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Epidermis-Derived Semaphorin Promotes Dendrite Self-Avoidance by Regulating Dendrite-Substrate Adhesion in Drosophila Sensory Neurons

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Epidermis-Derived Semaphorin Promotes Dendrite Self-Avoidance by Regulating Dendrite-Substrate Adhesion in Drosophila Sensory Neurons. / Meltzer, Shan; Yadav, Smita; Lee, Jiae; Soba, Peter; Younger, Susan H; Jin, Peng; Zhang, Wei; Parrish, Jay; Jan, Lily Yeh; Jan, Yuh-Nung.

in: NEURON, Jahrgang 89, Nr. 4, 17.02.2016, S. 741-55.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Meltzer, S, Yadav, S, Lee, J, Soba, P, Younger, SH, Jin, P, Zhang, W, Parrish, J, Jan, LY & Jan, Y-N 2016, 'Epidermis-Derived Semaphorin Promotes Dendrite Self-Avoidance by Regulating Dendrite-Substrate Adhesion in Drosophila Sensory Neurons', NEURON, Jg. 89, Nr. 4, S. 741-55. https://doi.org/10.1016/j.neuron.2016.01.020

APA

Meltzer, S., Yadav, S., Lee, J., Soba, P., Younger, S. H., Jin, P., Zhang, W., Parrish, J., Jan, L. Y., & Jan, Y-N. (2016). Epidermis-Derived Semaphorin Promotes Dendrite Self-Avoidance by Regulating Dendrite-Substrate Adhesion in Drosophila Sensory Neurons. NEURON, 89(4), 741-55. https://doi.org/10.1016/j.neuron.2016.01.020

Vancouver

Meltzer S, Yadav S, Lee J, Soba P, Younger SH, Jin P et al. Epidermis-Derived Semaphorin Promotes Dendrite Self-Avoidance by Regulating Dendrite-Substrate Adhesion in Drosophila Sensory Neurons. NEURON. 2016 Feb 17;89(4):741-55. https://doi.org/10.1016/j.neuron.2016.01.020

Bibtex

@article{1bc4d3aebc6c4d89802cce454df915a0,
title = "Epidermis-Derived Semaphorin Promotes Dendrite Self-Avoidance by Regulating Dendrite-Substrate Adhesion in Drosophila Sensory Neurons",
abstract = "Precise patterning of dendritic arbors is critical for the wiring and function of neural circuits. Dendrite-extracellular matrix (ECM) adhesion ensures that the dendrites of Drosophila dendritic arborization (da) sensory neurons are properly restricted in a 2D space, and thereby facilitates contact-mediated dendritic self-avoidance and tiling. However, the mechanisms regulating dendrite-ECM adhesion in vivo are poorly understood. Here, we show that mutations in the semaphorin ligand sema-2b lead to a dramatic increase in self-crossing of dendrites due to defects in dendrite-ECM adhesion, resulting in a failure to confine dendrites to a 2D plane. Furthermore, we find that Sema-2b is secreted from the epidermis and signals through the Plexin B receptor in neighboring neurons. Importantly, we find that Sema-2b/PlexB genetically and physically interacts with TORC2 complex, Tricornered (Trc) kinase, and integrins. These results reveal a novel role for semaphorins in dendrite patterning and illustrate how epidermal-derived cues regulate neural circuit assembly.",
keywords = "Animals, Animals, Genetically Modified, Cell Communication, Dendrites, Drosophila, Drosophila Proteins, Epidermis, Focal Adhesion Kinase 1, Gene Expression Regulation, Developmental, Green Fluorescent Proteins, Immunoprecipitation, Larva, Molecular Biology, Multiprotein Complexes, Mutation, Nerve Tissue Proteins, Receptors, Cell Surface, Semaphorins, Sensory Receptor Cells, TOR Serine-Threonine Kinases, Transfection, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S.",
author = "Shan Meltzer and Smita Yadav and Jiae Lee and Peter Soba and Younger, {Susan H} and Peng Jin and Wei Zhang and Jay Parrish and Jan, {Lily Yeh} and Yuh-Nung Jan",
note = "Copyright {\textcopyright} 2016 Elsevier Inc. All rights reserved.",
year = "2016",
month = feb,
day = "17",
doi = "10.1016/j.neuron.2016.01.020",
language = "English",
volume = "89",
pages = "741--55",
journal = "NEURON",
issn = "0896-6273",
publisher = "Cell Press",
number = "4",

