@article{oai:repo.qst.go.jp:00074638,
 author = {Shimojo, Masafumi and Madara, Joseph and Pankow, Sandra and Liu, Xinran and Yates III, John and Thomas, C Südhof and Maximov, Anton and Shimojo, Masafumi},
 issue = {5-6},
 journal = {Genes & development},
 month = {Feb},
 note = {Synaptotagmin-11 (Syt11) is a Synaptotagmin isoform that lacks an apparent ability to bind calcium, phospholipids, or SNARE proteins. While human genetic studies have linked mutations in the  gene to schizophrenia and Parkinson's disease, the localization or physiological role of Syt11 remain unclear. We found that in neurons, Syt11 resides on abundant vesicles that differ from synaptic vesicles and resemble trafficking endosomes. These vesicles recycle via the plasma membrane in an activity-dependent manner, but their exocytosis is slow and desynchronized. Constitutive knockout mice lacking Syt11 died shortly after birth, suggesting Syt11-mediated membrane transport is required for survival. In contrast, selective ablation of Syt11 in excitatory forebrain neurons using a conditional knockout did not affect life span but impaired synaptic plasticity and memory. Syt11-deficient neurons displayed normal secretion of fast neurotransmitters and peptides but exhibited a reduction of long-term synaptic potentiation. Hence, Syt11 is an essential component of a neuronal vesicular trafficking pathway that differs from the well-characterized synaptic vesicle trafficking pathway but is also essential for life.},
 pages = {365--376},
 title = {Synaptotagmin-11 mediates a vesicle trafficking pathway that is essential for development and synaptic plasticity.},
 volume = {33},
 year = {2019}
}