scholarly journals Combinatorial specification of blastomere identity by glp-1-dependent cellular interactions in the nematode Caenorhabditis elegans

Development ◽  
1994 ◽  
Vol 120 (11) ◽  
pp. 3325-3338 ◽  
Author(s):  
I.P. Moskowitz ◽  
S.B. Gendreau ◽  
J.H. Rothman
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Lineage ◽  
New Combination ◽  
Cellular Interaction ◽  
Specific Cell ◽  
Cellular Interactions ◽  
Nematode Caenorhabditis Elegans ◽  
Cell Embryo ◽  
Extensive Cell ◽  
A Cell

Most somatic cells in the nematode Caenorhabditis elegans arise from AB, the anterior blastomere of the 2-cell embryo. While the daughters of AB, ABa and ABp, are equivalent in potential at birth, they adopt different fates as a result of their unique positions. One such difference is that the distribution of epidermal precursors arising from ABp is reversed along the anterior-posterior axis relative to those arising from ABa. We have found that a strong mutation in the glp-1 gene eliminates this ABa/ABp difference. Furthermore, extensive cell lineage analyses showed that ABp adopts an ABa-like fate in this mutant. This suggests that glp-1 acts in a cellular interaction that makes ABp distinct from ABa. One ABp-specific cell type was previously shown to be induced by an interaction with a neighboring cell, P2. By removing P2 from early embryos, we have found that the widespread differences between ABa and ABp arise from induction of the entire ABp fate by P2. Lineage analyses of genetically and physically manipulated embryos further suggest that the identifies of the AB great-granddaughters (AB8 cells) are controlled by three regulatory inputs that act in various combinations. These inputs are: (1) induction of the ABp-specific fate by P2, (2) a previously described induction of particular AB8 cells by a cell called MS, and (3) a process that controls whether an AB8 cell is an epidermal precursor in the absence of either induction. When an AB8 cell is caused to receive a new combination of these regulatory inputs, its lineage pattern is transformed to resemble the lineage of the wild-type AB8 cell normally receiving that combination of inputs. These lineage patterns are faithfully reproduced irrespective of position in the embryo, suggesting that each combination of regulatory inputs directs a unique lineage program that is intrinsic to each AB8 cell.

Major sex-determining genes and the control of sexual dimorphism in Caenorhabditis elegans

Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 625-637 ◽  
Author(s):  
Jonathan Hodgkin ◽  
Andrew D. Chisholm ◽  
Michael M. Shen
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Germ Line ◽  
Cell Lineage ◽  
Regulatory Genes ◽  
Nematode Caenorhabditis Elegans ◽  
X Chromosomes ◽  
The Many ◽  
Lineage Analysis

Sex determination in Caenorhabditis elegans involves a cascade of major regulatory genes connecting the primary sex determining signal, X chromosome dosage, to key switch genes, which in turn direct development along either male or female pathways. Animals with one X chromosome (XO) are male, while animals with two X chromosomes (XX) are hermaphrodite: hermaphrodite development occurs because the action of the regulatory genes is modified in the germ line so that both sperm and oocytes are made inside a completely female soma. The regulatory genes are being examined by both genetic and molecular means. We discuss how these major genes, in particular the last switch gene in the cascade, tra-1, might regulate the many different sex-specific events that occur during the development of the hermaphrodite and of the male.Key words: nematode, Caenorhabditis elegans, sex determination, sexual differentiation, cell lineage analysis.

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 Microinjection into the Caenorhabditis elegans embryo using an uncoated glass needle enables cell lineage visualization and reveals cell-non-autonomous adhesion control

2018 ◽  
Author(s):  
Yohei Kikuchi ◽  
Akatsuki Kimura
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Biology ◽  
Cell Lineage ◽  
Special Equipment ◽  
Cell Stage ◽  
C Elegans ◽  
Carbon Coated ◽  
A Cell ◽  
Glass Needle ◽  
Time Specific

