Abstract
Polarity establishment, asymmetric division, and acquisition of cell fates are critical steps during early development. In this review, we discuss processes that set up the embryonic axes, with an emphasis on polarity establishment and asymmetric division. We begin with the first asymmetric division in the C. elegans embryo, where symmetry is broken by the local inactivation of actomyosin cortical contractility. This contributes to establishing a polarized distribution of PAR proteins and associated components on the cell cortex along the longitudinal embryonic axis, which becomes the anterior-posterior (AP) axis. Thereafter, AP polarity is maintained through reciprocal negative interactions between the anterior and posterior cortical domains. We then review the mechanisms that ensure proper positioning of the centrosomes and the mitotic spindle in the one-cell embryo by exerting pulling forces on astral microtubules. We explain how a ternary complex comprised of Gα (GOA-1/GPA-16), GPR-1/GPR-2, and LIN-5 is essential for anchoring the motor protein dynein to the cell cortex, where it is thought to exert pulling forces on depolymerizing astral microtubules. We proceed by providing an overview of cell cycle asynchrony in two-cell embryos, as well as the cell signaling and spindle positioning events that underly the subsequent asymmetric divisions, which establish the dorsal-ventral and left-right axes. We then discuss how AP polarity ensures the unequal segregation of cell fate regulators via the cytoplasmic proteins MEX-5/MEX-6 and other polarity mediators, before ending with an overview of how the fates of the early blastomeres are specified by these processes.
Highlights
During development, cells acquire distinct fates, and one prominent mechanism by which this is achieved is asymmetric division
This review provides an overview of the mechanisms governing polarity establishment, asymmetric division and segregation of cell fate determinants in early C. elegans embryos
RHO-1 inactivation in the vicinity of the centrosome plays a major role in initiating AP polarity establishment, more recent work revealed the existence of a partially redundant mechanism relying on the PAR protein PAR-2, which is discussed in Section 2.3 after the PAR proteins have been introduced just below
Summary
Cells acquire distinct fates, and one prominent mechanism by which this is achieved is asymmetric division. In the early embryo of C. elegans, five asymmetric divisions produce six founder cells: AB, MS, E, C, D, and P4 (Figure 1). The anterior-posterior (AP) axis is established in the one-cell embryo, with the sperm-derived centrosome determining the future posterior side. The left-right (LR) axis becomes apparent by the six-cell stage, with the ABal and ABpl cells defining the left side During these early divisions, asymmetries in cellular inheritance combined with cell signaling events act to refine the fates of the founder cells and their daughters. This review provides an overview of the mechanisms governing polarity establishment, asymmetric division and segregation of cell fate determinants in early C. elegans embryos. Some aspects that were covered extensively previously could not be mentioned in detail here; readers should refer to the 2005 contribution and the references therein in those cases
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