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Publication : Limk2 mediates semaphorin signalling in cortical interneurons migrating through the subpallium.

First Author  Andrews WD Year  2013
Journal  Biol Open Volume  2
Issue  3 Pages  277-82
PubMed ID  23519094 Mgi Jnum  J:195280
Mgi Id  MGI:5477850 Doi  10.1242/bio.20133202
Citation  Andrews WD, et al. (2013) Limk2 mediates semaphorin signalling in cortical interneurons migrating through the subpallium. Biol Open 2(3):277-82
abstractText  En route to the neocortex, interneurons migrate around and avoid the developing striatum. This is due to the chemorepulsive cues of class 3 semaphorins (Sema3A and Sema3F) acting through neuropilin and plexin co-receptors expressed in interneurons. In a recent genetic screen aimed at identifying novel components that may play a role in interneuron migration, we identified LIM-kinase 2 (Limk2), a kinase previously shown to be involved in cell movement and in Sema7A-PlexinC1 signalling. Here we show that Limk2 is differentially expressed in interneurons, with a higher expression in the subpallium compared to cortex, suggesting it may play a role in their migration through the subpallium. Chemotactic assays, carried out with small interfering RNAs (siRNAs), revealed that Limk2-siRNA transfected interneurons are less responsive to Sema3A, but respond to Sema3F. Lack of responsiveness to Sema3A resulted in their aberrant invasion of the developing striatum, as demonstrated in brain slice preparations and in in utero electroporated mouse embryos with the same siRNAs. Our results reveal a previously unknown role for Limk2 in interneuron migration and Sema3A signalling.
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