| First Author | Miller BC | Year | 2008 |
| Journal | Autophagy | Volume | 4 |
| Issue | 3 | Pages | 309-14 |
| PubMed ID | 18188005 | Mgi Jnum | J:222383 |
| Mgi Id | MGI:5644424 | Doi | 10.4161/auto.5474 |
| Citation | Miller BC, et al. (2008) The autophagy gene ATG5 plays an essential role in B lymphocyte development. Autophagy 4(3):309-14 |
| abstractText | 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. ATG5-/- progenitors exhibited a significant defect in B cell development at the pro- to pre-B cell transition, although a proportion of pre-B cells survived to populate the periphery. Inefficient B cell development in the bone marrow was associated with increased cell death, indicating that ATG5 is important for B cell survival during development. In addition, B-1a B cells require ATG5 for their maintenance in the periphery. We conclude that ATG5 is differentially required at discrete stages of development in distinct, but closely related, cell lineages. |
