Asymmetric Cell Division in the One-Cell C. elegans Embryo: Multiple Steps to Generate Cell Size Asymmetry

Author(s):  
Anne Pacquelet
2018 ◽  
Vol 29 (4) ◽  
pp. 419-434 ◽  
Author(s):  
Namal Abeysundara ◽  
Andrew J. Simmonds ◽  
Sarah C. Hughes

An intact actomyosin network is essential for anchoring polarity proteins to the cell cortex and maintaining cell size asymmetry during asymmetric cell division of Drosophila neuroblasts (NBs). However, the mechanisms that control changes in actomyosin dynamics during asymmetric cell division remain unclear. We find that the actin-binding protein, Moesin, is essential for NB proliferation and mitotic progression in the developing brain. During metaphase, phosphorylated Moesin (p-Moesin) is enriched at the apical cortex, and loss of Moesin leads to defects in apical polarity maintenance and cortical stability. This asymmetric distribution of p-Moesin is determined by components of the apical polarity complex and Slik kinase. During later stages of mitosis, p-Moesin localization shifts more basally, contributing to asymmetric cortical extension and myosin basal furrow positioning. Our findings reveal Moesin as a novel apical polarity protein that drives cortical remodeling of dividing NBs, which is essential for polarity maintenance and initial establishment of cell size asymmetry.


2018 ◽  
Author(s):  
Tri Thanh Pham ◽  
Arnaud Monnard ◽  
Jonne Helenius ◽  
Erik Lund ◽  
Nicole Lee ◽  
...  

AbstractMetazoan cells can generate unequal sized sibling cells during cell division. This form of asymmetric cell division depends on spindle geometry and Myosin distribution but the underlying mechanics are unclear. Here, we use atomic force microscopy and live cell imaging to elucidate the biophysical forces involved in the establishment of physical asymmetry in Drosophila neural stem cells. We show that the force driving initial apical membrane expansion is provided by hydrostatic pressure, peaking shortly after anaphase onset, and enabled by a relieve of actomyosin contractile tension on the apical cell cortex. The subsequent increase in contractile forces at the cleavage furrow, combined with the relocalization of basally located Myosin results in basal membrane extension and sustained apical expansion. We propose that spatiotemporally controlled actomyosin contractile tension and hydrostatic pressure enables stereotypic biased membrane expansion to generate sibling cell size asymmetry.


eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Chet Huan Oon ◽  
Kenneth E Prehoda

The Par complex dynamically polarizes to the apical cortex of asymmetrically dividing Drosophila neuroblasts where it directs fate determinant segregation. Previously we showed that apically directed cortical movements that polarize the Par complex require F-actin (Oon and Prehoda, 2019). Here we report the discovery of cortical actomyosin dynamics that begin in interphase when the Par complex is cytoplasmic but ultimately become tightly coupled to cortical Par dynamics. Interphase cortical actomyosin dynamics are unoriented and pulsatile but rapidly become sustained and apically-directed in early mitosis when the Par protein aPKC accumulates on the cortex. Apical actomyosin flows drive the coalescence of aPKC into an apical cap that is depolarized in anaphase when the flow reverses direction. Together with the previously characterized role of anaphase flows in specifying daughter cell size asymmetry, our results indicate that multiple phases of cortical actomyosin dynamics regulate 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

Development ◽  
2010 ◽  
Vol 137 (19) ◽  
pp. 3337-3345 ◽  
Author(s):  
Y. Arata ◽  
J.-Y. Lee ◽  
B. Goldstein ◽  
H. Sawa

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

2008 ◽  
Vol 321 (2) ◽  
pp. 368-378 ◽  
Author(s):  
Vincent Hyenne ◽  
Marianne Desrosiers ◽  
Jean-Claude Labbé

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