As demonstrated by the 2016 Nobel Prize winner, Yoshinori Ohsumi, autophagy is a fundamental process vital to cellular health. The molecular processes and signalling pathways controlling autophagy include numerous autophagy-related (Atg) genes, important stress-inducible intracellular protein, such as p62/A170/SQSTM1, and autophagosome localizing proteins such as LC3, among many others making this a complex network of control.
What Is Autophagy?
Definition: Autophagy is a vital cellular process for recycling of cellular constituents, allowing cells to balance energy sources during critical times of nutrient stress and development. The word autophagy is derived from the Greek words: auto, meaning "self" and phagein, "to eat".
Autophagy starts with the formation of a phagophore from a membrane; this expands and engulfs the molecules or “cargo” for degradation. The cargo can include ribosomes, organelles and protein aggregates and once engulfed, they are contained within the autophagosome. The autophagosome can then fuse with lysosomes which results in the release of lysosomal acid proteases to degrade the contents of the autophagosome.
The products of the degradation include amino acids amongst other molecules, all of which are released back into the cytoplasm and re-used in metabolism and for building macromolecules.
Gene deletion experiments in both mice and cell lines have implicated autophagy in the development of a number of diseases including; neurodegenerative diseases, cancer, infectious diseases, and metabolic diseases. Furthermore, SNPs and mutations in genes encoding proteins involved in autophagy have been implicated in a wide variety of conditions including asthma, Crohn’s disease and cancers.
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|Examples of popular knockout cell lines|
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Wild type Hap1 cells were either untreated (Panel A) or stimulated with10 nM Bafilomycin A and 250 nM Torin (Panel C) for 3 hours prior to staining for the autophagy marker LC3. Image analysis using CellProfilerTM software identified autophagosomes (segmented in red in Panels B and D). Quantification of the number of autophagosomes per cell area shows a robust response to stimulation (E), indicating that the Hap1 cells have a functioning autophagic stress response.
Images were acquired by the Ketteler Group at the Translational Research Resource Centre at University College London
Wild type Hap1 cells (Panel A) or Atg5 KO Hap1 cells (Panel C) were stimulated with Bafilomycin A and Torin for 3 hours prior to staining for the autophagy marker LC3. Image analysis using CellProfilerTM software identified autophagosomes (segmented in red in Panels B and D). Quantification of the number of autophagosomes per cell area shows that the Atg5 KO cells were unable to produce autophagosomes (E). This demonstrates the functionality of Hap1 knockout cells for investigating autophagic responses. The panel of available autophagy cell lines can be a valuable tool in analysing the mechanism of action of a gene or compound involved in autophagic regulation.
*Images were acquired by the Ketteler Group at the Translational Research Resource Centre at University College London