Cell cycle arrest in G0 and autophagy share features in common. The Bcl-2 family exerts cell cycle effects in addition to regulating apoptosis. Bcl-2 and Bcl-xL upregulate p27 and promote G0 arrest. Recently, we asked whether autophagy was involved in Bcl-2 and Bcl-x L-mediated cell cycle arrest, and found that autophagy was activated, but not required, for G0 arrest. We also discovered that the cell cycle function of Bcl-2 and Bcl-xL was dependent on Bax and Bak, and in bax-/- bak-/- double knockout cells, features of G 0 quiesecence were already present and p27 was constitutively elevated. Here, we queried the presence of autophagy in bax-/- bak-/- double knockout cells, and report the phosphorylation of p27 at Thr198, which is known to occur in autophagy, as well as constitutive Atg5 induction and LC3-I to -II conversion. These findings in bax-/- bak-/- cells suggest that a physiological role of Bax and Bak may be the suppression of autophagy. ©2009 Landes Bioscience.
CITATION STYLE
Cui, Q., Valentin, M., Janumyan, Y., & Yang, E. (2009). Bax-/- bak-/- cells exhibit p27 Thr198 phosphorylation and autophagy. Autophagy, 5(2), 263–264. https://doi.org/10.4161/auto.5.2.7618
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