@article{1117,
  abstract     = {GABAergic synapses in brain circuits generate inhibitory output signals with submillisecond latency and temporal precision. Whether the molecular identity of the release sensor contributes to these signaling properties remains unclear. Here, we examined the Ca^2+ sensor of exocytosis at GABAergic basket cell (BC) to Purkinje cell (PC) synapses in cerebellum. Immunolabeling suggested that BC terminals selectively expressed synaptotagmin 2 (Syt2), whereas synaptotagmin 1 (Syt1) was enriched in excitatory terminals. Genetic elimination of Syt2 reduced action potential-evoked release to ∼10%, identifying Syt2 as the major Ca^2+ sensor at BC-PC synapses. Differential adenovirus-mediated rescue revealed that Syt2 triggered release with shorter latency and higher temporal precision and mediated faster vesicle pool replenishment than Syt1. Furthermore, deletion of Syt2 severely reduced and delayed disynaptic inhibition following parallel fiber stimulation. Thus, the selective use of Syt2 as release sensor at BC-PC synapses ensures fast and efficient feedforward inhibition in cerebellar microcircuits. #bioimagingfacility-author},
  author       = {Chen, Chong and Arai, Itaru and Satterield, Rachel and Young, Samuel and Jonas, Peter M},
  issn         = {22111247},
  journal      = {Cell Reports},
  number       = {3},
  pages        = {723 -- 736},
  publisher    = {Cell Press},
  title        = {{Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse}},
  doi          = {10.1016/j.celrep.2016.12.067},
  volume       = {18},
  year         = {2017},
}

@article{672,
  abstract     = {Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration.},
  author       = {Vaahtomeri, Kari and Brown, Markus and Hauschild, Robert and De Vries, Ingrid and Leithner, Alexander F and Mehling, Matthias and Kaufmann, Walter and Sixt, Michael K},
  issn         = {22111247},
  journal      = {Cell Reports},
  number       = {5},
  pages        = {902 -- 909},
  publisher    = {Cell Press},
  title        = {{Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia}},
  doi          = {10.1016/j.celrep.2017.04.027},
  volume       = {19},
  year         = {2017},
}

@article{677,
  abstract     = {The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler that acts in transcription, replication, and genome stability. It is required for resistance against genotoxic agents and is involved in the repair of DNA double-strand breaks (DSBs) by homologous recombination (HR). However, the causes of the HR defect in INO80-C mutant cells are controversial. Here, we unite previous findings using a system to study HR with high spatial resolution in budding yeast. We find that INO80-C has at least two distinct functions during HR—DNA end resection and presynaptic filament formation. Importantly, the second function is linked to the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic filament formation is the crucial INO80-C function during HR.},
  author       = {Lademann, Claudio and Renkawitz, Jörg and Pfander, Boris and Jentsch, Stefan},
  issn         = {22111247},
  journal      = {Cell Reports},
  number       = {7},
  pages        = {1294 -- 1303},
  publisher    = {Cell Press},
  title        = {{The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination}},
  doi          = {10.1016/j.celrep.2017.04.051},
  volume       = {19},
  year         = {2017},
}

@article{749,
  abstract     = {Synaptotagmin 7 (Syt7) is thought to be a Ca2+ sensor that mediates asynchronous transmitter release and facilitation at synapses. However, Syt7 is strongly expressed in fast-spiking, parvalbumin-expressing GABAergic interneurons, and the output synapses of these neurons produce only minimal asynchronous release and show depression rather than facilitation. To resolve this apparent contradiction, we examined the effects of genetic elimination of Syt7 on synaptic transmission at the GABAergic basket cell (BC)-Purkinje cell (PC) synapse in cerebellum. Our results indicate that at the BC-PC synapse, Syt7 contributes to asynchronous release, pool replenishment, and facilitation. In combination, these three effects ensure efficient transmitter release during high-frequency activity and guarantee frequency independence of inhibition. Our results identify a distinct function of Syt7: ensuring the efficiency of high-frequency inhibitory synaptic transmission},
  author       = {Chen, Chong and Satterfield, Rachel and Young, Samuel and Jonas, Peter M},
  issn         = {22111247},
  journal      = {Cell Reports},
  number       = {8},
  pages        = {2082 -- 2089},
  publisher    = {Cell Press},
  title        = {{Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central GABAergic synapses}},
  doi          = {10.1016/j.celrep.2017.10.122},
  volume       = {21},
  year         = {2017},
}