Abstract
In quiescent cells, primary cilia function as a mechanosensor that converts mechanic signals into chemical activities. This unique organelle plays a critical role in restricting mechanistic target of rapamycin complex 1 (mTORC1) signaling, which is essential for quiescent cells to maintain their quiescence. Multiple mechanisms have been identified that mediate the inhibitory effect of primary cilia on mTORC1 signaling. These mechanisms depend on several tumor suppressor proteins localized within the ciliary compartment, including liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK), polycystin-1, and polycystin-2. Conversely, changes in mTORC1 activity are able to affect ciliogenesis and stability indirectly through autophagy. In this review, we summarize recent advances in our understanding of the reciprocal regulation of mTORC1 and primary cilia.
Highlights
Quiescence is a state of reversible cell cycle arrest and a stage when a cell acquires its specialty for sustaining tissue and organ functions
The accumulation of liver kinase B1 (LKB1) within the cilium activates AMPK localized at the basal body [41], which in turn phosphorylates Tsc2, leading to the inhibition of mechanistic target of rapamycin complex 1 (mTORC1) [42]
Evidence accumulated so far suggests that primary cilia play a negative role in mTORC1 signaling by converting mechanical stimuli into inhibitory activities
Summary
Quiescence is a state of reversible cell cycle arrest and a stage when a cell acquires its specialty for sustaining tissue and organ functions. In comparison with cycling cells, quiescent cells have a reduced mTORC1 activity, which is essential for maintaining the quiescent state. An increasing body of evidence suggests that primary cilia, a unique membranous protrusion at the apical surface of quiescent cells, play an important role in restricting mTORC1 signaling activity. Primary cilia functions as a cellular antenna to sense extracellular chemical and mechanic signals. It converts mechanic signals into chemical activities for mTORC1 inhibition. This primary cilium-dependent downregulation of mTORC1 appears to be important for maintaining cell quiescence, as the abnormal activation of mTORC1 is often associated with disease conditions caused by defects in primary cilia [3,4]. We summarize the molecular basis underlying the mutual regulation
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