The Enzyme Involved in Cell Division also Regulates Synaptic Maturation in the Brain

June 15, 2026

Mechanism by Which Neurons Use Oxidative Reactions to Regulate Synapse Formation Elucidated

Researchers at the National Center of Neurology and Psychiatry (NCNP), in collaboration with RIKEN CSRS, have demonstrated that neurons utilize oxidative signaling to regulate synapse formation, challenging the conventional view that oxidative stress merely damages cells. The team also revealed that Aurora-A kinase, a molecule best known for its role in cell division, is repurposed in neurons to promote synapse formation.

Neurons in the brain establish highly precise neural circuits by forming synapses with one another. While oxidative reactions are known to cause cellular damage when excessive, resulting in “oxidative stress,” this study found that localized oxidative reactions generated within neurons act as signaling cues that activate Aurora-A kinase and promote synapse maturation. The researchers further showed that this activation depends on a specialized chemical modification known as S-glutathionylation, which is tightly regulated by intracellular enzymes.

These findings provide a new molecular mechanism underlying the formation of precise neural circuits in the brain, addressing a fundamental question in neuroscience. The results are also expected to contribute to a better understanding of various neurological disorders associated with oxidative stress, including autism spectrum disorder and Alzheimer’s disease.

 

Original article

The Journal of Cell Biology　doi: 10.1083/jcb.202509200

S. Wakatsuki, A. Yumoto, T. Suzuki, N. Dohmae, T. Araki,

"Redox-dependent S-glutathionylation of Aurora-A kinase by Gstp promotes postsynaptic maturation".

Contact

Naoshi Dohmae
Associate Division Director / Unit Leader
Technology Platform Division / Biomolecular Characterization Unit