Neuronal migration - PubMed (original) (raw)
Review
. 2001 Jul;105(1-2):47-56.
doi: 10.1016/s0925-4773(01)00396-3.
Affiliations
- PMID: 11429281
- DOI: 10.1016/s0925-4773(01)00396-3
Free article
Review
Neuronal migration
C Lambert de Rouvroit et al. Mech Dev. 2001 Jul.
Free article
Abstract
Like other motile cells, neurons migrate in three schematic steps, namely leading edge extension, nuclear translocation or nucleokinesis, and retraction of the trailing process. In addition, neurons are ordered into architectonic patterns at the end of migration. Leading edge extension can proceed at the extremity of the axon, by growth cone formation, or from the dendrites, by formation of dendritic tips. Among both categories of leading edges, variation seems to be related to the rate of extension of the leading process. Leading edge extension is directed by microfilament polymerization following integration of extracellular cues and is regulated by Rho-type small GTPases. In humans, mutations of filamin, an actin-associated protein, result in heterotopic neurons, probably due to defective leading edge extension. The second event in neuron migration is nucleokinesis, a process which is critically dependent on the microtubule network, as shown in many cell types, from slime molds to vertebrates. In humans, mutations in the PAFAH1B1 gene (more commonly called LIS1) or in the doublecortin (DCX) gene result in type 1 lissencephalies that are most probably due to defective nucleokinesis. Both the Lis1 and doublecortin proteins interact with microtubules, and two Lis1-interacting proteins, Nudel and mammalian NudE, are components of the dynein motor complex and of microtubule organizing centers. In mice, mutations of Cdk5 or of its activators p35 and p39 result in a migration phenotype compatible with defective nucleokinesis, although an effect on leading edge formation is also likely. The formation of architectonic patterns at the end of migration requires the integrity of the Reelin signalling pathway. Other known components of the pathway include members of the lipoprotein receptor family, the intracellular adaptor Dab1, and possibly integrin alpha 3 beta 1. Defective Reelin leads to poor lamination and, in humans, to a lissencephaly phenotype different from type 1 lissencephaly. Although the action of Reelin is unknown, it may trigger some recognition-adhesion among target neurons. Finally, pattern formation requires the integrity of the external limiting membrane, defects of which lead to overmigration of neurons in meninges and to human type 2 lissencephaly.
Similar articles
- Lis1 and doublecortin function with dynein to mediate coupling of the nucleus to the centrosome in neuronal migration.
Tanaka T, Serneo FF, Higgins C, Gambello MJ, Wynshaw-Boris A, Gleeson JG. Tanaka T, et al. J Cell Biol. 2004 Jun 7;165(5):709-21. doi: 10.1083/jcb.200309025. Epub 2004 Jun 1. J Cell Biol. 2004. PMID: 15173193 Free PMC article. - Distinct dose-dependent cortical neuronal migration and neurite extension defects in Lis1 and Ndel1 mutant mice.
Youn YH, Pramparo T, Hirotsune S, Wynshaw-Boris A. Youn YH, et al. J Neurosci. 2009 Dec 9;29(49):15520-30. doi: 10.1523/JNEUROSCI.4630-09.2009. J Neurosci. 2009. PMID: 20007476 Free PMC article. - Potential mechanisms of mutations that affect neuronal migration in man and mouse.
Walsh CA, Goffinet AM. Walsh CA, et al. Curr Opin Genet Dev. 2000 Jun;10(3):270-4. doi: 10.1016/s0959-437x(00)00076-9. Curr Opin Genet Dev. 2000. PMID: 10826984 Review. - Global developmental gene expression and pathway analysis of normal brain development and mouse models of human neuronal migration defects.
Pramparo T, Libiger O, Jain S, Li H, Youn YH, Hirotsune S, Schork NJ, Wynshaw-Boris A. Pramparo T, et al. PLoS Genet. 2011 Mar;7(3):e1001331. doi: 10.1371/journal.pgen.1001331. Epub 2011 Mar 10. PLoS Genet. 2011. PMID: 21423666 Free PMC article. - [Molecular mechanism of lissencephaly--how LIS1 and NDEL1 regulate cytoplasmic dynein?].
Hirotsune S. Hirotsune S. Brain Nerve. 2008 Apr;60(4):375-81. Brain Nerve. 2008. PMID: 18421979 Review. Japanese.
Cited by
- Lissencephaly caused by a de novo mutation in tubulin TUBA1A: a case report and literature review.
Ren S, Kong Y, Liu R, Li Q, Shen X, Kong QX. Ren S, et al. Front Pediatr. 2024 May 14;12:1367305. doi: 10.3389/fped.2024.1367305. eCollection 2024. Front Pediatr. 2024. PMID: 38813542 Free PMC article. - Novel lissencephaly-associated NDEL1 variant reveals distinct roles of NDE1 and NDEL1 in nucleokinesis and human cortical malformations.
Tsai MH, Ke HC, Lin WC, Nian FS, Huang CW, Cheng HY, Hsu CS, Granata T, Chang CH, Castellotti B, Lin SY, Doniselli FM, Lu CJ, Franceschetti S, Ragona F, Hou PS, Canafoglia L, Tung CY, Lee MH, Wang WJ, Tsai JW. Tsai MH, et al. Acta Neuropathol. 2024 Jan 9;147(1):13. doi: 10.1007/s00401-023-02665-y. Acta Neuropathol. 2024. PMID: 38194050 Free PMC article. - Reelin Signaling and Synaptic Plasticity in Schizophrenia.
Markiewicz R, Markiewicz-Gospodarek A, Borowski B, Trubalski M, Łoza B. Markiewicz R, et al. Brain Sci. 2023 Dec 11;13(12):1704. doi: 10.3390/brainsci13121704. Brain Sci. 2023. PMID: 38137152 Free PMC article. Review. - An adhesion signaling axis involving Dystroglycan, β1-Integrin, and Cas adaptor proteins regulates the establishment of the cortical glial scaffold.
Wong W, Estep JA, Treptow AM, Rajabli N, Jahncke JN, Ubina T, Wright KM, Riccomagno MM. Wong W, et al. PLoS Biol. 2023 Aug 4;21(8):e3002212. doi: 10.1371/journal.pbio.3002212. eCollection 2023 Aug. PLoS Biol. 2023. PMID: 37540708 Free PMC article. - Subcellular mRNA localization and local translation of Arhgap11a in radial glial progenitors regulates cortical development.
Pilaz LJ, Liu J, Joshi K, Tsunekawa Y, Musso CM, D'Arcy BR, Suzuki IK, Alsina FC, Kc P, Sethi S, Vanderhaeghen P, Polleux F, Silver DL. Pilaz LJ, et al. Neuron. 2023 Mar 15;111(6):839-856.e5. doi: 10.1016/j.neuron.2023.02.023. Neuron. 2023. PMID: 36924763 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Research Materials
Miscellaneous