| First Author | Germain M | Year | 2011 |
| Journal | EMBO J | Volume | 30 |
| Issue | 2 | Pages | 395-407 |
| PubMed ID | 21139567 | Mgi Jnum | J:168794 |
| Mgi Id | MGI:4938240 | Doi | 10.1038/emboj.2010.327 |
| Citation | Germain M, et al. (2011) MCL-1 is a stress sensor that regulates autophagy in a developmentally regulated manner. EMBO J 30(2):395-407 |
| abstractText | Apoptosis has an important role during development to regulate cell number. In differentiated cells, however, activation of autophagy has a critical role by enabling cells to remain functional following stress. In this study, we show that the antiapoptotic BCL-2 homologue MCL-1 has a key role in controlling both processes in a developmentally regulated manner. Specifically, MCL-1 degradation is an early event not only following induction of apoptosis, but also under nutrient deprivation conditions where MCL-1 levels regulate activation of autophagy. Furthermore, deletion of MCL-1 in cortical neurons of transgenic mice activates a robust autophagic response. This autophagic response can, however, be converted to apoptosis by either reducing the levels of the autophagy regulator Beclin-1, or by a concomitant activation of BAX. Our results define a pathway whereby MCL-1 has a key role in determining cell fate, by coordinately regulating apoptosis and autophagy. |
