Principles and mechanisms of asymmetric cell division

Sunchu, Bharath; Cabernard, Clemens

doi:10.1242/dev.167650

Cited by 88 publications

(61 citation statements)

References 155 publications

(200 reference statements)

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“…Similarly, during the asymmetric division of S. cerevisiae cells, increased Cdc5 activity at the mother centrosome (spindle pole body) is essential for its asymmetric inheritance to the newly born daughter cell (Maekawa et al, 2017 ). Non-random inheritance of mother and daughter centrosomes is widespread and may contribute to the partitioning of aging/rejuvenation programs between daughter cells or in the asymmetric inheritance of centrosome-associated fate determinants (Macara and Mili, 2008 ; Pelletier and Yamashita, 2012 ; Manzano-Lopez et al, 2019 ; Sunchu and Cabernard, 2020 ). PLK1 has also been shown to regulate planar cell polarity in mammalian epithelial cells through phosphorylation of CELSR-1 (Flamingo in Drosophila ), which triggers CELSR-1 clearance from the cell surface as cells prepare to undergo cytokinesis (Shrestha et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

PLK-1 Regulation of Asymmetric Cell Division in the Early C. elegans Embryo

Kim

Griffin

2021

Front. Cell Dev. Biol.

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PLK1 is a conserved mitotic kinase that is essential for the entry into and progression through mitosis. In addition to its canonical mitotic functions, recent studies have characterized a critical role for PLK-1 in regulating the polarization and asymmetric division of the one-cell C. elegans embryo. Prior to cell division, PLK-1 regulates both the polarization of the PAR proteins at the cell cortex and the segregation of cell fate determinants in the cytoplasm. Following cell division, PLK-1 is preferentially inherited to one daughter cell where it acts to regulate the timing of centrosome separation and cell division. PLK1 also regulates cell polarity in asymmetrically dividing Drosophila neuroblasts and during mammalian planar cell polarity, suggesting it may act broadly to connect cell polarity and cell cycle mechanisms.

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Section: Discussionmentioning

confidence: 99%

PLK-1 Regulation of Asymmetric Cell Division in the Early C. elegans Embryo

Kim

Griffin

2021

Front. Cell Dev. Biol.

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“…royalsocietypublishing.org/journal/rsob Open Biol. 11: 200314 tissue [11][12][13]. Several stem cell systems have been reported to exhibit stereotypical centrosome inheritance during asymmetric stem cell divisions, where the mother or daughter centrosome is consistently inherited by stem cells.…”

Section: Asymmetric Centrosome Inheritance During Stem Cell Divisionsmentioning

confidence: 99%

Centrosome-centric view of asymmetric stem cell division

Chen

Yamashita

2021

Open Biol.

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The centrosome is a unique organelle: the semi-conservative nature of its duplication generates an inherent asymmetry between ‘mother’ and ‘daughter’ centrosomes, which differ in their age. This asymmetry has captivated many cell biologists, but its meaning has remained enigmatic. In the last two decades, many stem cell types have been shown to display stereotypical inheritance of either the mother or daughter centrosome. These observations have led to speculation that the mother and daughter centrosomes bear distinct information, contributing to differential cell fates during asymmetric cell divisions. This review summarizes recent progress and discusses how centrosome asymmetry may promote asymmetric fates during stem cell divisions.

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“…Protein polarization enables cell-fate determinants to be sequestered in a location within the progenitor cell that is partitioned to one of the two daughter cells after division. Accordingly, establishment of cell-fate asymmetry often requires protein polarization in ACD progenitor cells (Goldstein and Macara, 2007;Sunchu and Cabernard, 2020).…”

Section: Introductionmentioning

confidence: 99%

A Spatiotemporal Molecular Switch Governs Plant Asymmetric Cell Division

Guo

Park

Wang

et al. 2020

Preprint

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SummaryAsymmetric cell division (ACD) often requires protein polarization in the mother cell to produce daughter cells with distinct identities (“cell-fate asymmetry”). Here, we define a previously undocumented mechanism for establishing cell-fate asymmetry in Arabidopsis stomatal stem cells. In particular, we show that polarization of BSL protein phosphatases promotes stomatal ACD by establishing a “kinase-based signaling asymmetry” in the two daughter cells. BSL polarization in the stomatal ACD mother cell is triggered upon commitment to cell division. Polarized BSL is inherited by the differentiating daughter cell where it suppresses cell division and promotes cell-fate determination. Plants lacking BSL exhibit stomatal over-proliferation, demonstrating BSL plays an essential role in stomatal development. Our findings establish that BSL polarization provides a spatiotemporal molecular switch that enables cell-fate asymmetry in stomatal ACD daughter cells. We propose BSL polarization is triggered by an ACD “checkpoint” in the mother cell that monitors establishment of division-plane asymmetry.

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Principles and mechanisms of asymmetric cell division

Cited by 88 publications

References 155 publications

PLK-1 Regulation of Asymmetric Cell Division in the Early C. elegans Embryo

PLK-1 Regulation of Asymmetric Cell Division in the Early C. elegans Embryo

Centrosome-centric view of asymmetric stem cell division

A Spatiotemporal Molecular Switch Governs Plant Asymmetric Cell Division

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