Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Cell biology

Surviving import failure

Nature volume 524, pages 419–420 (2015)Cite this article

Subjects

Two studies reveal that dysfunction in organelles called mitochondria causes the toxic accumulation of mitochondrial proteins in the cell's cytosolic fluid, and identify ways in which damage is mitigated. See Letters p.481 & p.485

In an endosymbiotic event that occurred more than one billion years ago, a bacterium was engulfed by a cell, and eventually became an organelle — the mitochondrion. Over time, most of the roughly 1,000 genes that encode mitochondrial proteins were transferred from mitochondria to the nucleus, and are now translated into proteins in the intracellular fluid known as the cytosol. A crucial import mechanism then ensures that these proteins end up in the appropriate locations within mitochondria. Now, two complementary studies1,2 in this issue provide insight into the consequences of inefficient import of mitochondrial proteins — their accumulation in the cytosol — and demonstrate that the cell undergoes several adaptive responses to mitigate the toxicity caused by such accumulation.

Your institute does not have access to this article

Access options

Buy article

Get time limited or full article access on ReadCube.

$32.00

Buy

All prices are NET prices.

Figure 1: Effects of decreased mitochondrial-protein import.

Notes

  1. See all news & views

References

  1. Wang, X. & Chen, X. J. Nature 524, 481–484 (2015).

    ADS  CAS  Article  Google Scholar 

  2. Wrobel, L. et al. Nature 524, 485–488 (2015).

    ADS  CAS  Article  Google Scholar 

  3. Matsuo, Y. et al. Nature 505, 112–116 (2014).

    ADS  Article  Google Scholar 

  4. Le Tallec, B. et al. Mol. Cell 27, 660–674 (2007).

    CAS  Article  Google Scholar 

  5. Sammons, M. A., Samir, P. & Link, A. J. Biochem. Biophys. Res. Commun. 406, 13–19 (2011).

    CAS  Article  Google Scholar 

  6. Akerfelt, M., Morimoto, R. I. & Sistonen, L. Nature Rev. Mol. Cell Biol. 11, 545–555 (2010).

    CAS  Article  Google Scholar 

  7. Nargund, A. M., Pellegrino, M. W., Fiorese, C. J., Baker, B. M. & Haynes, C. M. Science 337, 587–590 (2012).

    ADS  CAS  Article  Google Scholar 

  8. Narendra, D. P. et al. PLoS Biol. 8, e1000298 (2010).

    Article  Google Scholar 

  9. Johnson, S. C. et al. Science 342, 1524–1528 (2013).

    ADS  CAS  Article  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Cole M. Haynes is at the Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.,

    Cole M. Haynes

Authors
  1. Cole M. Haynes
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Cole M. Haynes.

Rights and permissions

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Haynes, C. Surviving import failure. Nature 524, 419–420 (2015). https://doi.org/10.1038/nature14644

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nature14644

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing