Guidance Counselors

Cell-adhesion molecules help newborn neurons migrate to their intended destinations within the neocortex.

By | November 1, 2013

IN PLACE: Cerebral cortex neurons, like these from an adult mouse, reach their final destination with the help of guidance cells and binding molecules called nectins.COURTESY OF ULRICH MUELLER

EDITOR'S CHOICE IN NEUROSCIENCE

The paper
C. Gil-Sanz et al., “Cajal-Retzius cells instruct neuronal migration by coincidence signaling between secreted and contact-dependent
guidance cues,” Neuron, 79:461-77, 2013.

The finding
During development, a large signaling molecule named reelin coordinates the outward migration of neurons from the inner neocortex, with help from a cell-adhesion molecule, cadherin 2. “The problem is that cadherin 2 is expressed all over the cortex in all cell types,” says Ulrich Mueller, a neuroscientist at The Scripps Research Institute in La Jolla, Calif. “How could you use that to make a specific connection?” Now Mueller and his team have shown that two cell-adhesion and signaling proteins called nectins guide neurons to specific cortical destinations.

The migration
Mueller’s group used small hairpin RNAs (shRNAs) to knock down two nectins, nectin1 and nectin3, strongly expressed in the mouse embryonic neocortex. Fluorescent imaging indicated nectin expression and the final destinations of developing neurons.

The hook-up
The team discovered that nectin1 was expressed in short-lived guidance cells, called Cajal-Retzius cells, at the top of the cortex near the skull, whereas nectin3 was identified in the leading branches of migrating neurons deeper within the brain. When the neuronal processes contacted the guidance cells, the two nectins bound one another. “This is a really comprehensive study that fills some gaps in our understanding of the molecular mechanisms behind neuronal migration,” says Gabriella D’Arcangelo, a neuroscientist at Rutgers University, who was not involved in the study.

The compensation
Unlike mice that lack reelin or cadherin 2, mice lacking nectin do not display major neuronal defects, supporting the idea that other cell adhesion molecules may be upregulated to compensate for the loss of nectin—a possibility Mueller hopes to explore in the future.

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