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However, the functions of each BLOC-1 component remain enigmatic. Here, we use CRISPR to mutate each Drosophila BLOC-1 gene to investigate roles in synaptic growth, function, and homeostatic plasticity. First, we show that BLOC-1 mutations are viable, with no defects in synaptic growth, morphology, or baseline function. We then demonstrate distinct synaptic localization patterns of BLOC-1 components. Finally, we show that only two of the eight BLOC-1 components, dysbindin and snapin, are necessary for presynaptic homeostatic potentiation. These results indicate separable functions and distinct synaptic localization patterns of BLOC-1 subunits, and a need to reconsider predictions made from biochemical models of BLOC-1. <\/jats:p>","DOI":"10.1091\/mbc.e24-09-0392","type":"journal-article","created":{"date-parts":[[2025,8,13]],"date-time":"2025-08-13T15:35:18Z","timestamp":1755099318000},"source":"Crossref","is-referenced-by-count":2,"title":["Genetic dissection of the <i>Drosophila<\/i> BLOC-1 complex reveals distinctions in synaptic localization and homeostatic plasticity"],"prefix":"10.1091","volume":"36","author":[{"given":"Rebecca","family":"Stark","sequence":"first","affiliation":[{"name":"Department of Neurobiology, University of Southern California, Los Angeles, CA 90089"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Caleb","family":"Dehn","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, University of Southern California, Los Angeles, CA 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