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Novel Kidins220/ARMS Splice Isoforms: Potential Specific Regulators of Neuronal and Cardiovascular Development.

PLoS ONE. 2015 Jun 17;10(6):e0129944. eCollection 2015
Nathalie Schmieg 1 , Claire Thomas 2 , Arisa Yabe 2 , David S Lynch 3 , Teresa Iglesias 4 , Probir Chakravarty 2 , Giampietro Schiavo 5
Nathalie Schmieg 1 , Claire Thomas 2 , Arisa Yabe 2 , David S Lynch 3 , Teresa Iglesias 4 , Probir Chakravarty 2 , Giampietro Schiavo 5
+ et al

[No authors listed]

Author information
  • 1 Molecular Neuropathobiology Laboratory, Sobell Department of Motor Neuroscience & Movement Disorders, UCL Institute of Neurology, University College London, London WC1N 3BG, United Kingdom; The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, United Kingdom.
  • 2 The Francis Crick Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, United Kingdom.
  • 3 Molecular Neuropathobiology Laboratory, Sobell Department of Motor Neuroscience & Movement Disorders, UCL Institute of Neurology, University College London, London WC1N 3BG, United Kingdom; Leonard Wolfson Centre for Experimental Neurology, University College London, 8 Queen Anne Street, London W1G 9LD, United Kingdom.
  • 4 Instituto de Investigaciones Biomédicas "Alberto Sols" (CSIC-UAM), C/ Arturo Duperier, 4, Madrid 28029, Spain; CIBERNED (ISCIII), C/ Valderrebollo 5, Madrid 28031, Spain.
  • 5 Molecular Neuropathobiology Laboratory, Sobell Department of Motor Neuroscience & Movement Disorders, UCL Institute of Neurology, University College London, London WC1N 3BG, United Kingdom.

摘要

Kidins220/ARMS is a transmembrane protein playing a crucial role in neuronal and cardiovascular development. Kidins220/ARMS is a downstream target of neurotrophin receptors and interacts with several signalling and trafficking factors. Through computational modelling, we found two potential sites for alternative splicing of Kidins220/ARMS. The first is located between exon 24 and exon 29, while the second site replaces exon 32 by a short alternative terminal exon 33. Here we describe the conserved occurrence of several Kidins220/ARMS splice isoforms at RNA and protein levels. Kidins220/ARMS splice isoforms display spatio-temporal regulation during development with distinct patterns in different neuronal populations. Neurotrophin receptor stimulation in cortical and hippocampal neurons and neuroendocrine cells induces specific Kidins220/ARMS splice isoforms and alters the appearance kinetics of the full-length transcript. Remarkably, alternative terminal exon splicing generates Kidins220/ARMS variants with distinct cellular localisation: Kidins220/ARMS containing exon 32 is targeted to the plasma membrane and neurite tips, whereas Kidins220/ARMS without exon 33 mainly clusters the full-length protein in a perinuclear intracellular compartment in PC12 cells and primary neurons, leading to a change in neurotrophin receptor expression. Overall, this study demonstrates the existence of novel Kidins220/ARMS splice isoforms with unique properties, revealing additional complexity in the functional regulation of neurotrophin receptors, and potentially other signalling pathways involved in neuronal and cardiovascular development.

图表

基因

Kidins220, Kidins220, KIDINS220

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