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Reciprocal Regulation between Primary Cilia and mTORC1

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 qui...

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Detalles Bibliográficos
Autores principales: Lai, Yandong, Jiang, Yu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7349257/
https://www.ncbi.nlm.nih.gov/pubmed/32604881
http://dx.doi.org/10.3390/genes11060711
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author Lai, Yandong
Jiang, Yu
author_facet Lai, Yandong
Jiang, Yu
author_sort Lai, Yandong
collection PubMed
description 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.
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spelling pubmed-73492572020-07-22 Reciprocal Regulation between Primary Cilia and mTORC1 Lai, Yandong Jiang, Yu Genes (Basel) Review 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. MDPI 2020-06-26 /pmc/articles/PMC7349257/ /pubmed/32604881 http://dx.doi.org/10.3390/genes11060711 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Lai, Yandong
Jiang, Yu
Reciprocal Regulation between Primary Cilia and mTORC1
title Reciprocal Regulation between Primary Cilia and mTORC1
title_full Reciprocal Regulation between Primary Cilia and mTORC1
title_fullStr Reciprocal Regulation between Primary Cilia and mTORC1
title_full_unstemmed Reciprocal Regulation between Primary Cilia and mTORC1
title_short Reciprocal Regulation between Primary Cilia and mTORC1
title_sort reciprocal regulation between primary cilia and mtorc1
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7349257/
https://www.ncbi.nlm.nih.gov/pubmed/32604881
http://dx.doi.org/10.3390/genes11060711
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