Recent Research About The Mechanism of Disc Shedding
A 2007 paper offers a third new theory that builds on recent evidence that suggests that rhodopsin-deficient mice fail to develop OSS. Researchers at Cornell hypothesized that rhodopsin itself has a role in OS biogenesis, in addition to its role as a phototransduction receptor. While the molecular basis underlying rhodopsin’s participation in OS development is unknown, emerging evidence suggests that rhodopsin’s cytoplasmic C-terminal tail bears an “address signal” for its transport from its site of synthesis in the rod cell body to the OS.
The regulation of intracellular membrane trafficking by protein-lipid interactions has been gaining growing attention. A famous example is that of the ability of EEA1 (early endosomal antigen 1) to tether vesicles and regulate assembly of the SNARE (soluble NSF attachment receptor) complex to promote endocytic membrane fusion.
Similarly, the Weill Cornell researchers zeroed in on SARA – Smad anchor for receptor activation, which is also a FYVE domain protein located in early endosomes. They combined various approaches in mammalian photoreceptors to demonstrate that the rhodopsin C-terminal tail functionally interacts with SARA, thus regulating the targeting of these vesicles to nascent discs at the base of the OS. The incorporation of rhodopsin vesicles into discs completes the OS targeting of rhodopsin and directly participates in disc biogenesis.
Observe how the Besharse and others proposed models based on the morphological studies using rapid-freeze, deep-etch, and other techniques that suggested that tubule-vesicles are derived from the internalized distal ciliary membrane and/or the very basal OS plasma membrane. However, the Cornell researchers suggest that some of the axonemal vesicles were directly shipped from the IS through the connecting cilium as SARA was detected in the connecting cilium and basal body, possibly serving as an adaptor protein participating in rhodopsin's translocation.
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