@article{480,
  keywords = {Cell Biology, Cellular and Molecular Neuroscience, Pharmacology, Molecular Biology, Molecular Medicine},
  author = {Vilmos Tóth and Henrietta Vadászi and Lilla Ravasz and Dániel Mittli and Dominik Mátyás and Tamás Molnár and András Micsonai and Tamás Szaniszló and Péter Lőrincz and Réka Kovács and Tünde Juhász and Tamás Beke-Somfai and Gábor Juhász and Balázs Györffy and Katalin Kékesi and József Kardos},
  title = {Neuronal-specific septin-3 binds Atg8/LC3B, accumulates and localizes to autophagosomes during induced autophagy},
  abstract = {<p>AbstractIn synapses that show signs of local apoptosis and mitochondrial stress and undergo neuro-immunological synapse pruning, an increase in the levels of the presynaptic protein, neuronal-specific septin-3 can be observed. Septin-3 is a member of the septin GTPase family with the ability to form multimers and contribute to the cytoskeleton. However, the function of septin-3 remains elusive. Here, we provide evidence that septin-3 is capable of binding the most-studied autophagy protein Atg8 homolog microtubule-associated protein 1 light chain 3B (LC3B), besides another homolog, GABA receptor-associated protein-like 2 (GABARAPL2). Moreover, we demonstrate that colocalization of septin-3 and LC3B increases upon chemical autophagy induction in primary neuronal cells. Septin-3 is accumulated in primary neurons upon autophagy enhancement or blockade, similar to autophagy proteins. Using electron microscopy, we also show that septin-3 localizes to LC3B positive membranes and can be found at mitochondria. However, colocalization results of septin-3 and the early mitophagy marker PTEN-induced kinase 1 (PINK1) do not support that binding of septin-3 to mitochondria is mitophagy related. We conclude that septin-3 correlates with synaptic/neuronal autophagy, binds Atg8 and localizes to autophagic membranes that can be enhanced with chemical autophagy induction. Based on our results, elevated septin-3 levels might indicate enhanced or impeded autophagy in neurons.</p>
},
  year = {2022},
  journal = {Cellular and Molecular Life Sciences},
  volume = {79},
  publisher = {Springer Science and Business Media LLC},
  issn = {1420-682X, 1420-9071},
  doi = {10.1007/s00018-022-04488-8},
}