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The establishment of axon-dendrite polarity is fundamental for radial migration of neurons, cortical patterning, and formation of neuronal circuits. Here, we show that the receptor tyrosine kinases, Ltk and Alk, are required for proper neuronal polarization. In isolated primary mouse embryonic neurons, the loss of Ltk and/or Alk causes a multiple axon phenotype. In mouse embryos and newborn pups, the absence of Ltk and Alk delays neuronal migration and subsequent cortical patterning. In adult cortices, neurons with aberrant neuronal projections are evident and axon tracts in the corpus callosum are disrupted. Mechanistically, we show that the loss of Alk and Ltk increases the cell-surface expression and activity of the insulin-like growth factor 1 receptor (Igf-1r), which activates downstream PI3 kinase signaling to drive the excess axon phenotype. Our data reveal Ltk and Alk as new regulators of neuronal polarity and migration whose disruption results in behavioral abnormalities.

Titel:	LTK and ALK promote neuronal polarity and cortical migration by inhibiting IGF1R activity.
Autor/in / Beteiligte Person:	Christova, T ; Ho, SK ; Liu, Y ; Gill, M ; Attisano, L
Link:	Full Text Finder (Volltext)
Zeitschrift:	EMBO reports, Jg. 24 (2023-07-05), Heft 7, S. e56937
Veröffentlichung:	2024- : [London] : Nature Publishing Group ; <i>Original Publication</i>: Oxford, UK : Published for EMBO by Oxford University Press, 2000-, 2023
Medientyp:	academicJournal
ISSN:	1469-3178 (electronic)
DOI:	10.15252/embr.202356937
Schlagwort:	Animals Mice Axons metabolism Cell Polarity Neurogenesis genetics Signal Transduction Neurons metabolism Receptor Protein-Tyrosine Kinases genetics Receptor Protein-Tyrosine Kinases metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article Language: English [EMBO Rep] 2023 Jul 05; Vol. 24 (7), pp. e56937. <i>Date of Electronic Publication: </i>2023 Jun 09. MeSH Terms: Neurons* / metabolism ; Receptor Protein-Tyrosine Kinases* / genetics ; Receptor Protein-Tyrosine Kinases* / metabolism ; Animals ; Mice ; Axons / metabolism ; Cell Polarity ; Neurogenesis / genetics ; Signal Transduction References: Cell. 2011 Aug 5;146(3):435-47. (PMID: 21816278) ; Sci Signal. 2020 May 26;13(633):. (PMID: 32457113) ; Nature. 2021 Dec;600(7887):143-147. (PMID: 34646012) ; Curr Opin Investig Drugs. 2010 Dec;11(12):1477-90. (PMID: 21154129) ; Clin Adv Hematol Oncol. 2014 Jul;12(7):429-39. (PMID: 25322323) ; Development. 2015 Jun 15;142(12):2088-93. (PMID: 26081570) ; Sci Rep. 2017 Aug 9;7(1):7703. (PMID: 28794445) ; Lancet Oncol. 2018 Dec;19(12):1654-1667. (PMID: 30413378) ; Sci STKE. 2002 Jun 11;2002(136):pl9. 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LTK and ALK promote neuronal polarity and cortical migration by inhibiting IGF1R activity.