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      Call for Papers: Sex and Gender in Neurodegenerative Diseases

      Submit here before September 30, 2024

      About Neurodegenerative Diseases: 3.0 Impact Factor I 4.3 CiteScore I 0.695 Scimago Journal & Country Rank (SJR)

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      Tracing the Evolution and Function of the Trk Superfamily of Receptor Tyrosine Kinases

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      Publication date (Electronic):
      Journal: Brain, Behavior and Evolution
      Publisher: S. Karger AG
      Keywords: Ror, Musk, Discoidin, Ddr, IgCAM, Kringle, Frizzled

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          Abstract

          Most growth factors and their receptors have been strongly conserved during evolution. In contrast, Trks (Tropomyosin-related kinases) and related receptors in the Trk superfamily, Rors (receptor tyrosine kinase-like orphan receptors), Musks (muscle specific kinases) and Ddrs (discoidin domain receptor family), appear to be ancient, but their function has been lost in multiple lineages and the roles for the receptors have been modified over time. We will trace the evolution of the Trk superfamily and discuss possible conserved functional roles, including a unifying theme of target recognition by growing axons. We present an analogy between the evolution of G-protein-coupled receptors and receptor tyrosine kinases (RTKs), proposing that an important driving force for the divergence of receptors is the ease of divergence of their ligands.

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          BDNF function in adult synaptic plasticity: the synaptic consolidation hypothesis.

          Clive Bramham, Elhoucine Messaoudi (2005)
          Interest in BDNF as an activity-dependent modulator of neuronal structure and function in the adult brain has intensified in recent years. Localization of BDNF-TrkB to glutamate synapses makes this system attractive as a dynamic, activity-dependent regulator of excitatory transmission and plasticity. Despite individual breakthroughs, an integrated understanding of BDNF function in synaptic plasticity is lacking. Here, we attempt to distill current knowledge of the molecular mechanisms and function of BDNF in LTP. BDNF activates distinct mechanisms to regulate the induction, early maintenance, and late maintenance phases of LTP. Evidence from genetic and pharmacological approaches is reviewed and tabulated. The specific contribution of BDNF depends on the stimulus pattern used to induce LTP, which impacts the duration and perhaps the subcellular site of BDNF release. Particular attention is given to the role of BDNF as a trigger for protein synthesis-dependent late phase LTP--a process referred to as synaptic consolidation. Recent experiments suggest that BDNF activates synaptic consolidation through transcription and rapid dendritic trafficking of mRNA encoded by the immediate early gene, Arc. A model is proposed in which BDNF signaling at glutamate synapses drives the translation of newly transported (Arc) and locally stored (i.e., alphaCaMKII) mRNA in dendrites. In this model BDNF tags synapses for mRNA capture, while Arc translation defines a critical window for synaptic consolidation. The biochemical mechanisms by which BDNF regulates local translation are also discussed. Elucidation of these mechanisms should shed light on a range of adaptive brain responses including memory and mood resilience.
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            The receptor tyrosine kinase Ror2 is involved in non-canonical Wnt5a/JNK signalling pathway.

            Isao Oishi, Hiroaki Suzuki, Nobuyuki Onishi … (2003)
            Ror2 is an orphan receptor, belonging to the Ror family of receptor tyrosine kinases. Although Ror2 has been shown to play crucial roles in developmental morphogenesis, the precise signalling events that Ror2 mediates remain elusive. Since Ror2 possesses an extracellular cysteine-rich domain (CRD) that resembles the Wnt-binding sites of the Frizzled (Fz) proteins, it is conceivable that Ror2 interacts with members of the Wnt family. Both Ror2-/- and Wnt5a-/- mice exhibit dwarfism, facial abnormalities, short limbs and tails, dysplasia of lungs and genitals, and ventricular septal defects. In vitro binding assay revealed that Wnt5a binds to the CRD of Ror2. Furthermore, Ror2 associates via its CRD with rFz2, a putative receptor for Wnt5a. Interestingly, Wnt5a and Ror2 activate the non-canonical Wnt pathway, as assessed by activation of JNK in cultured cells and inhibition of convergent extension movements in Xenopus. Our findings indicate that Wnt5a and Ror2 interact physically and functionally. Ror2 may thus act as a receptor for Wnt5a to activate non-canonical Wnt signalling.
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              The receptor tyrosine kinase MuSK is required for neuromuscular junction formation in vivo.

              Thomas Dechiara, David C. Bowen, David M. Valenzuela … (1996)
              Formation of neuromuscular synapses requires a series of inductive interactions between growing motor axons and differentiating muscle cells, culminating in the precise juxtaposition of a highly specialized nerve terminal with a complex molecular structure on the postsynaptic muscle surface. The receptors and signaling pathways mediating these inductive interactions are not known. We have generated mice with a targeted disruption of the gene encoding MuSK, a receptor tyrosine kinase selectively localized to the postsynaptic muscle surface. Neuromuscular synapses do not form in these mice, suggesting a failure in the induction of synapse formation. Together with the results of an accompanying manuscript, our findings indicate that MuSK responds to a critical nerve-derived signal (agrin), and in turn activates signaling cascades responsible for all aspects of synapse formation, including organization of the postsynaptic membrane, synapse-specific transcription, and presynaptic differentiation.
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                Author and article information

                Journal
                Journal ID (publisher-id): BBE
                Journal ID (nlm-ta): Brain Behav Evol
                Journal ID (doi): 10.1159/issn.0006-8977
                Title: Brain, Behavior and Evolution
                Publisher: S. Karger AG
                ISBN: 978-3-8055-8181-3
                ISBN: 978-3-318-01400-6
                ISSN (Print): 0006-8977
                ISSN (Electronic): 1421-9743
                Publication date Subscription-year: 2006
                Publication date (Print): August 2006
                Publication date (Electronic): 16 August 2006
                Volume: 68
                Issue: 3
                Pages: 145-156
                Affiliations
                Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Canada
                Article
                Publisher ID: 94084 Other ID: Brain Behav Evol 2006;68:145–156
                DOI: 10.1159/000094084
                PubMed ID: 16912468
                SO-VID: 455c308a-6583-48b1-8785-1d60b0aa4cc1
                Copyright © © 2006 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 12 April 2006
                Date accepted : 18 April 2006
                Page count
                Figures: 4, Tables: 3, References: 58, Pages: 12
                Categories
                Subject: Paper

                ScienceOpen disciplines: Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Keywords: Kringle,Ror,Frizzled,Discoidin,Ddr,IgCAM,Musk
                Data availability:
                ScienceOpen disciplines: Geriatric medicine, Neurology, Cardiovascular Medicine, Neurosciences, Clinical Psychology & Psychiatry, Public health
                Keywords: Kringle, Ror, Frizzled, Discoidin, Ddr, IgCAM, Musk

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