AbstractMicroinjection is a useful method in cell biology, with which exogenous substances are introduced into a cell in a location- and time-specific manner. The Caenorhabditis elegans embryo is an important model system for cell and developmental biology. Applying microinjection to the C. elegans embryo had been difficult due to the rigid eggshell surrounding the embryo. In 2013, microinjection method using a carbon-coated quartz needle for the C. elegans embryo was reported. To prepare the needle, unfortunately, special equipment is required and thus a limited number of researchers can use this method. In this study, we established a method for the microinjection of drugs, dyes, and microbeads into the C. elegans embryo using an uncoated glass needle that can be produced in a general laboratory. This method enabled us to easily detect cell lineage up to adult stages by injecting a fluorescent dye into a blastomere. We also found a cell-non-autonomous control mechanism of cell adhesion; specifically, the injection of an actin inhibitor into one cell at the 2-cell stage enhanced adhesion between daughter cells of the other cell. Our microinjection method is expected to be used for broad studies and could facilitate various discoveries using C. elegans.

scholarly journals The Caenorhabditis elegans aristaless Orthologue, alr-1, Is Required for Maintaining the Functional and Structural Integrity of the Amphid Sensory Organs

2005 ◽  
Vol 16 (10) ◽  
pp. 4695-4704 ◽  
Author(s):  
Morgan Tucker ◽  
Matt Sieber ◽  
Mary Morphew ◽  
Min Han
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Shape ◽  
Structural Integrity ◽  
Genetic Interaction ◽  
Critical Role ◽  
Sensory Function ◽  
Specific Cell ◽  
Sensory Organs ◽  
Human Disorders ◽  
A Cell

The homeobox-containing aristaless-related protein ARX has been directly linked to the development of a number of human disorders involving mental retardation and epilepsy and clearly plays a critical role in development of the vertebrate central nervous system. In this work, we investigate the role of ALR-1, the Caenorhabditis elegans aristaless orthologue, in amphid sensory function. Our studies indicate that ALR-1 is required for maintenance of the amphid organ structure throughout larval development. Mutant analysis indicates a progressive loss in the amphid neurons' ability to fill with lipophilic dyes as well as a declining chemotactic response. The degeneration in amphid function corresponds with a failure of the glial-like amphid socket cell to maintain its specific cell shape and cell–cell contacts. Consistent with ALR-1 expression within the amphid socket cell, our results indicate a cell autonomous role for ALR-1 in maintaining cell shape. Furthermore, we demonstrate a role for ALR-1 in the proper morphogenesis of the anterior hypodermis. Genetic interaction tests also suggest that ALR-1 may function cooperatively with the cell adhesion processes in maintaining the amphid sensory organs.

scholarly journals Genes required for the engulfment of cell corpses during programmed cell death in Caenorhabditis elegans.

Genetics ◽  
1991 ◽  
Vol 129 (1) ◽  
pp. 79-94 ◽  
Author(s):  
R E Ellis ◽  
D M Jacobson ◽  
H R Horvitz
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Programmed Cell Death ◽  
Nematode Caenorhabditis Elegans ◽  
Electron Microscopic ◽  
New Genes ◽  
Microscopic Studies ◽  
A Cell ◽  
Cell Corpse ◽  
Dying Cells

Abstract After programmed cell death, a cell corpse is engulfed and quickly degraded by a neighboring cell. For degradation to occur, engulfing cells must recognize, phagocytose and digest the corpses of dying cells. Previously, three genes were known to be involved in eliminating cell corpses in the nematode Caenorhabditis elegans: ced-1, ced-2 and nuc-1. We have identified five new genes that play a role in this process: ced-5, ced-6, ced-7, ced-8 and ced-10. Electron microscopic studies reveal that mutations in each of these genes prevent engulfment, indicating that these genes are needed either for the recognition of corpses by other cells or for the initiation of phagocytosis. Based upon our study of double mutants, these genes can be divided into two sets. Animals with mutations in only one of these sets of genes have relatively few unengulfed cell corpses. By contrast, animals with mutations in both sets of genes have many unengulfed corpses. These observations suggest that these two sets of genes are involved in distinct and partially redundant processes that act in the engulfment of cell corpses.

