دورية أكاديمية
أعرض في EDS

Atg5-independent autophagy regulates mitochondrial clearance and is essential for iPSC reprogramming.

التفاصيل البيبلوغرافية
العنوان: Atg5-independent autophagy regulates mitochondrial clearance and is essential for iPSC reprogramming.
المؤلفون: Ma T; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA., Li J; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA.; Institute of Immunology, PLA, Third Military Medical University, Chongqing 400038, China., Xu Y; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA., Yu C; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA., Xu T; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA., Wang H; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA., Liu K; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA., Cao N; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA., Nie BM; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA., Zhu SY; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA., Xu S; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA., Li K; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA., Wei WG; Center for Stem Cell and Regenerative Medicine, Shanghai Advanced Research Institute, Chinese Academy of Sciences, No. 99, Haike Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai 201210, China., Wu Y; Institute of Immunology, PLA, Third Military Medical University, Chongqing 400038, China., Guan KL; Department of Pharmacology and Moores Cancer Center, University of California San Diego, La Jolla, California 92093, USA., Ding S; Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA.; Department of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, California 94158, USA.
المصدر: Nature cell biology [Nat Cell Biol] 2015 Nov; Vol. 17 (11), pp. 1379-87. Date of Electronic Publication: 2015 Oct 26.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Macmillan Magazines Ltd Country of Publication: England NLM ID: 100890575 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-4679 (Electronic) Linking ISSN: 14657392 NLM ISO Abbreviation: Nat Cell Biol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London : Macmillan Magazines Ltd., [1999-
مواضيع طبية MeSH: Autophagy* , Cellular Reprogramming*, Induced Pluripotent Stem Cells/*metabolism , Microtubule-Associated Proteins/*metabolism , Mitochondria/*metabolism, AMP-Activated Protein Kinases/metabolism ; Aminoimidazole Carboxamide/analogs & derivatives ; Aminoimidazole Carboxamide/pharmacology ; Animals ; Autophagy-Related Protein 5 ; Blotting, Western ; Cells, Cultured ; Embryo, Mammalian/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibroblasts/ultrastructure ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Induced Pluripotent Stem Cells/drug effects ; Mice, Inbred C57BL ; Mice, Knockout ; Microscopy, Electron ; Microscopy, Fluorescence ; Microtubule-Associated Proteins/genetics ; Octamer Transcription Factor-3/genetics ; Octamer Transcription Factor-3/metabolism ; RNA Interference ; Reverse Transcriptase Polymerase Chain Reaction ; Ribonucleotides/pharmacology ; Sirolimus/pharmacology
مستخلص: Successful generation of induced pluripotent stem cells entails a major metabolic switch from mitochondrial oxidative phosphorylation to glycolysis during the reprogramming process. The mechanism of this metabolic reprogramming, however, remains elusive. Here, our results suggest that an Atg5-independent autophagic process mediates mitochondrial clearance, a characteristic event involved in the metabolic switch. We found that blocking such autophagy, but not canonical autophagy, inhibits mitochondrial clearance, in turn, preventing iPSC induction. Furthermore, AMPK seems to be upstream of this autophagic pathway and can be targeted by small molecules to modulate mitochondrial clearance during metabolic reprogramming. Our work not only reveals that the Atg5-independent autophagy is crucial for establishing pluripotency, but it also suggests that iPSC generation and tumorigenesis share a similar metabolic switch.
References: Mol Biol Cell. 2008 Nov;19(11):4762-75. (PMID: 18768753)
Nature. 2009 Dec 3;462(7273):595-601. (PMID: 19898493)
Cell Metab. 2011 Aug 3;14(2):264-71. (PMID: 21803296)
Nat Cell Biol. 2009 Nov;11(11):1305-14. (PMID: 19801973)
Nat Rev Mol Cell Biol. 2007 Oct;8(10):774-85. (PMID: 17712357)
Nat Rev Mol Cell Biol. 2007 Nov;8(11):931-7. (PMID: 17712358)
J Vis Exp. 2013 Mar 28;(73):null. (PMID: 23568137)
Blood. 2008 Aug 15;112(4):1493-502. (PMID: 18539900)
Nat Commun. 2014 Jun 04;5:4004. (PMID: 24895007)
Cell. 2010 Feb 5;140(3):313-26. (PMID: 20144757)
J Biol Chem. 2010 Mar 5;285(10):7324-33. (PMID: 20018866)
Nat Chem Biol. 2007 Jun;3(6):331-8. (PMID: 17486044)
Nat Cell Biol. 2013 Jul;15(7):713-20. (PMID: 23817233)
Nature. 2009 Oct 1;461(7264):654-8. (PMID: 19794493)
EMBO J. 2000 Nov 1;19(21):5720-8. (PMID: 11060023)
Cell. 2006 Aug 25;126(4):663-76. (PMID: 16904174)
Nat Cell Biol. 2011 Feb;13(2):132-41. (PMID: 21258367)
Science. 2007 Dec 21;318(5858):1917-20. (PMID: 18029452)
Cell Stem Cell. 2009 May 8;4(5):381-4. (PMID: 19398399)
Curr Opin Cell Biol. 2010 Apr;22(2):132-9. (PMID: 20056399)
Nature. 2004 Dec 23;432(7020):1032-6. (PMID: 15525940)
Cell Metab. 2013 Sep 3;18(3):325-32. (PMID: 23850316)
Cell Res. 2011 Jan;21(1):196-204. (PMID: 20956998)
Nat Biotechnol. 2008 Aug;26(8):916-24. (PMID: 18594521)
Science. 2011 Jan 28;331(6016):456-61. (PMID: 21205641)
Cell. 2007 Nov 30;131(5):861-72. (PMID: 18035408)
J Cell Biol. 2001 Feb 19;152(4):657-68. (PMID: 11266458)
Cell Stem Cell. 2013 Nov 7;13(5):617-25. (PMID: 24209762)
Mol Cell Biol. 2005 Jul;25(14):6225-34. (PMID: 15988031)
المشرفين على المادة: 0 (Atg5 protein, mouse)
0 (Autophagy-Related Protein 5)
0 (Microtubule-Associated Proteins)
0 (Octamer Transcription Factor-3)
0 (Pou5f1 protein, mouse)
0 (Ribonucleotides)
147336-22-9 (Green Fluorescent Proteins)
360-97-4 (Aminoimidazole Carboxamide)
EC 2.7.11.31 (AMP-Activated Protein Kinases)
F0X88YW0YK (AICA ribonucleotide)
W36ZG6FT64 (Sirolimus)
تواريخ الأحداث: Date Created: 20151027 Date Completed: 20160314 Latest Revision: 20181113
رمز التحديث: 20231215
DOI: 10.1038/ncb3256
PMID: 26502054
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-4679
DOI:10.1038/ncb3256