}

RIS

TY - JOUR

T1 - Epidermis-Derived Semaphorin Promotes Dendrite Self-Avoidance by Regulating Dendrite-Substrate Adhesion in Drosophila Sensory Neurons

AU - Meltzer, Shan

AU - Yadav, Smita

AU - Lee, Jiae

AU - Soba, Peter

AU - Younger, Susan H

AU - Jin, Peng

AU - Zhang, Wei

AU - Parrish, Jay

AU - Jan, Lily Yeh

AU - Jan, Yuh-Nung

N1 - Copyright © 2016 Elsevier Inc. All rights reserved.

PY - 2016/2/17

Y1 - 2016/2/17

N2 - Precise patterning of dendritic arbors is critical for the wiring and function of neural circuits. Dendrite-extracellular matrix (ECM) adhesion ensures that the dendrites of Drosophila dendritic arborization (da) sensory neurons are properly restricted in a 2D space, and thereby facilitates contact-mediated dendritic self-avoidance and tiling. However, the mechanisms regulating dendrite-ECM adhesion in vivo are poorly understood. Here, we show that mutations in the semaphorin ligand sema-2b lead to a dramatic increase in self-crossing of dendrites due to defects in dendrite-ECM adhesion, resulting in a failure to confine dendrites to a 2D plane. Furthermore, we find that Sema-2b is secreted from the epidermis and signals through the Plexin B receptor in neighboring neurons. Importantly, we find that Sema-2b/PlexB genetically and physically interacts with TORC2 complex, Tricornered (Trc) kinase, and integrins. These results reveal a novel role for semaphorins in dendrite patterning and illustrate how epidermal-derived cues regulate neural circuit assembly.

AB - Precise patterning of dendritic arbors is critical for the wiring and function of neural circuits. Dendrite-extracellular matrix (ECM) adhesion ensures that the dendrites of Drosophila dendritic arborization (da) sensory neurons are properly restricted in a 2D space, and thereby facilitates contact-mediated dendritic self-avoidance and tiling. However, the mechanisms regulating dendrite-ECM adhesion in vivo are poorly understood. Here, we show that mutations in the semaphorin ligand sema-2b lead to a dramatic increase in self-crossing of dendrites due to defects in dendrite-ECM adhesion, resulting in a failure to confine dendrites to a 2D plane. Furthermore, we find that Sema-2b is secreted from the epidermis and signals through the Plexin B receptor in neighboring neurons. Importantly, we find that Sema-2b/PlexB genetically and physically interacts with TORC2 complex, Tricornered (Trc) kinase, and integrins. These results reveal a novel role for semaphorins in dendrite patterning and illustrate how epidermal-derived cues regulate neural circuit assembly.

KW - Animals

KW - Animals, Genetically Modified

KW - Cell Communication

KW - Dendrites

KW - Drosophila

KW - Drosophila Proteins

KW - Epidermis

KW - Focal Adhesion Kinase 1

KW - Gene Expression Regulation, Developmental

KW - Green Fluorescent Proteins

KW - Immunoprecipitation

KW - Larva

KW - Molecular Biology

KW - Multiprotein Complexes

KW - Mutation

KW - Nerve Tissue Proteins

KW - Receptors, Cell Surface

KW - Semaphorins

KW - Sensory Receptor Cells

KW - TOR Serine-Threonine Kinases

KW - Transfection

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

KW - Research Support, U.S. Gov't, Non-P.H.S.

U2 - 10.1016/j.neuron.2016.01.020

DO - 10.1016/j.neuron.2016.01.020

M3 - SCORING: Journal article

C2 - 26853303

VL - 89

SP - 741

EP - 755

JO - NEURON

JF - NEURON

SN - 0896-6273

IS - 4

ER -