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.

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.

The terminal differentiation factor LIN-29 is required for proper vulval morphogenesis and egg laying in Caenorhabditis elegans

Development ◽  
1997 ◽  
Vol 124 (21) ◽  
pp. 4333-4342 ◽  
Author(s):  
J.C. Bettinger ◽  
S. Euling ◽  
A.E. Rougvie
Keyword(s):  
Caenorhabditis Elegans ◽  
Terminal Differentiation ◽  
Egg Laying ◽  
Small Subset ◽  
Wild Type ◽  
Vulval Development ◽  
Genetic Mosaics ◽  
Hypodermal Cell ◽  
Heterochronic Gene ◽  
Final Molt

Caenorhabditis elegans vulval development culminates during exit from the L4-to-adult molt with the formation of an opening through the adult hypodermis and cuticle that is used for egg laying and mating. Vulva formation requires the heterochronic gene lin-29, which triggers hypodermal cell terminal differentiation during the final molt. lin-29 mutants are unable to lay eggs or mate because no vulval opening forms; instead, a protrusion forms at the site of the vulva. We demonstrate through analysis of genetic mosaics that lin-29 is absolutely required in a small subset of lateral hypodermal seam cells, adjacent to the vulva, for wild-type vulva formation and egg laying. However, lin-29 function is not strictly limited to the lateral hypodermis. First, LIN-29 accumulates in many non-hypodermal cells with known roles in vulva formation or egg laying. Second, animals homozygous for one lin-29 allele, ga94, have the vulval defect and cannot lay eggs, despite having a terminally differentiated adult lateral hypodermis. Finally, vulval morphogenesis and egg laying requires lin-29 activity within the EMS lineage, a lineage that does not generate hypodermal cells.

scholarly journals Cell lineage-dependent chiral actomyosin flows drive cellular rearrangements in early development

2019 ◽  
Author(s):  
Lokesh Pimpale ◽  
Teije C. Middelkoop ◽  
Alexander Mietke ◽  
Stephan W. Grill
Keyword(s):  
Cell Division ◽  
Cell Lineage ◽  
Early Embryo ◽  
Embryonic Cell ◽  
Rotating Flows ◽  
Cell Divisions ◽  
Fluid Theory ◽  
Division Axis ◽  
Cell Reorientation ◽  
Shed Light

ABSTRACTProper positioning of cells is important for many aspects of embryonic development, tissue homeostasis, and regeneration. A simple mechanism by which cell positions can be specified is via orienting the cell division axis. This axis is specified at the onset of cytokinesis, but can be reoriented as cytokinesis proceeds. Rotatory actomyosin flows have been implied in specifying and reorienting the cell division axis in certain cases, but how general such reorientation events are, and how they are controlled, remains unclear. In this study, we set out to address these questions by investigating early Caenorhabditis elegans development. In particular, we determined which of the early embryonic cell divisions exhibit chiral counter-rotating actomyosin flows, and which do not. We follow the first nine divisions of the early embryo, and discover that chiral counter-rotating flows arise systematically in the early AB lineage, but not in early P/EMS lineage cell divisions. Combining our experiments with thin film active chiral fluid theory we identify specific properties of the actomyosin cortex in the symmetric AB lineage divisions that favor chiral counter-rotating actomyosin flows of the two halves of the dividing cell. Finally, we show that these counter-rotations are the driving force of both the AB lineage spindle skew and cell reorientation events. In conclusion, we here have shed light on the physical basis of lineage-specific actomyosin-based processes that drive chiral morphogenesis during development.

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

scholarly journals Mosaic Analysis Using a ncl-1 (+) Extrachromosomal Array Reveals That lin-31 Acts in the Pn.p Cells During Caenorhabditis elegans Vulval Development

Genetics ◽  
1996 ◽  
Vol 143 (3) ◽  
pp. 1181-1191 ◽  
Author(s):  
Leilani M Miller ◽  
David A Waxing ◽  
Stuart K Kim
Keyword(s):  
Caenorhabditis Elegans ◽  
The Body ◽  
Specific Cell ◽  
Vulval Development ◽  
C Elegans ◽  
Genetic Mosaic ◽  
Extrachromosomal Array ◽  
Mosaic Analysis ◽  
Putative Transcription Factor ◽  
Sites Of Action

