Abstract
The first division of the one-cell C. elegans embryo has been a fundamental model in deciphering the mechanisms underlying asymmetric cell division. Polarization of the one-cell zygote is induced by a signal from the sperm centrosome and results in the asymmetric distribution of PAR proteins. Multiple mechanisms then maintain PAR polarity until the end of the first division. Once asymmetrically localized, PAR proteins control several essential aspects of asymmetric division, including the position of the mitotic spindle along the polarity axis. Coordination of the spindle and cytokinetic furrow positions is the next essential step to ensure proper asymmetric division. In this chapter, I review the different mechanisms underlying these successive steps of asymmetric division. Work from the last 30 years has revealed the existence of multiple and redundant regulatory pathways which ensure division robustness. Besides the essential role of PAR proteins, this work also emphasizes the importance of both microtubules and actomyosin throughout the different steps of asymmetric division.
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Acknowledgments
The author would like to thank members of the Michaux and Pécréaux labs for discussions and Ken Kemphues for helpful comments on the manuscript. Work in the Michaux lab is supported by grants from the Ligue contre le Cancer (22/29/35/36/72), the Fondation Maladies Rares, the CNRS, and Université de Rennes 1.
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Pacquelet, A. (2017). Asymmetric Cell Division in the One-Cell C. elegans Embryo: Multiple Steps to Generate Cell Size Asymmetry. In: Tassan, JP., Kubiak, J. (eds) Asymmetric Cell Division in Development, Differentiation and Cancer. Results and Problems in Cell Differentiation, vol 61. Springer, Cham. https://doi.org/10.1007/978-3-319-53150-2_5
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