Cell polarity and asymmetric cell division: the C. elegans early embryo

2012 ◽  
Vol 53 ◽  
pp. 1-14 ◽  
Author(s):  
Anna Noatynska ◽  
Monica Gotta
Keyword(s):  
Cell Migration ◽  
Cell Division ◽  
Cell Polarity ◽  
Asymmetric Cell Division ◽  
Early Embryo ◽  
Animal Cells ◽  
Par Proteins ◽  
C Elegans ◽  
Lethal Mutations ◽  
Tissue Organization

Cell polarity is crucial for many functions including cell migration, tissue organization and asymmetric cell division. In animal cells, cell polarity is controlled by the highly conserved PAR (PARtitioning defective) proteins. par genes have been identified in Caenorhabditis elegans in screens for maternal lethal mutations that disrupt cytoplasmic partitioning and asymmetric division. Although PAR proteins were identified more than 20 years ago, our understanding on how they regulate polarity and how they are regulated is still incomplete. In this chapter we review our knowledge of the processes of cell polarity establishment and maintenance, and asymmetric cell division in the early C. elegans embryo. We discuss recent findings that highlight new players in cell polarity and/or reveal the molecular details on how PAR proteins regulate polarity processes.

OOC-3, a novel putative transmembrane protein required for establishment of cortical domains and spindle orientation in the P(1) blastomere of C. elegans embryos

Development ◽  
2000 ◽  
Vol 127 (10) ◽  
pp. 2063-2073 ◽  
Author(s):  
S. Pichler ◽  
P. Gonczy ◽  
H. Schnabel ◽  
A. Pozniakowski ◽  
A. Ashford ◽  
...  
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
Transmembrane Protein ◽  
Cell Stage ◽  
Par Proteins ◽  
Asymmetric Cell Divisions ◽  
C Elegans ◽  
Membrane Compartment ◽  
Chromosome Ii

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.

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

2021 ◽  
Vol 8 ◽  
Author(s):  
Amelia J. Kim ◽  
Erik E. Griffin
Keyword(s):  
Cell Division ◽  
Cell Fate ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Asymmetric Cell Division ◽  
Critical Role ◽  
Cell Cortex ◽  
C Elegans ◽  
Mitotic Kinase ◽  
Centrosome Separation

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.

EGL-27 is similar to a metastasis-associated factor and controls cell polarity and cell migration in C. elegans

Development ◽  
1999 ◽  
Vol 126 (5) ◽  
pp. 1055-1064 ◽  
Author(s):  
M.A. Herman ◽  
Q. Ch'ng ◽  
S.M. Hettenbach ◽  
T.M. Ratliff ◽  
C. Kenyon ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Division ◽  
T Cell ◽  
Cell Polarity ◽  
Wnt Pathway ◽  
Hox Gene ◽  
C Elegans ◽  
Metastatic Cells ◽  
Mosaic Analysis ◽  
Wnt Pathways

Mutations in the C. elegans gene egl-27 cause defects in cell polarity and cell migration: the polarity of the asymmetric T cell division is disrupted and the descendants of the migratory QL neuroblast migrate incorrectly because they fail to express the Hox gene mab-5. Both of these processes are known to be controlled by Wnt pathways. Mosaic analysis indicates that egl-27 function is required in the T cell for proper cell polarity. We cloned egl-27 and discovered that a domain of the predicted EGL-27 protein has similarity to Mta1, a mammalian factor overexpressed in metastatic cells. Overlaps in the phenotypes of egl-27 and Wnt pathway mutants suggest that the EGL-27 protein interacts with Wnt signaling pathways in C. elegans.

Actin filament debranching regulates cell polarity during cell migration and asymmetric cell division

2021 ◽  
Vol 118 (37) ◽  
pp. e2100805118
Author(s):  
Chao Xie ◽  
Yuxiang Jiang ◽  
Zhiwen Zhu ◽  
Shanjin Huang ◽  
Wei Li ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Fate ◽  
Cell Polarity ◽  
Actin Filaments ◽  
Asymmetric Cell Division ◽  
Leading Edge ◽  
Cell Stage ◽  
Actin Networks ◽  
C Elegans

The formation of the branched actin networks is essential for cell polarity, but it remains unclear how the debranching activity of actin filaments contributes to this process. Here, we showed that an evolutionarily conserved coronin family protein, the Caenorhabditis elegans POD-1, debranched the Arp2/3-nucleated actin filaments in vitro. By fluorescence live imaging analysis of the endogenous POD-1 protein, we found that POD-1 colocalized with Arp2/3 at the leading edge of the migrating C. elegans neuroblasts. Conditional mutations of POD-1 in neuroblasts caused aberrant actin assembly, disrupted cell polarity, and impaired cell migration. In C. elegans one-cell−stage embryos, POD-1 and Arp2/3, moved together during cell polarity establishment, and inhibition of POD-1 blocked Arp2/3 motility and affected the polarized cortical flow, leading to symmetric segregation of cell fate determinants. Together, these results indicate that F-actin debranching organizes actin network and cell polarity in migrating neuroblasts and asymmetrically dividing embryos.

scholarly journals Cytokine receptor-Eb1 interaction couples cell polarity and fate during asymmetric cell division

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Cuie Chen ◽  
Ryan Cummings ◽  
Aghapi Mordovanakis ◽  
Alan J Hunt ◽  
Michael Mayer ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Division ◽  
Cell Fate ◽  
Cell Polarity ◽  
Adult Stem Cells ◽  
Asymmetric Cell Division ◽  
Cytokine Receptor ◽  
Spindle Orientation ◽  
Germline Stem Cells ◽  
Self Renewal

Asymmetric stem cell division is a critical mechanism for balancing self-renewal and differentiation. Adult stem cells often orient their mitotic spindle to place one daughter inside the niche and the other outside of it to achieve asymmetric division. It remains unknown whether and how the niche may direct division orientation. Here we discover a novel and evolutionary conserved mechanism that couples cell polarity to cell fate. We show that the cytokine receptor homolog Dome, acting downstream of the niche-derived ligand Upd, directly binds to the microtubule-binding protein Eb1 to regulate spindle orientation in Drosophila male germline stem cells (GSCs). Dome’s role in spindle orientation is entirely separable from its known function in self-renewal mediated by the JAK-STAT pathway. We propose that integration of two functions (cell polarity and fate) in a single receptor is a key mechanism to ensure an asymmetric outcome following cell division.

scholarly journals Cortical localization of the G  protein GPA-16 requires RIC-8function during C. elegans asymmetric cell division

Development ◽  
2005 ◽  
Vol 132 (20) ◽  
pp. 4449-4459 ◽  
Author(s):  
K. Afshar ◽  
F. S. Willard ◽  
K. Colombo ◽  
D. P. Siderovski ◽  
P. Gonczy
Keyword(s):  
Cell Division ◽  
G Protein ◽  
Asymmetric Cell Division ◽  
C Elegans ◽  
Cortical Localization
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