scholarly journals Physical determinants of asymmetric cell divisions in the early development of Caenorhabditis elegans

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Rolf Fickentscher ◽  
Matthias Weiss
Keyword(s):  
Caenorhabditis Elegans ◽  
Early Development ◽  
Asymmetric Cell Divisions ◽  
Cell Divisions

The Caenorhabditis elegans gene lin-44 controls the polarity of asymmetric cell divisions

Development ◽  
1994 ◽  
Vol 120 (5) ◽  
pp. 1035-1047 ◽  
Author(s):  
M.A. Herman ◽  
H.R. Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
The Body ◽  
Body Axis ◽  
Nematode Caenorhabditis Elegans ◽  
Asymmetric Cell Divisions ◽  
Cell Divisions ◽  
Sister Cells

The generation and orientation of cellular and organismic polarity are fundamental aspects of development. Mutations in the gene lin-44 of the nematode Caenorhabditis elegans reverse both the relative positions of specific sister cells and the apparent polarities of these cells. Thus, lin-44 mutants appear to generate polar cells but to misorient these cells along the body axis of the animal. We postulate that lin-44 acts to specify the orientation of polar cells.

Atypical protein kinase C cooperates with PAR-3 to establish embryonic polarity in Caenorhabditis elegans

Development ◽  
1998 ◽  
Vol 125 (18) ◽  
pp. 3607-3614 ◽  
Author(s):  
Y. Tabuse ◽  
Y. Izumi ◽  
F. Piano ◽  
K.J. Kemphues ◽  
J. Miwa ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Caenorhabditis Elegans ◽  
Protein Kinase ◽  
Atypical Protein Kinase C ◽  
Asymmetric Cell Divisions ◽  
Atypical Protein Kinase ◽  
Cell Divisions ◽  
Kinase C ◽  
Embryonic Polarity ◽  
Asymmetric Divisions

Asymmetric cell divisions, critically important to specify cell types in the development of multicellular organisms, require polarized distribution of cytoplasmic components and the proper alignment of the mitotic apparatus. In Caenorhabditis elegans, the maternally expressed protein, PAR-3, is localized to one pole of asymmetrically dividing blastomeres and is required for these asymmetric divisions. In this paper, we report that an atypical protein kinase C (PKC-3) is essential for proper asymmetric cell divisions and co-localizes with PAR-3. Embryos depleted of PKC-3 by RNA interference die showing Par-like phenotypes including defects in early asymmetric divisions and mislocalized germline-specific granules (P granules). The defective phenotypes of PKC-3-depleted embryos are similar to those exhibited by mutants for par-3 and another par gene, par-6. Direct interaction of PKC-3 with PAR-3 is shown by in vitro binding analysis. This result is reinforced by the observation that PKC-3 and PAR-3 co-localize in vivo. Furthermore, PKC-3 and PAR-3 show mutual dependence on each other and on three of the other par genes for their localization. We conclude that PKC-3 plays an indispensable role in establishing embryonic polarity through interaction with PAR-3.

scholarly journals Assessment of asymmetric cell divisions in the early development of Caenorhabditis elegans

2017 ◽  
Author(s):  
Rolf Fickentscher ◽  
Matthias Weiss
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Size ◽  
Somatic Cells ◽  
Metaphase Plate ◽  
Early Embryogenesis ◽  
Asymmetric Cell Divisions ◽  
C Elegans ◽  
Light Sheet Microscopy ◽  
Cell Divisions ◽  
A Cell

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.

ISOLATION AND GENETIC CHARACTERIZATION OF CELL-LINEAGE MUTANTS OF THE NEMATODE CAENORHABDITIS ELEGANS

Genetics ◽  
1980 ◽  
Vol 96 (2) ◽  
pp. 435-454 ◽  
Author(s):  
H Robert Horvitz ◽  
John E Sulston
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Lineage ◽  
Embryonic Cell ◽  
Null Alleles ◽  
Recessive Mutation ◽  
Incomplete Penetrance ◽  
Nematode Caenorhabditis Elegans ◽  
Cell Lineages ◽  
Cell Divisions ◽  
Recessive Mutations

ABSTRACT Twenty-four mutants that alter the normally invariant post-embryonic cell lineages of the nematode Caenorhabditis elegans have been isolated and genetically characterized. In some of these mutants, cell divisions fail that occur in wild-type animals; in other mutants, cells divide that do not normally do so. The mutants differ in the specificities of their defects, so that it is possible to identify mutations that affect some cell lineages but not others. These mutants define 14 complementation groups, which have been mapped. The abnormal phenotype of most of the cell-lineage mutants results from a single recessive mutation; however, the excessive cell divisions characteristic of one strain, CB1322, require the presence of two unlinked recessive mutations. All 24 cell-lineage mutants display incomplete penetrance and/or variable expressivity. Three of the mutants are suppressed by pleiotropic suppressors believed to be specific for null alleles, suggesting that their phenotypes result from the complete absence of gene activity.

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