The Neurexin/N-Ethylmaleimide-sensitive Factor (NSF) Interaction Regulates Short Term Synaptic Depression

Li, Tao; Tian, Yao; Li, Qian; Lv, Huihui; Xie, Wei; Han, Junhai

doi:10.1074/jbc.m115.644583

Cited by 20 publications

(20 citation statements)

References 60 publications

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“…Neurexins function in the formation and transmission of synapses (Dean et al, 2003;Li et al, 2015;Missler et al, 2003;Qiu et al, 2007;Scheiffele, 2003;Zeng et al, 2007) and were also shown to interact directly with neuroligin on the postsynaptic membrane to influence dendrite growth and stability in Xenopus (Chen et al, 2010). In addition, a-neurexin knockout mice exhibit shortened distal dendritic branches (Dudanova et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Neurexin Restricts Axonal Branching in Columns by Promoting Ephrin Clustering

et al. 2017

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Columnar restriction of neurites is critical for forming nonoverlapping receptive fields and preserving spatial sensory information from the periphery in both vertebrate and invertebrate nervous systems, but the underlying molecular mechanisms remain largely unknown. Here, we demonstrate that Drosophila homolog of α-neurexin (DNrx) plays an essential role in columnar restriction during L4 axon branching. Depletion of DNrx from L4 neurons resulted in misprojection of L4 axonal branches into neighboring columns due to impaired ephrin clustering. The proper ephrin clustering requires its interaction with the intracellular region of DNrx. Furthermore, we find that Drosophila neuroligin 4 (DNlg4) in Tm2 neurons binds to DNrx and initiates DNrx clustering in L4 neurons, which subsequently induces ephrin clustering. Our study demonstrates that DNrx promotes ephrin clustering and reveals that ephrin/Eph signaling from adjacent L4 neurons restricts axonal branches of L4 neurons in columns.

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Section: Introductionmentioning

confidence: 99%

Neurexin Restricts Axonal Branching in Columns by Promoting Ephrin Clustering

et al. 2017

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“…Neurexins and neuroligins are cell adhesion molecules that function in synapse formation8910 and synaptic transmission1112. Mutations in neurexin and neuroligin genes have been linked to autism1314.…”

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confidence: 99%

Neurexin regulates nighttime sleep by modulating synaptic transmission

Tong

Zhang

et al. 2016

Sci Rep

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Neurexins are cell adhesion molecules involved in synaptic formation and synaptic transmission. Mutations in neurexin genes are linked to autism spectrum disorders (ASDs), which are frequently associated with sleep problems. However, the role of neurexin-mediated synaptic transmission in sleep regulation is unclear. Here, we show that lack of the Drosophila α-neurexin homolog significantly reduces the quantity and quality of nighttime sleep and impairs sleep homeostasis. We report that neurexin expression in Drosophila mushroom body (MB) αβ neurons is essential for nighttime sleep. We demonstrate that reduced nighttime sleep in neurexin mutants is due to impaired αβ neuronal output, and show that neurexin functionally couples calcium channels (Cac) to regulate synaptic transmission. Finally, we determine that αβ surface (αβs) neurons release both acetylcholine and short neuropeptide F (sNPF), whereas αβ core (αβc) neurons release sNPF to promote nighttime sleep. Our findings reveal that neurexin regulates nighttime sleep by mediating the synaptic transmission of αβ neurons. This study elucidates the role of synaptic transmission in sleep regulation, and might offer insights into the mechanism of sleep disturbances in patients with autism disorders.

