Genetic evidence for selective transport of opsin and arrestin by kinesin-II in mammalian photoreceptors.

摘要: Abstract To test whether kinesin-II is important for transport in the mammalian photoreceptor cilium, and to identify its potential cargoes, we used Cre-loxP mutagenesis remove subunit, KIF3A, specifically from photoreceptors. Complete loss of KIF3A caused large accumulations opsin, arrestin, membranes within inner segment, while localization α-transducin was unaffected. Other membrane, organelle, markers, as well opsin processing appeared normal. Loss ultimately apoptotic cell death similar a known mutant. The data suggest that required arrestin outer segment blocks this pathway lead found retinitis pigmentosa.