期刊
CELLULAR SIGNALLING
卷 28, 期 9, 页码 1380-1388出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2016.06.015
关键词
RPIA; Autophagy; CRISPR; Cas9; Pentose phosphate pathway; shRNA
类别
资金
- UK Medical Research Council [MC_EX_G0800785]
- BBSRC [BB/J015881/1]
- Biotechnology and Biological Sciences Research Council [BB/J015881/1] Funding Source: researchfish
- Medical Research Council [1068278, MC_EX_G0800785] Funding Source: researchfish
- BBSRC [BB/J015881/1] Funding Source: UKRI
- MRC [MC_EX_G0800785] Funding Source: UKRI
Autophagy and cellular metabolism are tightly linked processes, but how individual metabolic enzymes regulate the process of autophagy is not well understood. This study implicates ribose-5-phosphate isomerase (RPIA), a key regulator of the pentose phosphate pathway, in the control of autophagy. We used a dual gene deletion strategy, combining shRNA-mediated knockdown studies with CRISPR/Cas9 genome editing. Knockdown of RPIA by shRNA or genomic deletion by CRISPR/Cas9 genome editing, results in an increase of ATG4B-mediated LC3 processing and in the appearance of LC3-positive autophagosomes in cells. Increased LC3 processing upon knockdown of RPIA can be reversed by treatment with the antioxidant N-acetyl cysteine. The results are consistent with a model in which RPIA suppresses autophagy and LC3 processing by modulation of redox signaling. (C) 2016 The Authors. Published by Elsevier Inc.
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