scholarly journals Ceramide glucosyltransferase of the nematode Caenorhabditis elegans is involved in oocyte formation and in early embryonic cell division

Glycobiology ◽  
2011 ◽  
Vol 21 (6) ◽  
pp. 834-848 ◽  
Author(s):  
K. H. Nomura ◽  
D. Murata ◽  
Y. Hayashi ◽  
K. Dejima ◽  
S. Mizuguchi ◽  
...  
Keyword(s):  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Embryonic Cell ◽  
Nematode Caenorhabditis Elegans

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.

scholarly journals The ncl-1 gene and genetic mosaics of Caenorhabditis elegans.

Genetics ◽  
1995 ◽  
Vol 141 (3) ◽  
pp. 989-1006 ◽  
Author(s):  
E M Hedgecock ◽  
R K Herman
Keyword(s):  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Embryonic Cell ◽  
Vulval Development ◽  
Genetic Mosaics ◽  
Cell Divisions ◽  
Mosaic Analysis ◽  
A Cell ◽  
Intercellular Signal

Abstract A ncl-1 mutation results in enlarged nucleoli, which can be detected in nearly all cells of living animals by Nomarski microscopy. Spontaneous mitotic loss of a ncl-1(+)-containing free duplication in an otherwise homozygous ncl-1 mutant animal results in mosaicism for ncl-1 expression, and the patterns of mosaicism lead us to conclude that ncl-1 acts cell autonomously. The probability of mitotic loss of the duplication sDp3 is approximately constant over many cell divisions. About 60% of the losses of sDp3 at the first embryonic cell division involve nondisjunction. Frequencies of mitotic loss of different ncl-1(+)-bearing free duplications varied over a 200-fold range. The frequencies of mitotic loss were enhanced by a chromosomal him-10 mutation. We have used ncl-1 as a cell autonomous marker in the mosaic analysis of dpy-1 and lin-37. The focus of action of dpy-1 is in hypodermis. A mutation in lin-37 combined with a mutation in another gene results in a synthetic multivulva phenotype. We show that lin-37 acts cell nonautonomously and propose that it plays a role, along with the previously studied gene lin-15, in the generation of an intercellular signal by hyp7 that represses vulval development.

scholarly journals A Genetic Screen for Temperature-Sensitive Cell-Division Mutants of Caenorhabditis elegans

Genetics ◽  
1998 ◽  
Vol 149 (3) ◽  
pp. 1303-1321
Author(s):  
Kevin F O'Connell ◽  
Charles M Leys ◽  
John G White
Keyword(s):  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Mitotic Spindle ◽  
Embryonic Cell ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Mitotic Spindles ◽  
Wild Type ◽  
Cell Cycles ◽  
Maternal Expression

Abstract A novel screen to isolate conditional cell-division mutants in Caenorhabditis elegans has been developed. The screen is based on the phenotypes associated with existing cell-division mutations: some disrupt postembryonic divisions and affect formation of the gonad and ventral nerve cord—resulting in sterile, uncoordinated animals—while others affect embryonic divisions and result in lethality. We obtained 19 conditional mutants that displayed these phenotypes when shifted to the restrictive temperature at the appropriate developmental stage. Eighteen of these mutations have been mapped; 17 proved to be single alleles of newly identified genes, while 1 proved to be an allele of a previously identified gene. Genetic tests on the embryonic lethal phenotypes indicated that for 13 genes, embryogenesis required maternal expression, while for 6, zygotic expression could suffice. In all cases, maternal expression of wild-type activity was found to be largely sufficient for embryogenesis. Cytological analysis revealed that 10 mutants possessed embryonic cell-division defects, including failure to properly segregate DNA, failure to assemble a mitotic spindle, late cytokinesis defects, prolonged cell cycles, and improperly oriented mitotic spindles. We conclude that this approach can be used to identify mutations that affect various aspects of the cell-division cycle.

