scholarly journals C. elegans Brat homologs regulate PAR protein-dependent polarity and asymmetric cell division

2008 ◽  
Vol 321 (2) ◽  
pp. 368-378 ◽  
Author(s):  
Vincent Hyenne ◽  
Marianne Desrosiers ◽  
Jean-Claude Labbé
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
C Elegans

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

scholarly journals Extracellular control of PAR protein localization during asymmetric cell division in the C. elegans embryo

Development ◽  
2010 ◽  
Vol 137 (19) ◽  
pp. 3337-3345 ◽  
Author(s):  
Y. Arata ◽  
J.-Y. Lee ◽  
B. Goldstein ◽  
H. Sawa
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
Protein Localization ◽  
C Elegans

scholarly journals Regulation of anterior cell-specific mec-3 expression during asymmetric cell division in C. elegans

1992 ◽  
Vol 194 (4) ◽  
pp. 289-302 ◽  
Author(s):  
Jeffrey C. Way ◽  
Jin-Quan Run ◽  
Alice Y. Wang
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
C Elegans

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.

A C. elegans Ror receptor tyrosine kinase regulates cell motility and asymmetric cell division

Nature ◽  
10.1038/23722 ◽  
1999 ◽  
Vol 400 (6747) ◽  
pp. 881-885 ◽  
Author(s):  
Wayne C. Forrester ◽  
Megan Dell ◽  
Elliot Perens ◽  
Gian Garriga
Keyword(s):  
Cell Division ◽  
Tyrosine Kinase ◽  
Cell Motility ◽  
Receptor Tyrosine Kinase ◽  
Asymmetric Cell Division ◽  
C Elegans

scholarly journals Roles of Actin in the Morphogenesis of the Early Caenorhabditis elegans Embryo

2020 ◽  
Vol 21 (10) ◽  
pp. 3652
Author(s):  
Dureen Samandar Eweis ◽  
Julie Plastino
Keyword(s):  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Asymmetric Cell Division ◽  
Cell Types ◽  
Actin Dynamics ◽  
Actin Binding ◽  
Asymmetric Cell Divisions ◽  
C Elegans ◽  
Asymmetric Divisions ◽  
Different Cell Types

The cell shape changes that ensure asymmetric cell divisions are crucial for correct development, as asymmetric divisions allow for the formation of different cell types and therefore different tissues. The first division of the Caenorhabditis elegans embryo has emerged as a powerful model for understanding asymmetric cell division. The dynamics of microtubules, polarity proteins, and the actin cytoskeleton are all key for this process. In this review, we highlight studies from the last five years revealing new insights about the role of actin dynamics in the first asymmetric cell division of the early C. elegans embryo. Recent results concerning the roles of actin and actin binding proteins in symmetry breaking, cortical flows, cortical integrity, and cleavage furrow formation are described.

scholarly journals MAP Kinase Signaling Antagonizes PAR-1 Function During Polarization of the Early Caenorhabditis elegans Embryo

Genetics ◽  
2009 ◽  
Vol 183 (3) ◽  
pp. 965-977 ◽  
Author(s):  
Annina C. Spilker ◽  
Alexia Rabilotta ◽  
Caroline Zbinden ◽  
Jean-Claude Labbé ◽  
Monica Gotta
Keyword(s):  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Cell Fate ◽  
Asymmetric Cell Division ◽  
Asymmetric Distribution ◽  
Kinase Signaling ◽  
C Elegans ◽  
Link Type ◽  
Map Kinase Signaling

PAR proteins (partitioning defective) are major regulators of cell polarity and asymmetric cell division. One of the par genes, par-1, encodes a Ser/Thr kinase that is conserved from yeast to mammals. In Caenorhabditis elegans, par-1 governs asymmetric cell division by ensuring the polar distribution of cell fate determinants. However the precise mechanisms by which PAR-1 regulates asymmetric cell division in C. elegans remain to be elucidated. We performed a genomewide RNAi screen and identified six genes that specifically suppress the embryonic lethal phenotype associated with mutations in par-1. One of these suppressors is mpk-1, the C. elegans homolog of the conserved mitogen activated protein (MAP) kinase ERK. Loss of function of mpk-1 restored embryonic viability, asynchronous cell divisions, the asymmetric distribution of cell fate specification markers, and the distribution of PAR-1 protein in par-1 mutant embryos, indicating that this genetic interaction is functionally relevant for embryonic development. Furthermore, disrupting the function of other components of the MAPK signaling pathway resulted in suppression of par-1 embryonic lethality. Our data therefore indicates that MAP kinase signaling antagonizes PAR-1 signaling during early C. elegans embryonic polarization.

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