Version of Record online: 22 DEC 2010
© 2010 The Societies and Blackwell Publishing Asia Pty Ltd
Microbiology and Immunology
Volume 55, Issue 1, pages 1–11, January 2011
How to Cite
Tanida, I. (2011), Autophagy basics. Microbiology and Immunology, 55: 1–11. doi: 10.1111/j.1348-0421.2010.00271.x
- Issue online: 22 DEC 2010
- Version of Record online: 22 DEC 2010
- Accepted manuscript online: 27 SEP 2010 04:57PM EST
- Received 28 July 2010; revised 16 August 2010; accepted 2 September 2010.
Autophagy (macroautophagy) is a dynamic process for degradation of cytosolic components. Autophagy has intracellular anti-viral and anti-bacterial functions, and plays a role in the initiation of innate and adaptive immune system responses to viral and bacterial infections. Some viruses encode virulence factors for blocking autophagy, whereas others utilize some autophagy components for their intracellular growth or cellular budding. The “core” autophagy-related (Atg) complexes in mammals are ULK1 protein kinase, Atg9-WIPI-1 and Vps34-beclin1 class III PI3-kinase complexes, and the Atg12 and LC3 conjugation systems. In addition, PI(3)-binding proteins, PI3-phosphatases, and Rab proteins contribute to autophagy. The autophagy process consists of continuous dynamic membrane formation and fusion. In this review, the relationships between these Atg complexes and each process are described. Finally, the critical points for monitoring autophagy, including the use of GFP-LC3 and GFP-Atg5, are discussed.