The researchers then tried the procedure in blind mice, which still had rods and

cones, but lacked two key genes that allow those photoreceptors to transmit
signals. Alongside the three genes that encourage rod development, researchers also
introduced the gene that corrects the signaling defect in rods—so that any newly
created ones would be functional. When exposed to light, the treated mice showed
activity in the part of the brain that receives visual signals. New rods had
apparently wired up to retinal ganglion cells and transmitted their messages
successfully, the team concluded.

“No one has made a photoreceptor that looks and functions as much like a
photoreceptor as they have,” says Deborah Otteson, a cell and developmental
neurobiologist at the University of Houston’s College of Optometry in Texas. But
even in the mice that regenerated the most new rods, she notes, their density was
just 0.2% of what you’d expect in a healthy mouse retina. As a result, the treated
mice probably perceived light, but they couldn’t make out shapes or objects.