells and cystoblast which persists up to stage 10 egg chambers. Accumulates in the cytoplasm of dividing pNBs. Colocalizes with Actn at the Z-line of IFMs. Expression concentrates at the post-synaptic region of NMJs in larval brain. In late first instar larvae, expressed in pNBs. Expression increases as the pNBs enlarge, with the highest accumulation observed in dividing pNBs of second and third instar larvae. Enriched in type ID (thoracic and brain lobe), type IA and all the mira-expressing NBs of the brain lobes. In larvae, also expressed in muscle fibers. In larval and adult testis, expressed in germline stem cells and gonialblast, expression decreases as cells differentiate into cysts and spermatocytes. In adult fly thorax, expressed in the IFMs. In adult ovary, expressed in germline stem cells, cystoblasts, follicle cells, nurse cells and oocyte (at protein level). Also expressed in larval salivary glands. Expressed both maternally and zygotically. Expressed ubiquitously throughout development. Expression is high during embryogenesis but decreases 30-fold in adult flies (at protein level). Embryos lacking maternal and zygotic Smn die between 0 and 4 hours after egg laying. Zygotic mutants never initiate pupation but instead persist as third instar larvae, often surviving at this stage for several days. Mutant larvae exhibit reduced CNS, testes and muscle size, decreased locomotion and altered rhythmic motor activity. At the NMJ, mutant larvae show an overall decrease in the number of synaptic boutons, but an increase in enlarged ones, loss of large glutamate receptor clusters and an aberrant increase in evoked excitatory postsynaptic potential (eEPSP) amplitude and in miniature EPSP frequency. Mutant larvae also show defective mira subcellular localization in pNBs. Mutant larvae show a decrease of spliceosomal snRNA levels and splicing defects in U12 intron-containing genes (PubMed:23063131). But appreciable splicing defects in U12 intron-containing genes are not observed in mutant larvae, although a decrease in spliceosomal snRNA levels is detected, in PubMed:22813737. RNAi-mediated knockdown in tracheal cells results in defective gas-filling lumen in terminal branches (PubMed:23029159). Belongs to the SMN family.