Glucose deprivation induces primary cilium formation through mTORC1 inactivation

Kengo Takahashi, Tomoaki Nagai, Shuhei Chiba, Keiko Nakayama, Kensaku Mizuno

研究成果: Article査読

12 被引用数 (Scopus)

抄録

Primary cilia are antenna-like sensory organelles extending from the surface of many cell types that play critical roles in tissue development and homeostasis. Here, we examined the effect of nutrient status on primary cilium formation. Glucose deprivation significantly increased the number of ciliated cells under both serum-fed and -starved conditions. Glucose deprivation-induced ciliogenesis was suppressed by overexpression of Rheb, an activator of the mammalian target of rapamycin complex-1 (mTORC1). InactivatingmTORC1 by rapamycin treatment or Raptor knockdown significantly promoted ciliogenesis. These results indicate that glucose deprivation promotes primary cilium formation through mTORC1 inactivation. Rapamycin treatment did not promote autophagy or degradation of OFD1, a negative regulator of ciliogenesis. In contrast, rapamycin treatment increased the level of the p27 KIP1 (also known as CDKN1B) cyclin-dependent kinase inhibitor, and rapamycin-induced ciliogenesis was abrogated in p27 KIP1 -depleted cells. These results indicate that mTORC1 inactivation induces ciliogenesis through p27 KIP1 upregulation, but not through autophagy. By contrast, glucose deprivation or rapamycin treatment shortened the cilium length. Thus, glucose deprivation and subsequent inactivation of mTORC1 play dual roles in ciliogenesis: triggering primary cilium formation and shortening cilium length.

本文言語English
論文番号jcs.208769
ジャーナルJournal of cell science
131
1
DOI
出版ステータスPublished - 2018 1 1

ASJC Scopus subject areas

  • Cell Biology

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