AI Article Synopsis
- Neuronal migration is crucial for proper brain circuit formation, and defects in this process can contribute to neurological and psychiatric issues.
- Researchers discovered that the protein Chromodomain Y-like (CDYL) is essential for the proper migration of newborn neurons in mice, with its knockdown leading to migration issues and altered neuron transitions.
- CDYL works by repressing the activity of RhoA, and its absence not only affects neuronal movement but also makes cortical neurons more excitable, increasing the risk of seizures in mice.
Article Abstract
During brain development, the correct migration of newborn neurons is one of the determinants of circuit formation, and neuronal migration defects may lead to neurological and psychiatric disorders. The molecular mechanisms underlying neuronal migration and related disorders are poorly understood. Here, we report that Chromodomain Y-like (CDYL) is critical for neuronal migration in mice. Knocking down CDYL caused neuronal migration defects and disrupted both mobility and multipolar-to-bipolar transition of migrating neurons. We find that CDYL regulates neuronal migration by transcriptionally repressing RhoA. In addition, CDYL deficiency increased the excitability of cortical pyramidal neurons and the susceptibility of mice to convulsant-induced seizures. These results demonstrate that CDYL is a regulator of neuronal migration and shed light on the pathogenesis of seizure-related neurodevelopmental disorders.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.celrep.2016.12.043 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!