Dr. Mason has studied this question for the past 15 years and has found that the key lies in receptors that are situated on the tips of the growing axons. When one kind of RGC reaches the optic chiasm, molecules there attach to the receptors and block the axon from crossing over, but when another kind arrives, its receptors interact with other molecules and it is allowed to keep going. “It’s like one RGC has the correct subway pass, while the other does not so it can’t get through,” Dr. Mason says. She is now trying to characterize molecular differences between these two RGC types.

To do this, her lab uses several methods. In one approach, they mutate particular genes in mice and observe how the cells with mutated genes grow. In another, they apply dye or chemical labels to the RGCs and later inspect the brain with a method called clearing. This technique renders the brain transparent except for the highlighted pathways. With high-resolution photography, they can then construct 3D computer renderings of the axons. One important finding from these methods is that the RGCs that cross the optic chiasm arise during an earlier period of gestation, compared to those that do not. “It’s like the oldest born are endowed with the receptors to choose one path, and the youngest born choose a different one,” Dr. Mason says.

Her work also has direct implications for restoring vision. Dr. Mason is looking at how gene activity turns stem cells into RGCs, knowledge that could be used for possible transplantation therapy. Relatedly, she is looking at how to revert mature RGCs to a younger, stem cell–like state so that damaged optic nerves might regrow. “All of our work,” she says, “is done with the hope of someday recreating what happened during development, even in the adult.”