When cells are faced with an inadequate supply of nutrients in their extracellular fluid (ECF), they may begin to cannibalize some of their internal macromolecules (e.g., proteins) and even organelles (e.g. mitochondria) for re-use of their components.
This phenomenon is called autophagy.Three different mechanisms of autophagy have been discovered.
In microautophagy and chaperone-mediated autophagy, the material to be degraded is delivered directly to the lysosome.
Early in embryonic development when the genes in the zygote nucleus begin to be expressed [Link], the messenger RNAs and proteins that the mother earlier had deposited in her egg are destroyed by autophagy.
Autophagy occurs in many types of cells as their tissue is remodelled during development.
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. Mice lacking certain autophagy genes die shortly after birth.
Macroautophagy is also a mechanism by which the cell gets rid of defective organelles (e.g., mitochondria, peroxisomes — too big to fit into proteasomes) 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].
Aging Drosophila adults accumulate degraded proteins in the neurons of their brain.
Autophagy helps cells to destroy bacteria that invade them.
Autophagy also provides a mechanism for presenting intracellular antigens 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 and enter the class II pathway. [Link to discussion of the pathways of antigen presentation.]The intracellular antigens diverted into the class II pathway by autophagy include