2010
DOI: 10.1523/jneurosci.6140-09.2010
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LKB1-Mediated Spatial Control of GSK3  and Adenomatous Polyposis Coli Contributes to Centrosomal Forward Movement and Neuronal Migration in the Developing Neocortex

Abstract: Neuronal migration is an essential process for the development of the cerebral cortex. We have previously shown that LKB1, an evolutionally conserved polarity kinase, plays a critical role in neuronal migration in the developing neocortex. Here we show that LKB1 mediates Ser9 phosphorylation of GSK3␤ to inactivate the kinase at the leading process tip of migrating neurons in the developing neocortex. This enables the microtubule plus-end binding protein adenomatous polyposis coli (APC) to localize at the dista… Show more

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Cited by 59 publications
(66 citation statements)
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“…MACF1 is implicated in GKS-3 signaling in skin stem cells (Wu et al, 2011), and GSK-3 is shown to regulate cortical placement and radial migration of pyramidal neurons (Asada and Sanada, 2010; Yokota et al, 2009). We wondered whether MACF1 interacts with GSK-3 in the developing brain.…”
Section: Resultsmentioning
confidence: 99%
“…MACF1 is implicated in GKS-3 signaling in skin stem cells (Wu et al, 2011), and GSK-3 is shown to regulate cortical placement and radial migration of pyramidal neurons (Asada and Sanada, 2010; Yokota et al, 2009). We wondered whether MACF1 interacts with GSK-3 in the developing brain.…”
Section: Resultsmentioning
confidence: 99%
“…It has been suggested that dynein anchored in the membrane of the leading process is pulling microtubules attached to the centrosome and leading process. Recent work with migrating pyramidal neurons has shown that microtubule plus-end binding protein adenomatous polyposis coli (APC) is required to anchor microtubules to the distal end of the leading process (Asada and Sanada, 2010). If the localization of APC to the distal tips of the leading process is prevented, radial migration is impaired and the neurons exhibited longer leading processes.…”
Section: Discussionmentioning
confidence: 99%
“…Interestingly, similar migration defects were also observed after inactivation of various molecules that are known to act downstream of Sema3A/neuropilin-1 such as the cycling-dependent kinase Cdk5 (Gupta et al 2003), the Src Kynase Fyn (Sasaki et al 2002), or Tag-1 (Law et al 2008;Namba et al 2014). In addition, Sema3A inhibits the activity of protein kinase A on the phosphorylation of GSK3" and LKB1, two kinases acting on radial migration and neuronal polarity (Asada et al 2007;Asada and Sanada 2010). However, the exact mechanism of action of Sema3A remains unknown, and the apparently normal cortical layering in the Sema3A knockout (Catalano et al 1998) suggests that Sema3A acts redundantly with other factors.…”
Section: Fig 41 Role Of Secreted Semaphorins In Cortical Neuron Migmentioning
confidence: 99%