The embryonic cell lineage of the nematode Caenorhabditis elegans

1983 ◽  
Vol 100 (1) ◽  
pp. 64-119 ◽  
Author(s):  
J.E. Sulston ◽  
E. Schierenberg ◽  
J.G. White ◽  
J.N. Thomson
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Lineage ◽  
Embryonic Cell ◽  
Nematode Caenorhabditis Elegans

scholarly journals Identification of novel chondroitin proteoglycans in Caenorhabditis elegans: embryonic cell division depends on CPG-1 and CPG-2

2006 ◽  
Vol 173 (6) ◽  
pp. 985-994 ◽  
Author(s):  
Sara K. Olson ◽  
Joseph R. Bishop ◽  
John R. Yates ◽  
Karen Oegema ◽  
Jeffrey D. Esko
Keyword(s):  
Caenorhabditis Elegans ◽  
Embryonic Development ◽  
Embryonic Cell ◽  
Tissue Mechanics ◽  
Nematode Caenorhabditis Elegans ◽  
Biochemical Purification ◽  
Hydra Vulgaris ◽  
C Elegans ◽  
Core Proteins ◽  
Embryonic Viability

Vertebrates produce multiple chondroitin sulfate proteoglycans that play important roles in development and tissue mechanics. In the nematode Caenorhabditis elegans, the chondroitin chains lack sulfate but nevertheless play essential roles in embryonic development and vulval morphogenesis. However, assignment of these functions to specific proteoglycans has been limited by the lack of identified core proteins. We used a combination of biochemical purification, Western blotting, and mass spectrometry to identify nine C. elegans chondroitin proteoglycan core proteins, none of which have homologues in vertebrates or other invertebrates such as Drosophila melanogaster or Hydra vulgaris. CPG-1/CEJ-1 and CPG-2 are expressed during embryonic development and bind chitin, suggesting a structural role in the egg. RNA interference (RNAi) depletion of individual CPGs had no effect on embryonic viability, but simultaneous depletion of CPG-1/CEJ-1 and CPG-2 resulted in multinucleated single-cell embryos. This embryonic lethality phenocopies RNAi depletion of the SQV-5 chondroitin synthase, suggesting that chondroitin chains on these two proteoglycans are required for cytokinesis.

scholarly journals Many Genomic Regions Are Required for Normal Embryonic Programmed Cell Death in Caenorhabditis elegans

Genetics ◽  
2001 ◽  
Vol 158 (1) ◽  
pp. 237-252
Author(s):  
Asako Sugimoto ◽  
Ayumi Kusano ◽  
Rebecca R Hozak ◽  
W Brent Derry ◽  
Jiangwen Zhu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Programmed Cell Death ◽  
Embryonic Cell ◽  
Direct Result ◽  
Class Iii ◽  
Cell Corpse ◽  
Genomic Regions

Abstract To identify genes involved in programmed cell death (PCD) in Caenorhabditis elegans, we screened a comprehensive set of chromosomal deficiencies for alterations in the pattern of PCD throughout embryonic development. From a set of 58 deficiencies, which collectively remove ∼74% of the genome, four distinct classes were identified. In class I (20 deficiencies), no significant deviation from wild type in the temporal pattern of cell corpses was observed, indicating that much of the genome does not contain zygotic genes that perform conspicuous roles in embryonic PCD. The class II deficiencies (16 deficiencies defining at least 11 distinct genomic regions) led to no or fewer-than-normal cell corpses. Some of these cause premature cell division arrest, probably explaining the diminution in cell corpse number; however, others have little effect on cell proliferation, indicating that the reduced cell corpse number is not a direct result of premature embryonic arrest. In class III (18 deficiencies defining at least 16 unique regions), an excess of cell corpses was observed. The developmental stage at which the extra corpses were observed varied among the class III deficiencies, suggesting the existence of genes that perform temporal-specific functions in PCD. The four deficiencies in class IV (defining at least three unique regions), showed unusually large corpses that were, in some cases, attributable to extremely premature arrest in cell division without a concomitant block in PCD. Deficiencies in this last class suggest that the cell death program does not require normal embryonic cell proliferation to be activated and suggest that while some genes required for cell division might also be required for cell death, others are not. Most of the regions identified by these deficiencies do not contain previously identified zygotic cell death genes. There are, therefore, a substantial number of as yet unidentified genes required for normal PCD in C. elegans.

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