Roles of Actin in the Morphogenesis of the Early Caenorhabditis elegans Embryo.

Dureen Samandar Eweis,Julie Plastino

doi:10.3390/ijms21103652

Abstract

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.

Highlights

Actin is one of the most abundant proteins in the cell, existing as globular monomers (G-actin) that polymerize into helical filaments (F-actin)
Many actin binding proteins, including the main polymerization nucleators and myosin, are regulated by the small GTPases Rho, Rac, and Cdc42, which are in turn controlled by guanine-nucleotide-exchange factors (GEFs) and GTPase-activating proteins (GAPs) downstream of extracellular signals
We review results from the last five years that address some of the outstanding questions in the field and demonstrate the multitude of roles played by the actin cytoskeleton in the C. elegans embryo

Summary

Introduction

Actin is one of the most abundant proteins in the cell, existing as globular monomers (G-actin) that polymerize into helical filaments (F-actin). The result of this polarization phase in the embryo is the formation of two cortical domains that have different actomyosin activity and different PAR protein occupancy During this period, known as the maintenance phase, a complex network of reciprocally supportive and antagonistic interactions between PAR proteins exists reinforcing their localization at the poles of the embryo. Known as the maintenance phase, a complex network of reciprocally supportive and antagonistic interactions between PAR proteins exists reinforcing their localization at the poles of the embryo This includes effects on actomyosin wherein PAR-1 and PAR-2 at the posterior pole have a role in inhibiting the posterior localization of non-muscle myosin II (NMY-2), while anterior PARs—PAR-3 and PAR-6/PKC-3—lead to the accumulation of NMY-2 at the anterior, establishing and maintaining a more contractile anterior pole [9].

Role of Actin in the Just-Fertilized Embryo during Completion of Meiosis

Actomyosin Dynamics in Symmetry Breaking

Cortical Actin Architecture and Dynamics

Contractile Ring Formation and Positioning

Conclusions