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Protein aggregates act as a deterministic disruptor during bacterial cell size homeostasis

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Abstract

Mechanisms underlying deviant cell size fluctuations among clonal bacterial siblings are generally considered to be cryptic and stochastic in nature. However, by scrutinizing heat-stressed populations of the model bacterium Escherichia coli, we uncovered the existence of a deterministic asymmetry in cell division that is caused by the presence of intracellular protein aggregates (PAs). While these structures typically locate at the cell pole and segregate asymmetrically among daughter cells, we now show that the presence of a polar PA consistently causes a more distal off-center positioning of the FtsZ division septum. The resulting increased length of PA-inheriting siblings persists over multiple generations and could be observed in both E. coli and Bacillus subtilis populations. Closer investigation suggests that a PA can physically perturb the nucleoid structure, which subsequently leads to asymmetric septation.

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The datasets generated by this study will be made available by the corresponding author upon request.

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Acknowledgements

We would like to thank the Research Foundation-Flanders (FWO-Vlaanderen) and the KU Leuven Research Fund for providing funding for this study.

Funding

This work was supported by doctoral fellowships (11B0519N to J.M., 11J6222N to R.V.E., and 1135116N to A.C.) and research grants (G0C7118N and G0D8220N) from the Research Foundation-Flanders (FWO-Vlaanderen), and a postdoctoral fellowship (PDM/20/118 to J.M.) and a start-up grant (STG/21/068 to S.K.G.) from the KU Leuven Research Fund.

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Mortier, J., Govers, S.K., Cambré, A. et al. Protein aggregates act as a deterministic disruptor during bacterial cell size homeostasis. Cell. Mol. Life Sci. 80, 360 (2023). https://doi.org/10.1007/s00018-023-05002-4

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