ArticleJournal of cell science2019
A homeostatic mechanism rapidly corrects aberrant nucleocytoplasmic ratios maintaining nuclear size in fission yeast.
Article in Journal of cell science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- ASCL1 promotes nuclear shrinkage in transdifferentiation by suppressing NUP37.Stem cell reports · 2026Article
- How the chromatin landscape influences nuclear morphology.Frontiers in cell and developmental biology · 2025Review
- Chemical transformation of the multibudding yeast, Aureobasidium pullulans.The Journal of cell biology · 2024Article
- Eukaryotic cell size regulation and its implications for cellular function and dysfunction.Physiological reviews · 2024Review
- A deep learning-based toolkit for 3D nuclei segmentation and quantitative analysis in cellular and tissue context.Development (Cambridge, England) · 2024Article
- The fission yeast cell size control system integrates pathways measuring cell surface area, volume, and time.Current biology : CB · 2023Article
- Control of nuclear size by osmotic forces ineLife · 2022Article
- Pomegranate: 2D segmentation and 3D reconstruction for fission yeast and other radially symmetric cells.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Nuclear size scales with cell size across a wide range of cell types. The mechanism by which this scaling is maintained in growing cells remains unclear. Here, we investigate the mechanism of nuclear size homeostasis in the simple eukaryote fission yeast, by monitoring the recovery of aberrant nuclear volume to cell volume (N/C) ratios following perturbation. We demonstrate that both high and low N/C ratios correct rapidly, maintaining nuclear size homeostasis. We assess the kinetics of nuclear and cellular growth and of N/C ratio correction, and demonstrate that nuclear and cellular growth rates are not directly coupled. We propose that the mechanism underlying nuclear size homeostasis involves multiple limiting factors implicated in processes including nucleocytoplasmic transport, lipid biogenesis and RNA processing. We speculate that these link cellular size increases to changes in nuclear contents, which in turn lead to changes in nuclear membrane surface area. Our study reveals that there is rapid nuclear size homeostasis in cells, informing understanding of nuclear size control and size homeostasis of other membrane-bound organelles.
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Registered trials
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