Researchers based at the Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine in Baltimore, have published research data suggesting that the trans-membrane proteins, semaphorin 6A and its receptor plexin A2, are critical to the wiring process required to mediate object-motion detection by the retina, a critical component of animal vision. The direction-selective responses to varying levels of light are understood to depend upon the correct connectivity between inhibitory starburst amacrine cells (SACs) and direction-selective ganglion cells (DSGCs). Under normal circumstances, “On” and “Off “SACs are found in separate discrete layers with a clear radial dendrite morphology typical of neuronal cells. Knocking out one or other of the Sema6A or Plex A2 genes caused the “On” and “Off” layers to run into each other while causing a distortion of normal dendrite development. According to the authors, the results “correlate the elaboration of symmetric SAC dendritic morphology and asymmetric responses to motion, shedding light on the development of visual pathways that use the same cell types for divergent outputs”.