scholarly journals Wnt Signaling Polarizes C. elegans Asymmetric Cell Divisions During Development

Author(s):  
Arielle Koonyee Lam ◽  
Bryan T. Phillips
Development ◽  
2000 ◽  
Vol 127 (21) ◽  
pp. 4587-4598 ◽  
Author(s):  
J. Whangbo ◽  
J. Harris ◽  
C. Kenyon

Wnt signaling systems play important roles in the generation of cell and tissue polarity during development. We describe a Wnt signaling system that acts in a new way to orient the polarity of an epidermal cell division in C. elegans. In this system, the EGL-20/Wnt signal acts in a permissive fashion to polarize the asymmetric division of a cell called V5. EGL-20 regulates this polarization by counteracting lateral signals from neighboring cells that would otherwise reverse the polarity of the V5 cell division. Our findings indicate that this lateral signaling pathway also involves Wnt pathway components. Overexpression of EGL-20 disrupts both the asymmetry and polarity of lateral epidermal cell divisions all along the anteroposterior (A/P) body axis. Together our findings suggest that multiple, inter-related Wnt signaling systems may act together to polarize asymmetric cell divisions in this tissue.


Development ◽  
1996 ◽  
Vol 122 (9) ◽  
pp. 2579-2588 ◽  
Author(s):  
M. Labouesse ◽  
E. Hartwieg ◽  
H.R. Horvitz

The C. elegans gene lin-26, which encodes a presumptive zinc-finger transcription factor, is required for hypodermal cells to acquire their proper fates. Here we show that lin-26 is expressed not only in all hypodermal cells but also in all glial-like cells. During asymmetric cell divisions that generate a neuronal cell and a non-neuronal cell, LIN-26 protein is symmetrically segregated and then lost from the neuronal cell. Expression in glial-like cells (socket and sheath cells) is biologically important, as some of these neuronal support cells die or seem sometimes to be transformed to neuron-like cells in embryos homozygous for strong loss-of-function mutations. In addition, most of these glial-like cells are structurally and functionally defective in animals carrying the weak loss-of-function mutation lin-26(n156). lin-26 mutant phenotypes and expression patterns together suggest that lin-26 is required to specify and/or maintain the fates not only of hypodermal cells but also of all other non-neuronal ectodermal cells in C. elegans. We speculate that lin-26 acts by repressing the expression of neuronal-specific genes in non-neuronal cells.


Cell ◽  
1995 ◽  
Vol 83 (1) ◽  
pp. 101-110 ◽  
Author(s):  
Michael A. Herman ◽  
Larissa L. Vassilieva ◽  
H.Robert Horvitz ◽  
Jocelyn E. Shaw ◽  
Robert K. Herman

Development ◽  
2001 ◽  
Vol 128 (21) ◽  
pp. 4301-4314 ◽  
Author(s):  
José-Eduardo Gomes ◽  
Sandra E. Encalada ◽  
Kathryn A. Swan ◽  
Christopher A. Shelton ◽  
J. Clayton Carter ◽  
...  

C. elegans embryogenesis begins with a stereotyped sequence of asymmetric cell divisions that are largely responsible for establishing the nematode body plan. These early asymmetries are specified after fertilization by the widely conserved, cortically enriched PAR and PKC-3 proteins, which include three kinases and two PDZ domain proteins. During asymmetric cell divisions in the early embryo, centrosome pairs initially are positioned on transverse axes but then rotate to align with the anteroposterior embryonic axis. We show that rotation of the centrosomal/nuclear complex in an embryonic cell called P1 requires a maternally expressed gene we name spn-4. The predicted SPN-4 protein contains a single RNA recognition motif (RRM), and belongs to a small subfamily of RRM proteins that includes one Drosophila and two human family members. Remarkably, in mutant embryos lacking spn-4 function the transversely oriented ‘P1’ mitotic spindle appears to re-specify the axis of cell polarity, and the division remains asymmetric. spn-4 also is required for other developmental processes, including the specification of mesendoderm, the restriction of mesectoderm fate to P1 descendants, and germline quiescence during embryogenesis. We suggest that SPN-4 post-transcriptionally regulates the expression of multiple developmental regulators. Such SPN-4 targets might then act more specifically to generate a subset of the anterior-posterior asymmetries initially specified after fertilization by the more generally required PAR and PKC-3 proteins.


2017 ◽  
Author(s):  
Rolf Fickentscher ◽  
Matthias Weiss

AbstractAsymmetric cell divisions are of fundamental importance for developmental processes, e.g. for the generation of founder cells. Prime examples are asymmetric cell divisions in the P lineage during early embryogenesis of the model organism Caenorhabditis elegans. However, due to a lack of quantitative data it has remained unclear how frequent unequal daughter cell sizes emerge in the nematode’s early embryogenesis, and whether these originate from sterical or biochemical cues. Using quantitative light-sheet microscopy, we have found that about 40% of all cell divisions in C. elegans until gastrulation generate daughter cells with significantly different volumes. Removing the embryo’s rigid eggshell revealed asymmetric divisions in somatic cells to be primarily induced by steric effects. Division asymmetries in the germline remained unaltered and were correctly reproduced by a model based on a cell-size independent, eccentric displacement of the metaphase plate. Our data suggest asymmetric cell divisions to be essential for establishing important cell-cell interactions that eventually fuel a successful embryogenesis.Summary statementAbout 40% of all cell divisions in early C. elegans embryogenesis are found to be asymmetric. A cell-size independent displacement of the mitotic spindle explains division asymmetries in the germline whereas the confining eggshell induces asymmetries of somatic cells.


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