Identification of Atg5-dependent transcriptional changes and increases in mitochondrial mass in Atg5-deficient T lymphocytes.

Autophagy is implicated in many functions of mammalian cells such as organelle recycling, survival and differentiation, and is essential for the maintenance of T and B lymphocytes. Here, we demonstrate that autophagy is a constitutive process during T cell development. Deletion of the essential autophagy genes Atg5 or Atg7 in T cells resulted in decreased thymocyte and peripheral T cell numbers, and Atg5-deficient T cells had a decrease in cell survival.

The autophagy gene ATG5 plays an essential role in B lymphocyte development.

Macroautophagy (herein autophagy) is an evolutionarily conserved process, requiring the gene ATG5, by which cells degrade cytoplasmic constituents and organelles. Here we show that ATG5 is required for efficient B cell development and for the maintenance of B-1a B cell numbers. Deletion of ATG5 in B lymphocytes using Cre-LoxP technology or repopulation of irradiated mice with ATG5-/- fetal liver progenitors resulted in a dramatic reduction in B-1 B cells in the peritoneum.

Coronavirus replication does not require the autophagy gene ATG5.

Macroautophagy (herein autophagy) is a cellular process, requiring ATG5, by which cells deliver double membrane-bound packets containing cytoplasm or cytoplasmic organelles to the lysosome. This process has been reported in some cases to be antiviral, while in other cases it has been reported to be required for efficient viral replication or release. A role for autophagy in RNA virus replication has been an attractive hypothesis because of the association of RNA virus replication with complex membrane rearrangements in the cytoplasm that can generate opposed double membranes.