Finding cures for children's genetic diseases


CMRI scientists discover control point for neuron branching and development


Scientists at Children’s Medical Research Institute (CMRI), Annie Quan and Prof Phil Robinson, have identified a specific site in the protein Syndapin I that controls neuron outgrowth, a discovery which provides a better understanding of brain development. Their work will be published in the online early edition of the Proceedings of the National Academy of Sciences (USA) for the week of 20 February 2012.

In the brain, neurons are the cells responsible for learning, memory, emotions and form the control centres for the human body. To achieve this, they make an extensive network of connections between each other during development and continuing on into the first years after birth. The connection process involves the cells actively growing protrusions or ‘arms’ called neurites, which extend long distances across the brain and mature into dendrites (the ‘wires’).

Ms Quan and Prof Robinson found that a single site on the Syndapin I protein (called T181) can be modified to increase or decrease neurite outgrowth. The T181 site is modified during brain development by a process called phosphorylation, and the amount of neurite branching is also increased during development. However, in the adult brain, the level of T181 modification is very low and neurite branching is reduced. This means T181 modification is a new control point for neurite outgrowth and branching.

Indeed, the team found they could control the T181 modification by stimulating the neurons or by providing neuronal growth factors. This means the T181 modification can be encouraged to increase the formation of new connections, providing a possible new way to regulate syndapin's function during development.

The identification of a single site with so much control over neuron growth and shape means CMRI scientists now have a target to aim at when developing therapeutic drugs that may one day help treat or prevent some neural birth defects.