Ephrin Bs and canonical Reelin signalling.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 27882975.
- Also identified by DOI 10.1038/nature20129 and PMC identifier PMC6675355.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
Reeler mice exhibit loss of the signaling protein Reelin (Reln) which affects radial pyramidal neuron migration and results in cortical layer malformation. During cortical development Eph receptor/ephrin ligand (Eph/Efn) cell-cell interactions are important for neuronal migration, axonal/dendritic growth, synaptogenesis, and pruning. Recently it has been claimed that Ephb/Efnb and Reln pathways interact genetically and layering defects in triple Efnb1;2;3−/− mutants and Efnb3−/−;Reln+/− compound mice are similar to those present in reeler. Here we demonstrate that contrary to this previous report the compound mutant Efnb3−/−;Reln+/− as well as the triple mutant Efnb1;2;3−/− do not show defects of cortical layering or elevated Dab1 levels. While protein-protein interactions between Efnbs and Reln have been confirmed, they do not affect the radial positioning of migrating neocortical pyramidal neurons.