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In apoptotic cells, phosphatidylserine externalization is driven by caspase-dependent activation of Xkr scramblases\n                  <jats:sup>1<\/jats:sup>\n                  and inactivation of specific flippases\n                  <jats:sup>2<\/jats:sup>\n                  . Localized caspase activation at neuronal synapses can mediate spatially-restricted synaptic phosphatidylserine exposure leading to synapse pruning by glial cells during development and neurodegeneration\n                  <jats:sup>3\u20136<\/jats:sup>\n                  . It is unknown which caspase-regulated flippases and scramblases promote synaptic phosphatidylserine exposure and whether there are any caspase-independent mechanisms of phosphatidylserine exposure relevant for synapse elimination. To address this question, we here develop a scalable CRISPR screening approach, COMPASS-seq (compartment-anchored sgRNA screen sequencing), to uncover the genetic underpinnings of subcellular phenotypes. COMPASS-seq is compatible with\n                  <jats:italic>in vitro<\/jats:italic>\n                  and\n                  <jats:italic>in vivo<\/jats:italic>\n                  systems and a wide range of subcellular compartments; we here apply it to the neuronal synapse. We discover that inhibition of the caspase-independent, calcium-activated anoctamin ANO3 (TMEM16C) is sufficient to increase synapse numbers\n                  <jats:italic>in vivo<\/jats:italic>\n                  . ANO3 co-localizes with IP3 receptor 1 (ITPR1), a calcium channel in the endoplasmic reticulum, to form a postsynaptic signaling platform that drives spatially restricted phosphatidylserine exposure at synapses. Activation of the ITPR1 calcium channel activity is sufficient to drive synaptic phosphatidylserine exposure via an ANO3-dependent but caspase-independent mechanism. Our results suggest a mechanism for integrating synaptic activity information to control synaptic pruning. The role of ANO3 in regulating synapses could shed light on the mechanisms underlying its numerous associations with both dementia\n                  <jats:sup>7<\/jats:sup>\n                  and other neurological diseases\n                  <jats:sup>8,9<\/jats:sup>\n                  .\n                <\/jats:p>","DOI":"10.64898\/2026.06.26.734915","type":"posted-content","created":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T18:53:38Z","timestamp":1782845618000},"source":"Crossref","is-referenced-by-count":1,"title":["Synaptic activity controls local exposure of an \u2018eat-me\u2019 signal via ANO3-ITPR1 signaling"],"prefix":"10.64898","author":[{"given":"Kunal","family":"Shroff","sequence":"first","affiliation":[{"name":"Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, US"},{"name":"Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA"},{"name":"Neuroscience Graduate Program, University of California, San Francisco, San Francisco, CA, USA"},{"name":"Medical Scientist Training Program, University of California, San Francisco, San Francisco, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Molly C.","family":"O\u2019Brien","sequence":"additional","affiliation":[{"name":"Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, US"},{"name":"Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tyler J.","family":"Smith","sequence":"additional","affiliation":[{"name":"Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, US"},{"name":"Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jialing","family":"Fang","sequence":"additional","affiliation":[{"name":"Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, US"},{"name":"Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA"},{"name":"UC Berkeley-UCSF Graduate Program in Bioengineering, University of California, San Francisco, San Francisco, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelly S.","family":"Yu","sequence":"additional","affiliation":[{"name":"Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, US"},{"name":"Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sonia I.","family":"Lombroso","sequence":"additional","affiliation":[{"name":"Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, CA, US"},{"name":"Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shengjie","family":"Feng","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of California at San Francisco, San Francisco, CA 94143, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chao","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of California at San Francisco, San Francisco, CA 94143, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory A.","family":"Mohl","sequence":"additional","affiliation":[{"name":"Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA"},{"name":"Fein Memory & Aging Center, University of California San Francisco; 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