Autophagy

When cells are faced with an inadequate supply of nutrients in their extracellular fluid (ECF), they may begin to cannibalize some of their internal organelles (e.g. mitochondria) for re-use of their components.

• formation of a double membrane within the cell which
• envelops the materials to be degraded into a vesicle called an autophagosome.
• The autophagosome then fuses with a lysosome whose
• hydrolytic enzymes degrade the materials.

Autophagy also occurs in many types of cells as their tissue changes during development.

Example: as the Drosophila larva gets ready to pupate, the rising level of ecdysone triggers autophagy in some of its cells.

In mice, autophagy provides essential nutrients — especially amino acids — to the newborn pup during the critical hours after it has separated from its placenta but before nursing begins.

Autophagy is also a mechanism by which the cell gets rid of defective organelles (e.g., mitochondria) and recycles their constituents. This ability declines with age, which may account for the accumulation of cellular debris in the cells of aged animals [Link].

Autophagy may also help cells to destroy bacteria that invade them.

• After Mycobacterium tuberculosis — the agent of "tb" — is engulfed into phagosomes, it survives by preventing their fusion with lysosomes [Link]. However, infected macrophages can get around this problem by destroying the phagosomes — and the bacteria within them — by autophagy instead.
• Autophagy can also destroy bacteria (e.g., Listeria monocytogenes) that get into the cytosol.

Autophagy also provides a mechanism for presenting intracellular antigens (e.g., proteins synthesized by an infecting virus) to CD4⁺ T cells. Normally intracellular antigens enter the class I pathway of antigen presentation to generate cytotoxic (CD8⁺) T cells while CD4⁺ T cells specialize in extracellular antigens (e.g., bacteria) that have been engulfed by endocytosis. [Link to discussion of the pathways of antigen presentation.]