Noboru H. Komiyama Ph.D.
Centre for Centre for Neuroregeneration and Centre for Clinical Brain Sciences
The University of Edinburgh,
Chancellor's Building,
49 Little France Crescent,
Edinburgh,
EH16 4SB
Tel: +44(0)131 242 9240
e-mail: nkomiya2@staffmail.ed.ac.uk
Biographical Profile
Noboru Komiyama received a degree in Biophysics from Osaka University and did his
Ph.D. with Dr. Max Perutz and Dr. Kiyoshi Nagai in the MRC Laboratory of Molecular
Biology, Cambridge. He worked as a postdoctoral fellow in Prof. Seth Grant Lab in the
University of Edinburgh and a senior staff scientist in the Wellcome Trust Sanger
Institute, Cambridge. He is a senior lecturer and member of Centre for Neuroregeneration
and Centre for Clinical Brain Sciences in the University of Edinburgh.
Research Overview
We are interested in how complex brain functions such as synaptic plasticity,
cognition, learning and memory formation are achieved at a molecular level. We
want to understand the precise molecular mechanisms underlining those higher
brain functions and try to find out how these synaptic molecules are organized and
how they evolved to fulfil a variety of very complex tasks in the brain. We are
primarily focusing on NMDA subtype of glutamate receptors, especially the
structural and functional roles of large cytoplasmic C-terminal domains of
NR2/GluN2 subunits and their interacting proteins that form large macro-molecular
complexes at excitatory synapses in mammalian central nervous system. Recently a
large number of human genetic studies have identified mutations in genes encoding
NMDA receptor subunits and their interacting proteins that can either cause various
psychiatric disorders or increase the susceptibility for these diseases including
intellectual disability, autism, schizophrenia, epilepsy and addiction. Thus we have
been systematically engineering defined mutations in these genes to study their
physical and functional organization in normal brain and their alterations in
pathological conditions in vivo. We are also involved in developing genetic tools that
will further help us to understand detailed molecular interaction and precise
localization of these proteins in the brain. These studies will provide vital
information about basic synaptic biology and better understanding of mechanisms
for many human brain disorders.
Recent Publications
A polygenic burden of rare disruptive mutations in schizophrenia.
Purcell SM, Moran JL, Fromer M, Ruderfer D, Solovieff N, Roussos P, O'Dushlaine C, Chambert K,
Bergen SE, Kähler A, Duncan L, Stahl E, Genovese G, Fernández E, Collins MO, Komiyama NH,
Choudhary JS, Magnusson PK, Banks E, Shakir K, Garimella K, Fennell T, DePristo M, Grant SG,
Haggarty SJ, Gabriel S, Scolnick EM, Lander ES, Hultman CM, Sullivan PF, McCarroll SA, Sklar P.
Nature. 2014 Feb 13;506(7487):185-90. doi: 10.1038/nature12975.
Novel MPDZ/MUPP1 transgenic and knockdown models confirm Mpdz's role in ethanol withdrawal
and support its role in voluntary ethanol consumption.
Milner LC, Shirley RL, Kozell LB, Walter NA, Kruse LC, Komiyama NH, Grant SG, Buck KJ.
Addict Biol. 2013 Oct 10. doi: 10.1111/adb.12087.
CYFIP1 coordinates mRNA translation and cytoskeleton remodeling to ensure proper dendritic
spine formation.
De Rubeis S, Pasciuto E, Li KW, Fernández E, Di Marino D, Buzzi A, Ostroff LE, Klann E, Zwartkruis FJ,
Komiyama NH, Grant SG, Poujol C, Choquet D, Achsel T, Posthuma D, Smit AB, Bagni C.
Neuron. 2013 Sep 18;79(6):1169-82. doi: 10.1016/j.neuron.2013.06.039.
Synaptic scaffold evolution generated components of vertebrate cognitive complexity.
Nithianantharajah J, Komiyama NH, McKechanie A, Johnstone M, Blackwood DH, St Clair D, Emes RD,
van de Lagemaat LN, Saksida LM, Bussey TJ, Grant SG.
Nat Neurosci. 2013 Jan;16(1):16-24. doi: 10.1038/nn.3276.
Evolution of GluN2A/B cytoplasmic domains diversified vertebrate synaptic plasticity and behavior.
Ryan TJ, Kopanitsa MV, Indersmitten T, Nithianantharajah J, Afinowi NO, Pettit C, Stanford LE, Sprengel
R, Saksida LM, Bussey TJ, O'Dell TJ, Grant SG, Komiyama NH.
Nat Neurosci. 2013 Jan;16(1):25-32. doi: 10.1038/nn.3277.
TNiK is required for postsynaptic and nuclear signaling pathways and cognitive function.
Coba MP*, Komiyama NH*, Nithianantharajah J*, Kopanitsa MV, Indersmitten T, Skene NG, Tuck EJ,
Fricker DG, Elsegood KA, Stanford LE, Afinowi NO, Saksida LM, Bussey TJ, O'Dell TJ, Grant SG.
J Neurosci. 2012 Oct 3;32(40): doi: 10.1523/JNEUROSCI.2433-12.2012.
SynGAP isoforms exert opposing effects on synaptic strength.
McMahon AC, Barnett MW, O'Leary TS, Stoney PN, Collins MO, Papadia S, Choudhary JS, Komiyama
NH, Grant SG, Hardingham GE, Wyllie DJ, Kind PC.
Nat Commun. 2012 Jun 12;3:99 doi: 10.1038/ncomms1900.
The subtype of GluN2 C-terminal domain determines the response to excitotoxic insults.
Martel MA, Ryan TJ, Bell KF, Fowler JH, McMahon A, Al-Mubarak B, Komiyama NH, Horsburgh K,
Kind PC, Grant SG, Wyllie DJ, Hardingham GE.
Neuron. 2012 May 10;74(3):543-56. doi: 10.1016/j.neuron.2012.03.021.
De novo CNV analysis implicates specific abnormalities of postsynaptic signalling complexes in the
pathogenesis of schizophrenia.
Kirov G, Pocklington AJ, Holmans P, Ivanov D, Ikeda M, Ruderfer D, Moran J, Chambert K, Toncheva D,
Georgieva L, Grozeva D, Fjodorova M, Wollerton R, Rees E, Nikolov I, van de Lagemaat LN, Bayés A,
Fernandez E, Olason PI, Böttcher Y, Komiyama NH, Collins MO, Choudhary J, Stefansson K, Stefansson
H, Grant SG, Purcell S, Sklar P, O'Donovan MC, Owen MJ.
Mol Psychiatry. 2012 Feb;17(2):142-53. doi: 10.1038/mp.2011.154.