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Cellular stress induces Bax-regulated nuclear bubble budding and rupture followed by nuclear protein release

机译：细胞应力诱导Bax调节的核气泡出芽和破裂，随后释放核蛋白

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Cellular stress triggers many pathways including nuclear protein redistribution. We previously discovered that this process is regulated by Bax but the underlying mechanism has not yet been studied. Here we define this mechanism by showing that apoptotic stimuli cause Bax-regulated disturbances in lamin A/C and nuclear envelope (NE)-associated proteins which results in the g eneration and subsequent rupture of nuclear protein-containing bubbles. The bubbles do not contain DNA and are encapsulated by impaired nuclear pore-depleted NE. Stress-induced generation and rupture of nuclear bubbles ultimately leads to the discharge of nuclear proteins into the cytoplasm. This process precedes morphological changes of apoptosis and occurs independently of caspases. Rescue experiments revealed that this Bax effect is non-canonical, i.e. it requires the BH3 domain and α-helices 5 and 6 but it is not inhibited by Bcl~(-)x_(L). Targeting Bax to the NE by the Klarsicht/ANC-1/Syne-1 homology (KASH) domain effectively triggers the generation and rupture of nuclear bubbles. Overall, our findings provide evidence for a novel stress-response, which is regulated by a non-canonical action of Bax on the NE.
机译：细胞应激触发许多途径，包括核蛋白的再分布。我们先前发现该过程受Bax调控，但尚未研究其潜在机制。在这里，我们通过显示凋亡刺激会导致Lamin A / C和核包膜（NE）相关蛋白中Bax调节的紊乱，从而导致含核蛋白的气泡破裂并随后破裂，来定义这种机制。气泡不包含DNA，并且被受损的核孔贫化NE封装。应力诱导的核气泡的产生和破裂最终导致核蛋白释放到细胞质中。该过程在凋亡的形态学改变之前发生并且独立于胱天蛋白酶而发生。救援实验表明，这种Bax效应是非经典的，即它需要BH3结构域和α-螺旋5和6，但不受Bcl〜（-）x_（L）的抑制。通过Klarsicht / ANC-1 / Syne-1同源性（KASH）域将Bax靶向NE，可有效触发核气泡的产生和破裂。总的来说，我们的发现为新的应激反应提供了证据，该应激反应受Bax对NE的非典型作用的调节。

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