Polarity controls forces governing asymmetric spindle positioning in the Caenorhabditis elegans embryo

Pierre Gönczy
2001
Article

Cell divisions that create daughter cells of different sizes are crucial for the generation of cell diversity during animal development. In such asymmetric divisions, the mitotic spindle must be asymmetrically positioned at the end of anaphase. The mechanisms by which cell polarity translates to asymmetric spindle positioning remain unclear. Here we examine the nature of the forces governing asymmetric spindle positioning in the single-cell-stage Caenorhabditis elegans embryo. To reveal the forces that act on each spindle pole, we removed the central spindle in living embryos either physically with an ultraviolet laser microbeam, or genetically by RNA-mediated interference of a kinesin. We show that pulling forces external to the spindle act on the two spindle poles. A stronger net force acts on the posterior pole, thereby explaining the overall posterior displacement seen in wild-type embryos. We also show that the net force acting on each spindle pole is under control of the par genes that are required for cell polarity along the anterior-posterior embryonic axis. Finally, we discuss simple mathematical models that describe the main features of spindle pole behaviour. Our work suggests a mechanism for generating asymmetry in spindle positioning by varying the net pulling force that acts on each spindle pole, thus allowing for the generation of daughter cells with different sizes.

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Pierre Gönczy
2001
Article

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https://infoscience.epfl.ch/record/89329?ln=fr

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Caenorhabditis elegans

Caenorhabditis elegans (C. elegans en abrégé) est un petit ver d'un millimètre environ, transparent et non parasitaire. C'est un nématode de la famille des Rhabditidae. Le nom est formé de

Division cellulaire

thumb|upright=1.2| Schémas des différents types de divisions cellulaires. La division cellulaire est le mode de multiplication de toute cellule. Elle lui permet de se diviser en plusieurs cellules (de

Asymmetric cell division

An asymmetric cell division produces two daughter cells with different cellular fates. This is in contrast to symmetric cell divisions which give rise to daughter cells of equivalent fates. Notably,

Characterization of RGS-7 as a regulator of forces involved in C. elegans early cell divisions

Simon Germann

Proper regulation of cell division is crucial to most organisms. Asymmetric division and unequal cleavage are one of the many mechanisms by which spatial regulation of cell division might be achieved. Indeed, by varying its polarity cues or by modulating the size of its daughters, a cell can potentially influence its cellular neighborhood and possibly act upon it. In C. elegans, asymmetric cell division occurs at early stages of development, and is induced by an asymmetric positioning of the spindle during mitosis. RGS-7, a member of the RGS protein family, is a potential candidate as a regulator of this process, and was shown to affect the balance of pulling forces responsible for the asymmetric position of the spindle, possibly acting through Gα and/or Gβ, which are heterotrimeric G-protein complex subunits involved in force generation in C. elegans early cell divisions. However, many aspects of the role this protein may have in this process remain to be elucidated. Using available rgs-7 mutants, RNA interference, spindle severing experiments and immunofluorescence assays, this study highlights the potential functions RGS-7 may provide to a dividing C. elegans embryo

2008

Chargement

Asymmetric cell divisions require the establishment of an axis of polarity, which is subsequently communicated to downstream events. During the asymmetric cell division of the P(1) blastomere in C. elegans, establishment of polarity depends on the establishment of anterior and posterior cortical domains, defined by the localization of the PAR proteins, followed by the orientation of the mitotic spindle along the previously established axis of polarity. To identify genes required for these events, we have screened a collection of maternal-effect lethal mutations on chromosome II of C. elegans. We have identified a mutation in one gene, ooc-3, with mis-oriented division axes at the two-cell stage. Here we describe the phenotypic and molecular characterization of ooc-3. ooc-3 is required for the correct localization of PAR-2 and PAR-3 cortical domains after the first cell division. OOC-3 is a novel putative transmembrane protein, which localizes to a reticular membrane compartment, probably the endoplasmic reticulum, that spans the whole cytoplasm and is enriched on the nuclear envelope and cell-cell boundaries. Our results show that ooc-3 is required to form the cortical domains essential for polarity after cell division.

2000

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PLK-1 asymmetry contributes to asynchronous cell division of C. elegans embryos

Yemima Suryani Budirahardja, Pierre Gönczy

Acquisition of lineage-specific cell cycle duration is an important feature of metazoan development. In Caenorhabditis elegans, differences in cell cycle duration are already apparent in two-cell stage embryos, when the larger anterior blastomere AB divides before the smaller posterior blastomere P1. This time difference is under the control of anterior-posterior (A-P) polarity cues set by the PAR proteins. The mechanisms by which these cues regulate the cell cycle machinery differentially in AB and P1 are incompletely understood. Previous work established that retardation of P1 cell division is due in part to preferential activation of an ATL-1/CHK-1 dependent checkpoint in P1, but how the remaining time difference is controlled is not known. Here, we establish that differential timing relies also on a mechanism that promotes mitosis onset preferentially in AB. The polo-like kinase PLK-1, a positive regulator of mitotic entry, is distributed in an asymmetric manner in two-cell stage embryos, with more protein present in AB than in P1. We find that PLK-1 asymmetry is regulated by A-P polarity cues through preferential protein retention in the embryo anterior. Importantly, mild inactivation of plk-1 by RNAi delays entry into mitosis in P1, but not in AB, in a manner that is independent of ATL-1/CHK-1. Together, our findings support a model in which differential timing of mitotic entry in C. elegans embryos relies on two complementary mechanisms: ATL-1/CHK-1-dependent preferential retardation in P1 and PLK-1-dependent preferential promotion in AB, which together couple polarity cues and cell cycle progression during early development

2008

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