ER Membrane Protein Complex (EMC) Is Key Factor in Biogenesis of Multi-Pass Trans-Membrane Proteins, Including Rh1; Loss of EMC Causes Retinal Degeneration; Finding May Contribute to Advance in Treatment of Retinitis Pigmentosa

The endoplasmic reticulum (ER) membrane protein complex (EMC) has been shown to be a key factor in the biosynthesis and stable expression of multi-pass transmembrane proteins, and its loss is thought to cause retinal degeneration. The factor works especially for multi-pass membrane proteins, in the integration of polypeptides into the membrane and/or protein folding. Understanding the mechanisms underlying protein folding and trafficking may contribute to the large-scale, therapy-based production of target proteins. In 2013, the Nobel Prize in Physiology or Medicine was awarded to Randy W. Schekman, James E. Rothman, and Thomas C. Südhof for their discovery of how cells deliver thousands of membrane proteins to the right place at the right time. It is important for scientists to understand the molecular mechanisms underlying intracellular vesicular traffic. Associate Professor Akiko K. Satoh, in the Division of Life Science, Graduate School of Integral Arts and Science, Hiroshima University, Japan, and her collaborators have been investigating the mechanism of intracellular vesicular traffic using Drosophila photoreceptors. The team has previously shown that the protein Rab1 is involved in the transport of materials from the endoplasmic reticulum to Golgi, that glycosylphoshatidylinositol (GPI) synthesis is necessary for rhodopsin sorting in the trans-Golgi network, and that the Rab11/dRip11/Myo V complex is essential for post-Golgi transport of rhodopsin. Recently, Dr. Satoh’s group performed the genome-wide screening of Drosophila mutants, and identified 233 mutants that failed to synthesize and/or transport rhodopsin to the photosensitive membrane of the rhabdomeres.
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