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“…Different cell types show different levels of NSF/NSF2 expression (Ordway et al, 1994;Boulianne and Trimble, 1995;Pallanck et al, 1995;Golby et al, 2001;Mohtashami et al, 2001), indicating they have different demands for its function. We detected both genes by qRT-PCR from ovaries, and found high expression levels of NSF protein in the early germline and follicle cells, including polar cells, by antibody staining (Li et al, 2015) (not shown). Next, we overexpressed NSF2 in follicle cells.…”

Section: Introductionmentioning

confidence: 91%

“…The following primary antibodies were used: mouse anti-Eya (10H6, DSHB; 1:100) (Bonini et al, 1993), mouse anti-Armadillo (N27A1, DSHB; 1:40) (Riggleman et al, 1990), rabbit anti-Apt ( provided by S. Hirose, National Institute of Genetics, Mishima, Japan; 1:1000) (Liu et al, 2003), guinea pig anti-Apt from GST-Apt (Pocono Rabbit Farm, 1:5000), rat anti-Slbo ( provided by P. Rorth, Institute of Molecular and Cell Biology A-STAR, Proteos, Singapore; 1:1000) (Beccari et al, 2002), anti-rabbit GFP (Life Technologies; 1:250), rat anti-Drosophila E-Cad (DCAD2, DSHB;1:20) (Oda et al, 1997), rat anti-human influenza hemagglutinin (HA) (11867423001, Roche; at 0.5 µg/ml), mouse anti-FasIII (7G10, DSHB;1:50) (Patel et al, 1987), rabbit anti-NSF ( provided by J. Han, Southeast University, Nanjing, China; 1:50; Li et al, 2015) and α-Snap ( provided by L. Pallanck, University of Washington, Seattle, WA; 1:600; Babcock et al, 2004). Images were acquired with a Carl Zeiss AxioImager Z1 and Apotome optical sectioning with Axiovision acquisition software.…”

Section: Immunofluorescence Labeling and Phenotypic Analysismentioning

confidence: 99%

“…Although a few specific roles have been suggested for NSF and α-Snap, their distinct developmental functions remain largely unknown. NSF and α-Snap are required for Drosophila neurotransmission (Kawasaki et al, 1998;Babcock et al, 2004;Yu et al, 2011;Li et al, 2015), and in hypothalamus and neuron development in zebrafish and mice, respectively (Chae et al, 2004;Hong et al, 2004;Kurrasch et al, 2009). Two genes encode NSF proteins in Drosophilacomatose (comt) and NSF2with some tissue-specific requirements (Siddiqi and Benzer, 1976;Boulianne and Trimble, 1995;Pallanck et al, 1995;Golby et al, 2001;Zhao et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Cytokine exocytosis and JAK/STAT activation in the Drosophila ovary requires the vesicle trafficking regulator α-Snap

Saadin

Starz‐Gaiano

2018

Journal of Cell Science

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How vesicle trafficking components actively contribute to regulation of paracrine signaling is unclear. We genetically uncovered a requirement for α-soluble NSF attachment protein (α-Snap) in the activation of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway during Drosophila egg development. α-Snap, a well-conserved vesicle trafficking regulator, mediates association of N-ethylmaleimide-sensitive factor (NSF) and SNAREs to promote vesicle fusion. Depletion of α-Snap or the SNARE family member Syntaxin1A in epithelia blocks polar cells maintenance and prevents specification of motile border cells. Blocking apoptosis rescues polar cell maintenance in α-Snapdepleted egg chambers, indicating that the lack of border cells in mutants is due to impaired signaling. Genetic experiments implicate α-Snap and NSF in secretion of a STAT-activating cytokine. Live imaging suggests that changes in intracellular Ca 2+ are linked to this event. Our data suggest a cell-type specific requirement for particular vesicle trafficking components in regulated exocytosis during development. Given the central role for STAT signaling in immunity, this work may shed light on regulation of cytokine release in humans.

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The Neurexin/N-Ethylmaleimide-sensitive Factor (NSF) Interaction Regulates Short Term Synaptic Depression

Cited by 20 publications

References 60 publications

Neurexin Restricts Axonal Branching in Columns by Promoting Ephrin Clustering

Neurexin Restricts Axonal Branching in Columns by Promoting Ephrin Clustering

Neurexin regulates nighttime sleep by modulating synaptic transmission

Cytokine exocytosis and JAK/STAT activation in the Drosophila ovary requires the vesicle trafficking regulator α-Snap

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