Prof Dies Meijer
Prof. Meijer's biography and research focus, plus details of the Meijer Lab
Dies Meijer received his BSc and MSc in Molecular Sciences from Wageningen University and his PhD in Molecular Genetics and Developmental Biology from Erasmus University Rotterdam in 1992. After postdoctoral training at the National Institute for Medical Research, Mill Hill London, he established his research group in the department of Genetics at the Erasmus University Medical Center and initiated research into glial cell development and myelination of the peripheral nervous system. In 2013 he moved to the University of Edinburgh, where he joined the Centre for Neuroregeneration and Centre for Clinical Brain Sciences.
Prof Meijer was appointed as the CNR's Postgraduate Director in March 2016.
Dynamic interactions between neuronal cells shape key morphological and functional properties of the nervous system during ontogeny and adult life. This is most profoundly illustrated by the elaboration of the myelin sheath that surrounds many axons, and by the assembly and dynamics of the neuronal synapse. We are interested in the molecular interactions that coordinate these complex cell-cell interactions and shape the transcriptional programs of cell differentiation and homeostasis in the nervous system.
One class of molecules that play important roles in these processes are the LGI (Leucine-rich Glioma Inactivated) glycoproteins. They have been implicated in tumorigenesis, hereditary forms of epilepsy, limbic encephalitis and peripheral nerve amyelination. Our previous work revealed that Schwann cells secrete LGI4, which through binding to the axonal receptor ADAM22 drives axonal ensheathment and myelination in the peripheral nervous system. More recent experiments also implicate LGI2 and LGI3 in the cyto-architecture of myelinated nerve fibers and synapse biology. Our current work aims to identify the mechanism(s) through which LGI molecules coordinate formation and organization of the myelin sheath and contribute to synapse formation and strength. In a second line of research, we are building on our earlier work of the transcription factors Oct6 and Brn2 to define the complete transcriptional network of myelination in the peripheral nervous system.
- Dan Booth, Post-doctoral Fellow
- Gavin Steel, Senior Technical Officer
- Nina Kozar, PhD student (BBSRC, EASTBIO programme)
- Ella Mercer, PhD student Tissue Repair (Wellcome Trust)
Dr Dick Jaarsma, Erasmus MC, the Netherlands
Dr Martine Jaegle, Erasmus MC, the Netherlands
- Professor Masaki Fukatu and Dr Yuko Fukata, National Institute for Physiological Sciences (NIPS), Japan
- Dr Iris Oren, University of Edinburgh
- Prof Richard Ribchester, University of Edinburgh
- Yokoi N, Fukata Y, Kase D, Miyazaki T, Jaegle M, Ohkawa T, Takahashi N, Iwanari H, Mochizuki Y, Hamakubo T, Imoto, K, Meijer D, Watanabe M, Fukata M (2015). Chemical Corrector Treatment Ameliorates Increased Seizure Susceptibility in a Mouse Model of Familial Epilepsy. Nature Medicine 21, 19-26.
- Kegel L, Jaegle M, Driegen S, Aunin E, Leslie K, Fukata Y, Watanabe M, Fukata M, Meijer D (2014). Functional Phylogenetic Analysis of LGI Proteins Identifies an Interaction Motif Crucial for Myelination. Development 141: 1749-1756.
- Kegel L, Aunin E, Meijer D, Bermingham Jr J (2013). LGI Proteins in The Nervous System. ASN Neuro. 5(3).
- Jagalur NB, Ghazvini M, Mandemakers W, Driegen S, Maas A, Jones EA, Jaegle M, Grosveld F, Svaren J, Meijer D (2011). Functional Dissection of the Oct6 Schwann Cell Enhancer Reveals an Essential Role for Dimeric Sox10 Binding. Journal of Neuroscience 31,8585-8594.
- Ogawa Y, Oses-Prieto J, Kim MY, Horresh I, Peles E, Burlingame AL, Trimmer JS, Meijer D, Rasband MN (2010) ADAM22, A Kv1 Channel-Interacting Protein, Recruits Membrane-Associated Guanylate Kinases to Juxtaparanodes of Myelinated Axons. Journal of Neuroscience 30:1038-1048.
- Özkaynak E, Abello G, Jaegle M, van Berge L, Hamer D, Kegel L, Driegen S, Sagane K, Bermingham JR, Jr., Meijer D (2010). Adam22 is a Major Neuronal Receptor for lgi4-mediated Schwann Cell Signalling. Journal of Neuroscience 30:3857-3864.
Key Earlier Publications
- Bermingham, J.R., Shearin, H., Pennington, J., O'Moore, J., Jaegle, M., Driegen, S., van Zon, A., Darbas, A., Ozkaynak, E., Milbrandt, J. & Meijer, D (2006). The Claw Paw Mutation Reveals a Role for Lgi4 in Peripheral Nerve Development. Nature Neuroscience 9, 76-84.
- Darbas, A., Jaegle, M., Walbeehm, E., van den Burg, H., Driegen, S., Broos, L., Uyl, M., Visser, P., Grosveld, F. & Meijer, D (2004). Cell Autonomy of the Mouse Claw Paw Mutation. Developmental Biology 272, 470-82.
- Jaegle, M., Ghazvini, M., Mandemakers, W., Piirsoo, M., Driegen, S., Levavasseur, F., Raghoenath, S., Grosveld, F. & Meijer, D (2003). The POU Proteins Brn-2 and Oct-6 Share Important Functions in Schwann Cell Development. Genes & Development 17, 1380-91.
- Ghazvini, M., Mandemakers, W., Jaegle, M., Piirsoo, M., Driegen, S., Koutsourakis, M., Smit, X., Grosveld, F. & Meijer, D (2002). A Cell Type-specific Allele of the POU Gene Oct-6 Reveals Schwann Cell Autonomous Function in Nerve Development and Regeneration. The Embo Journal 21, 4612-20.
- Mandemakers, W., Zwart, R., Jaegle, M., Walbeehm, E., Visser, P., Grosveld, F. & Meijer, D (2000). A Distal Schwann Cell-specific Enhancer Mediates Axonal Regulation of the Oct-6 Transcription Factor During Peripheral Nerve Development and Regeneration. The Embo Journal 19, 2992-3003.