Cells cope with altered chromosome numbers by enhancing protein breakdown

Storchová, Zuzana

doi:10.1038/d41586-024-01360-6

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22 May 2024

Cells cope with altered chromosome numbers by enhancing protein breakdown

When chromosomes are lost or gained, massive changes in gene expression disrupt the delicate balance of proteins in a cell. Yeasts with incorrect chromosome numbers counteract this by degrading excess proteins.

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Zuzana Storchová ORCID: http://orcid.org/0000-0003-2376-7047⁰

Zuzana Storchová
1. Zuzana Storchová is in the Department of Molecular Genetics, Rhineland-Palatinate Technical University of Kaiserslautern, Kaiserlautern 67663, Germany.
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Most organisms have a species-specific number of chromosomes, an attribute known as euploidy. But a condition in which cells have an incorrect number of chromosomes — aneuploidy — also exists in nature. The deviation from euploidy leads to imbalances in gene expression, resulting in an altered abundance of hundreds of messenger RNAs and proteins in accordance with the changes in chromosome copy number. Consequently, imbalances in the full set of proteins in a cell (known as the proteome) inflict a burden on cells, which manifests as proteotoxic stress and a proliferative disadvantage, as seen in laboratory-engineered budding yeast (Saccharomyces cerevisiae) strains that carry extra chromosomes¹. But aneuploidy can also be beneficial in varying environments, in which wide-ranging changes to the proteome can offer rapid adaptive solutions². Aneuploidy is found in nearly 20% of naturally occurring yeast strains, for example³. Writing in Nature, Muenzner et al.⁴ sought to find the molecular processes that allow these strains to thrive with aneuploid genomes.

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Nature 630, 41-43 (2024)

doi: https://doi.org/10.1038/d41586-024-01360-6

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The author declares no competing interests.

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[1] Torres, E. M. et al. Science 317, 916–924 (2007).
Article PubMed Google Scholar

[2] Yona, A. H. et al. Proc. Natl Acad. Sci. USA 109, 21010–21015 (2012).
Article PubMed Google Scholar

[3] Peter, J. et al. Nature 556, 339–344 (2018).
Article PubMed Google Scholar

[4] Muenzner, J. et al. Nature 630, 149–157 (2024).
Article Google Scholar

[5] Torres, E. M. et al. Cell 143, 71–83 (2010).
Article PubMed Google Scholar

[6] Caudal, E. et al. Preprint at bioRxiv https://doi.org/10.1101/2023.05.17.541122 (2023).

[7] McShane, E. et al. Cell 167, 803–815 (2016).
Article PubMed Google Scholar

[8] Dephoure, N. et al. eLife 3, e03023 (2014).
Article PubMed Google Scholar

[9] Tsai, H.-J. et al. Nature 570, 117–121 (2019).
Article PubMed Google Scholar

[10] Ben-David, U. & Amon, A. Nature Rev. Genet. 21, 44–62 (2020).
Article PubMed Google Scholar

[11] Stingele, S. et al. Mol. Syst. Biol. 8, 608 (2012).
Article PubMed Google Scholar

[12] Chunduri, N. K. et al. Nature Commun. 12, 5576 (2021).
Article PubMed Google Scholar

[13] Liu, Y. et al. Nature Commun. 8, 1212 (2017).
Article PubMed Google Scholar

[14] Schukken, K. M. & Sheltzer, J. Genome Res. 32, 1254–1270 (2022).
Article PubMed Google Scholar

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