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Chronic chest congestion, blurry vision, brain disorder, obesity, and kidney cysts – what is so common underlying these disorders? The answer is - the possible malfunctioning of a tiny cellular organelle, called cilium. Known for more than a hundred years, the primary cilia have been considered a vestigial cellular organelle for a long part of the last century. Fortunately, no more, it is now one of the most extensively studied aspects of a eukaryotic cell. A lot of inherited rare genetic diseases, such as Bardet-Biedl Syndrome (BBS), Joubert Syndrome (JBTS), Polycystic Kidney Disease (PKD), etc., are now established to be caused by mutations in the genes coding for a ciliary protein. Why does the disruption of a cilium cause so many defects? This is because the cells receive and send signals through their cilia. Extensive research in the past two decades has revealed a complex mechanism that builds and maintains signal receptivity through the cilium by regulating the timing and quantity of receptor transport into and out of the cilium. In this colloquium, I will discuss some of the recent results from our laboratory indicating a possible feedback-driven mechanism underlying this process.
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