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Autophagy

In the hands of HMGB1

Nature Reviews Molecular Cell Biology volume 11, page 757 (2010)Cite this article

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In addition to its established role in the nucleus, HMGB1 has been shown to contribute to apoptosis and necrosis, so the authors tested whether HMGB1 is also involved in autophagy. First, they analysed the localization of HMGB1 in cultured cells in response to autophagic stimuli and found that HMGB1 translocated from the nucleus to the cytoplasm following both starvation and rapamycin treatment. This redistribution seemed to occur specifically in response to reactive oxygen species (ROS) generated downstream of autophagic stimuli.

Tang et al. next observed that Hmgb1−/− mouse embryonic fibroblasts (MEFs) had fewer autophagic punctae than wild-type cells, and this could be restored by HMGB1 overexpression. The role of cytoplasmic HMGB1 in the autophagic process was assessed both by pharmacological inhibition of HMGB1 translocation from the nucleus and by the generation of cytoplasts (anucleate cells) that retain only cytoplasmic HMGB1. These experiments showed that the generation of autophagic punctae is greatly enhanced by the translocation of nuclear HMGB1, which suggests that HMGB1 translocation induces autophagy following prolonged cellular stress.

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ORIGINAL RESEARCH PAPER

  1. Tang, D. et al. Endogenous HMGB1 regulates autophagy. J. Cell. Biol. 190, 881–892 (2010)

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  1. Consulting Editor, NCI–Nature Pathway Interaction Database,

    Mhairi Skinner

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  1. Mhairi Skinner
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Skinner, M. In the hands of HMGB1. Nat Rev Mol Cell Biol 11, 757 (2010). https://doi.org/10.1038/nrm2994

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