Interplay Between Toxoplasma gondii, Autophagy, and Autophagy Proteins

This article provides an overview of this interplay with an emphasis on autophagy. Lysosomal degradation is an important mechanism of defense against numerous pathogens. This can be accomplished not only through the endocytic pathway but also through macroautophagy (called herein autophagy) (Levine et al., 2011). Autophagy is a homeostatic mechanism whereby large portions of cytosol or entire organelles are encircled by a double membrane (isolation membrane) leading to the formation of an autophagosome (Klionsky and Emr, 2000; Yoshimori, 2004; Mizushima et al., 2010). This structure fuses with lysosomes resulting in the formation of an autolysosome and cargo degradation (Mizushima et al., 2010). Autophagy is dependent on a cascade of autophagy proteins (ATG). However, these proteins can have functions independent of autophagosome formation and lysosomal degradation (Subramani and Malhotra, 2013). This led to the use of the terms canonical and non-canonical autophagy where the latter was frequently used for processes that are non-degradative and/or not dependent on a core component(s) of the autophagy cascade [ATG3, ATG5, ATG7, Unc-51-like kinase 1 (ULK1), Beclin 1, and/or Phosphatidylinositol 3-kinase catalytic subunit type 3, PI3KC3, also known as VPS34] (Galluzzi et al., 2017). To avoid confusion, an expert panel recommended against the use of the terms “canonical”/“non-canonical,” and advised that the term autophagy be used solely fo...
Source: Frontiers in cellular and infection microbiology - Category: Microbiology Source Type: research