Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo

The unequal segregation of organelles has been proposed to be an intrinsic mechanism that contributes to cell fate divergence during asymmetric cell division; however, in vivo evidence is sparse. Using super-resolution microscopy, we analysed the segregation of organelles during the division of the neuroblast QL.p in C. elegans larvae. QL.p divides to generate a daughter that survives, QL.pa, and a daughter that dies, QL.pp. We found that mitochondria segregate unequally by density and morphology and that this is dependent on mitochondrial dynamics. Furthermore, we found that mitochondrial density in QL.pp correlates with the time it takes QL.pp to die. We propose that low mitochondrial density in QL.pp promotes the cell death fate and ensures that QL.pp dies in a highly reproducible and timely manner. Our results provide in vivo evidence that the unequal segregation of mitochondria can contribute to cell fate divergence during asymmetric cell division in a developing animal.

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Publication Details

Journal
Nature Communications
Published
2025-08-04
DOI
https://doi.org/10.1038/s41467-025-62484-5
Citations
3
Primary Topic
Genetics, Aging, and Longevity in Model Organisms
Type
article
Field-Weighted Citation Impact
2.86

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article

Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo

Nikhil Mishra, Simon Berger, Eric J. Lambie, Barbara Conradt et al.
3 citations
Nature Communications
Genetics, Aging, and Longevity in Model Organisms
2.86
article

Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo

Nikhil Mishra, Simon Berger, Eric J. Lambie, Barbara Conradt, Ioannis Segos, Jens Van Eeckhoven
article en
3 citations

Abstract

The unequal segregation of organelles has been proposed to be an intrinsic mechanism that contributes to cell fate divergence during asymmetric cell division; however, in vivo evidence is sparse. Using super-resolution microscopy, we analysed the segregation of organelles during the division of the neuroblast QL.p in C. elegans larvae. QL.p divides to generate a daughter that survives, QL.pa, and a daughter that dies, QL.pp. We found that mitochondria segregate unequally by density and morphology and that this is dependent on mitochondrial dynamics. Furthermore, we found that mitochondrial density in QL.pp correlates with the time it takes QL.pp to die. We propose that low mitochondrial density in QL.pp promotes the cell death fate and ensures that QL.pp dies in a highly reproducible and timely manner. Our results provide in vivo evidence that the unequal segregation of mitochondria can contribute to cell fate divergence during asymmetric cell division in a developing animal.

Nature CommunicationsVol. 16(1)
Institute of Science and Technology Austria (AT), University of Zurich (CH), Helmholtz Zentrum München (DE), MRC Laboratory for Molecular Cell Biology (GB), University College London (GB), Ludwig-Maximilians-Universität München (DE)
Royal Society, Eidgenössische Technische Hochschule Zürich, Studienstiftung des Deutschen Volkes, Universität Zürich, National Institutes of Health, Directorate for Biological Sciences, Biotechnology and Biological Sciences Research Council
Good health and well-being
Openalex Percentile: Top 8%
Genetics, Aging, and Longevity in Model Organisms
2.86
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