Abstract We describe a genetic mosaic analysis procedure in which Caenorhabditis elegans mosaics are generated by spontaneous loss of an extrachromosomal array. This technique allows almost any C. elegans gene that can be used in germline transformation experiments to be used in mosaic analysis experiments. We identified a cosmid clone that rescues the mutant phenotype of ncl-1, so that this cell-autonomous marker could be used to analyze mosaic animals. To determine the sites of action for unc-29 and lin-31, an extrachromosomal array was constructed containing the ncl-1(+) cosmid linked to lin-31(+) and unc-29(+) cosmids. This array is mitotically unstable and can be lost to produce a clone of mutant cells. The specific cell division at which the extrachromosomal array had been lost was deduced by scoring the Ncl phenotypes of individual cells in genetic mosaics. The Unc-29 and Lin-31 phenotypes were then scored in these animals to determine in which cells these genes are required. This analysis showed that unc-29, which encodes a subunit of the acetylcholine receptor, acts in the body muscle cells. Furthermore, lin-31, which specifies cell fates during vulval induction and encodes a putative transcription factor similar to HNF-3/fork head, acts in the Pn.p cells

scholarly journals The multivulva phenotype of certain Caenorhabditis elegans mutants results from defects in two functionally redundant pathways.

Genetics ◽  
1989 ◽  
Vol 123 (1) ◽  
pp. 109-121 ◽  
Author(s):  
E L Ferguson ◽  
H R Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Lineage ◽  
Gene Families ◽  
Precursor Cells ◽  
Wild Type ◽  
Vulval Development ◽  
Vulval Precursor Cells ◽  
New Mutations ◽  
Intercellular Signal

Abstract We previously identified Caenorhabditis elegans mutants in which certain of the six vulval precursor cells adopt fates normally expressed by other vulval precursor cells. These mutants define genes that appear to function in the response to an intercellular signal that induces vulval development. The multivulva (Muv) phenotype of one such mutant, CB1322, results from an interaction between two unlinked mutations, lin-8(n111) II and lin-9(n112) III. In this paper, we identify 18 new mutations, which are alleles of eight genes, that interact with either lin-8(n111) or lin-9(n112) to generate a Muv phenotype. None of these 20 mutations alone causes any vulval cell lineage defects. The "silent Muv" mutations fall into two classes; hermaphrodites carrying a mutation of each class are Muv, while hermaphrodites carrying two mutations of the same class have a wild-type vulval phenotype. Our results indicate that the Muv phenotype of these mutants results from defects in two functionally-redundant pathways, thereby demonstrating that redundancy can occur at the level of gene pathways as well as at the level of gene families.

Multiple levels of regulation specify the polarity of an asymmetric cell division in C. elegans

Development ◽  
2000 ◽  
Vol 127 (21) ◽  
pp. 4587-4598 ◽  
Author(s):  
J. Whangbo ◽  
J. Harris ◽  
C. Kenyon
Keyword(s):  
Cell Division ◽  
Wnt Signaling ◽  
Epidermal Cell ◽  
Asymmetric Cell Division ◽  
Asymmetric Cell Divisions ◽  
Signaling Systems ◽  
Tissue Polarity ◽  
C Elegans ◽  
Cell Divisions ◽  
A Cell

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.

scholarly journals Cell lineage-dependent chiral actomyosin flows drive cellular rearrangements in early Caenorhabditis elegans development

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Lokesh G Pimpale ◽  
Teije C Middelkoop ◽  
Alexander Mietke ◽  
Stephan W Grill
Keyword(s):  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Daughter Cell ◽  
Cell Lineage ◽  
Rotating Flows ◽  
Physical Processes ◽  
Cell Divisions ◽  
Fluid Theory ◽  
Division Axis ◽  
Cell Reorientation

Proper positioning of cells is essential for many aspects of development. Daughter cell positions can be specified via orienting the cell division axis during cytokinesis. Rotatory actomyosin flows during division have been implied in specifying and reorienting the cell division axis, but how general such reorientation events are, and how they are controlled, remains unclear. We followed the first nine divisions of Caenorhabditis elegans embryo development and demonstrate that chiral counter-rotating flows arise systematically in early AB lineage, but not in early P/EMS lineage cell divisions. Combining our experiments with thin film active chiral fluid theory we identify a mechanism by which chiral counter-rotating actomyosin flows arise in the AB lineage only, and show that they drive lineage-specific spindle skew and cell reorientation events. In conclusion, our work sheds light on the physical processes that underlie chiral morphogenesis in early 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.

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