論文

査読有り
2016年

Lysosomal putative RNA transporter SIDT2 mediates direct uptake of RNA by lysosomes

AUTOPHAGY
  • Shu Aizawa
  • ,
  • Yuuki Fujiwara
  • ,
  • Viorica Raluca Contu
  • ,
  • Katsunori Hase
  • ,
  • Masayuki Takahashi
  • ,
  • Hisae Kikuchi
  • ,
  • Chihana Kabuta
  • ,
  • Keiji Wada
  • ,
  • Tomohiro Kabuta

12
3
開始ページ
565
終了ページ
578
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1080/15548627.2016.1145325
出版者・発行元
TAYLOR & FRANCIS INC

Lysosomes are thought to be the major intracellular compartment for the degradation of macromolecules. We recently identified a novel type of autophagy, RNautophagy, where RNA is directly taken up by lysosomes in an ATP-dependent manner and degraded. However, the mechanism of RNA translocation across the lysosomal membrane and the physiological role of RNautophagy remain unclear. In the present study, we performed gain-and loss-of-function studies with isolated lysosomes, and found that SIDT2 (SID1 transmembrane family, member 2), an ortholog of the Caenorhabditis elegans putative RNA transporter SID-1 (systemic RNA interference deficient-1), mediates RNA translocation during RNautophagy. We also observed that SIDT2 is a transmembrane protein, which predominantly localizes to lysosomes. Strikingly, knockdown of Sidt2 inhibited up to 50% of total RNA degradation at the cellular level, independently of macroautophagy. Moreover, we showed that this impairment is mainly due to inhibition of lysosomal RNA degradation, strongly suggesting that RNautophagy plays a significant role in constitutive cellular RNA degradation. Our results provide a novel insight into the mechanisms of RNA metabolism, intracellular RNA transport, and atypical types of autophagy.


リンク情報
DOI
https://doi.org/10.1080/15548627.2016.1145325
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000373983300010&DestApp=WOS_CPL
URL
https://www.tandfonline.com/doi/full/10.1080/15548627.2016.1145325
ID情報
  • DOI : 10.1080/15548627.2016.1145325
  • ISSN : 1554-8627
  • eISSN : 1554-8635
  • Web of Science ID : WOS:000373983300010

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