Abstract
Asymmetric positioning of the mitotic spindle contributes to the generation of two daughter cells with distinct sizes and fates. Here, we investigated an asymmetric division in the Caenorhabditis elegans Q neuroblast lineage. In this division, beginning with an asymmetrically positioned spindle, the daughter-cell size differences continuously increased during cytokinesis, and the smaller daughter cell in the posterior eventually underwent apoptosis. We found that Arp2/3-dependent F-actin assembled in the anterior but not posterior cortex during division, suggesting that asymmetric expansion forces generated by actin polymerization may enlarge the anterior daughter cell. Consistent with this, inhibition of cortical actin polymerization or artificially equalizing actin assembly led to symmetric cell division. Furthermore, disruption of the Wnt gradient or its downstream components impaired asymmetric cortical actin assembly and caused symmetric division. Our results show that Wnt signaling establishes daughter cell asymmetry by polarizing cortical actin polymerization in a dividing cell.
Highlights
Asymmetric cell divisions (ACDs) are essential for organismal development and tissue homeostasis
We observed that the anterior of the dividing cell progressively expanded during division, causing a continuous increase in the anterior-to-posterior cell size ratio from 1.2-fold at the onset of anaphase to 2.7-fold upon completion of cytokinesis (Figs. 1b, c, 2d; Supplementary Video S3)
By measuring the two-dimensional area of the central cross-section of the dividing cells at metaphase and cytokinesis, we found that the plasma membrane was modestly enlarged 14% from metaphase to the completion of cytokinesis (Supplementary Fig. S1a), which suggests that membrane remodeling might be a significant driver of asymmetric membrane expansion in the anterior[7,8]
Summary
Asymmetric cell divisions (ACDs) are essential for organismal development and tissue homeostasis. Daughter-cell-size asymmetry can result from asymmetric cleavage furrow positioning or unequal myosinbased contractility in the cortex[3,4]. During the ACD of the one-cell stage embryo, dynein-mediated pulling forces displace the spindle toward the posterior pole at the end of the metaphase. The cleavage furrow forms at the center of the spindle but is shifted toward the rear, creating a large anterior daughter and a small posterior one[5]. The C. elegans Q.a and Drosophila neuroblast use a similar myosin asymmetry-based mechanism to generate two daughter cells of different sizes. During their ACDs, spindles are aligned in the middle of the dividing cells without any apparent displacement.
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