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LC3 lipidation is essential for TFEB activation during the lysosomal damage response to kidney injury

by Shigeyama Saki , Komatsu Masaaki , Akayama Shiori , Takabatake Yoshitsugu , Kuma Akiko , Tokumura Ayaka , Ballabio Andrea , Yoshimori Tamotsu , Shima Takayuki , Terawaki Seigo , Nakamura, Jun , Takahashi, Atsushi , Yamamoto Kenichi , Nagai Takeharu , Esposito, Alessandra , Xu Haoxing , Matsuda Tomoki , Oe Yukako , Hamasaki Maho , Okada Yukinori , Nakamura, Shuhei , Sasai Miwa , Miyamoto Mika , Namba-Hamano Tomoko , Napolitano Gennaro , Isaka Yoshitaka , Fujita Toshiharu , Minami Satoshi , Yamamoto Masahiro

in Activation / Autophagy / Biosynthesis / Calcium / Calcium channels / Calcium efflux / Conjugation / Crystals / Damage / Efflux / Homeostasis / Injuries / Kidneys / Lysosomes / Nephropathy / Oxalic acid / Phagocytosis

2020

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LC3 lipidation is essential for TFEB activation during the lysosomal damage response to kidney injury

2020

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2020

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Journal Article

LC3 lipidation is essential for TFEB activation during the lysosomal damage response to kidney injury

Shigeyama Saki,

Komatsu Masaaki,

Akayama Shiori,

Takabatake Yoshitsugu,

Kuma Akiko,

Tokumura Ayaka,

Ballabio Andrea,

Yoshimori Tamotsu,

Shima Takayuki,

Terawaki Seigo,

Nakamura, Jun,

Takahashi, Atsushi,

Yamamoto Kenichi,

Nagai Takeharu,

Esposito, Alessandra,

Xu Haoxing,

Matsuda Tomoki,

Oe Yukako,

Hamasaki Maho,

Okada Yukinori,

Nakamura, Shuhei,

Sasai Miwa,

Miyamoto Mika,

Namba-Hamano Tomoko,

Napolitano Gennaro,

Isaka Yoshitaka,

Fujita Toshiharu,

Minami Satoshi,

Yamamoto Masahiro

2020

Overview

Sensing and clearance of dysfunctional lysosomes is critical for cellular homeostasis. Here we show that transcription factor EB (TFEB)—a master transcriptional regulator of lysosomal biogenesis and autophagy—is activated during the lysosomal damage response, and its activation is dependent on the function of the ATG conjugation system, which mediates LC3 lipidation. In addition, lysosomal damage triggers LC3 recruitment on lysosomes, where lipidated LC3 interacts with the lysosomal calcium channel TRPML1, facilitating calcium efflux essential for TFEB activation. Furthermore, we demonstrate the presence and importance of this TFEB activation mechanism in kidneys in a mouse model of oxalate nephropathy accompanying lysosomal damage. A proximal tubule-specific TFEB-knockout mouse exhibited progression of kidney injury induced by oxalate crystals. Together, our results reveal unexpected mechanisms of TFEB activation by LC3 lipidation and their physiological relevance during the lysosomal damage response.Nakamura et al. find that the master transcriptional regulator of lysosomal biogenesis and autophagy TFEB is activated following LC3 lipidation during lysosomal damage and show the importance of this mechanism during kidney injury.

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Publisher

Nature Publishing Group

Subject

/ Calcium