Mechanism of the stress-induced collapse of the Ran distribution
- Department of Frontier Biosciences, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871 (Japan)
- Department of Cell Biology and Neuroscience, Graduate School of Medicine, Osaka University, 2-2 Yamda-oka, Suita, Osaka 565-0871 (Japan)
- Department of Frontier Biosciences, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871 (Japan) and Department of Cell Biology and Neuroscience, Graduate School of Medicine, Osaka University, 2-2 Yamda-oka, Suita, Osaka 565-0871 (Japan)
The small GTPase Ran plays a central role in several key nuclear functions, including nucleocytoplasmic transport, cell cycle progression, and assembly of the nuclear envelope. In a previous study, we showed that cellular stress induces the nuclear accumulation of importin {alpha}, and that this appears to be triggered by a collapse in the Ran gradient, leading to the down-regulation of classical nuclear transport. We report here that a decrease in stress-induced ATP is associated with an increase in cytoplasmic Ran levels. A luciferin-luciferase assay showed that cellular stress decreased the intracellular levels of ATP. Treatment of the cells with ATP-depleting agents altered the distribution of Ran. Furthermore, when exogenous ATP was introduced in oxidative stress-treated cells, a normal distribution of Ran was restored. In addition, a pull-down experiment with an importin {beta}1 variant that binds to RanGTP showed that oxidative stress was accompanied by a decrease in intracellular RanGTP levels. These findings indicate that the decrease in ATP levels induced by cellular stress causes a decrease in RanGTP levels and a collapse of Ran distribution.
- OSTI ID:
- 20775340
- Journal Information:
- Experimental Cell Research, Vol. 312, Issue 4; Other Information: DOI: 10.1016/j.yexcr.2005.11.017; PII: S0014-4827(05)00550-1; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
- Country of Publication:
- United States
- Language:
- English
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