4.8 Editorial Material

Autophagy-independent function of lipidated LC3 essential for TFEB activation during the lysosomal damage responses

期刊

AUTOPHAGY
卷 17, 期 2, 页码 581-583

出版社

TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2020.1846292

关键词

Autophagy; LC3; lysosome; TFEB; TRPML1

资金

  1. AMED-PRIME [17gm6110003h0001]
  2. JSPS KAKENHI
  3. Senri Life Science Foundation
  4. Takeda Science Foundation
  5. Nakajima Foundation
  6. MSD Life Science Foundation
  7. Astellas Foundation for Research on Metabolic Disorders
  8. Mochida Memorial Foundation for Medical and Pharmaceutical Research
  9. JST CREST [JPMJCR17H6]
  10. AMED [JP17gm5010001, JP17gm06 10005]
  11. HFSP Research grant

向作者/读者索取更多资源

Lysosomes play a crucial role in cellular digestion and maintaining cellular homeostasis. Cells have developed defense mechanisms, including the regulation of transcription factors like TFEB and LC3, to cope with damaged lysosomes.
Lysosomes are digestive organelles in cells containing many hydrolases, and also serve as a signaling hub to integrate intracellular and extracellular inputs; therefore, the integrity of lysosomes is critical for cellular homeostasis. Many agents and conditions can damage lysosomal membranes, which lead to leakage of lysosomal acidic contents into the cytosol thus becoming harmful for cells. Accordingly, cells have developed several defense systems to cope with damaged lysosomes, but underlying mechanisms of each system and their cross-talks are unclear. In our recent study, we found that a master transcription factor regulating autophagy and lysosomal biogenesis, TFEB (transcription factor EB) is activated during lysosomal damage, and this activation depends on an autophagy-independent function of lipidated LC3, which localizes on lysosomes. We further showed that this regulatory mechanism is essential to prevent the progression of the crystal nephropathy that accompanies lysosomal damage.

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