scholarly journals Plasticity of chemotaxis revealed by paired presentation of a chemoattractant and starvation in the nematode Caenorhabditis elegans

2001 ◽  
Vol 204 (10) ◽  
pp. 1757-1764 ◽  
Author(s):  
S. Saeki ◽  
M. Yamamoto ◽  
Y. Iino
Keyword(s):  
Caenorhabditis Elegans ◽  
Water Soluble ◽  
Behavioural Plasticity ◽  
Nematode Caenorhabditis Elegans ◽  
Cellular Mechanisms ◽  
C Elegans ◽  
A Cell ◽  
Behavioural Alteration ◽  
Altered Response ◽  
Conditioning Stimuli

While the basic functioning of the nervous system of Caenorhabditis elegans has been extensively studied, its behavioural plasticities have not been fully explored because of the limited availability of assay systems. We report here a simple form of chemotaxis plasticity in this organism: when worms are starved on plates that contain NaCl, their chemotaxis towards NaCl falls dramatically. This conditioning requires both the presence of NaCl and the absence of a bacterial food source, indicating that it is not merely adaptation or habituation, but that it is likely to be a form of associative learning. While chemotaxis towards volatile chemoattractants does not change significantly after conditioning with NaCl, chemotaxis towards other water-soluble attractants does decrease. This suggests that an altered response of a cell or a group of cells specifically involved in chemotaxis towards water-soluble chemoattractants is responsible for the behavioural alteration. The decrease in chemotaxis occurred slowly over 3–4 h of conditioning and returned quickly to the original level when either of the conditioning stimuli, NaCl or starvation, was removed. The application of serotonin partially blocked this reduction in chemotaxis, consistent with the proposed function of this neurotransmitter in food signalling. Using this assay, we have isolated three mutants with reduced plasticity. This assay system expands the opportunities for studying the molecular and cellular mechanisms of behavioural plasticity in C. elegans.

scholarly journals A Cell Fate Switch in the Caenorhabditis elegans Seam Cell Lineage Occurs Through Modulation of the Wnt Asymmetry Pathway in Response to Temperature Increase

Genetics ◽  
2020 ◽  
Vol 214 (4) ◽  
pp. 927-939 ◽  
Author(s):  
Mark Hintze ◽  
Sneha L. Koneru ◽  
Sophie P. R. Gilbert ◽  
Dimitris Katsanos ◽  
Julien Lambert ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Single Molecule ◽  
Cell Lineage ◽  
Cell Number ◽  
Culture Temperature ◽  
Cell Fate Decisions ◽  
Seam Cell ◽  
In The Wild ◽  
A Cell

Populations often display consistent developmental phenotypes across individuals despite inevitable biological stochasticity. Nevertheless, developmental robustness has limits, and systems can fail upon change in the environment or the genetic background. We use here the seam cells, a population of epidermal stem cells in Caenorhabditis elegans, to study the influence of temperature change and genetic variation on cell fate. Seam cell development has mostly been studied so far in the laboratory reference strain (N2), grown at 20° temperature. We demonstrate that an increase in culture temperature to 25° introduces variability in the wild-type seam cell lineage, with a proportion of animals showing an increase in seam cell number. We map this increase to lineage-specific symmetrization events of normally asymmetric cell divisions at the fourth larval stage, leading to the retention of seam cell fate in both daughter cells. Using genetics and single-molecule imaging, we demonstrate that this symmetrization occurs via changes in the Wnt asymmetry pathway, leading to aberrant Wnt target activation in anterior cell daughters. We find that intrinsic differences in the Wnt asymmetry pathway already exist between seam cells at 20° and this may sensitize cells toward a cell fate switch at increased temperature. Finally, we demonstrate that wild isolates of C. elegans display variation in seam cell sensitivity to increased culture temperature, although their average seam cell number is comparable at 20°. Our results highlight how temperature can modulate cell fate decisions in an invertebrate model of stem cell patterning.

scholarly journals gon-4, a Cell Lineage Regulator Required for Gonadogenesis in Caenorhabditis elegans

2000 ◽  
Vol 228 (2) ◽  
pp. 350-362 ◽  
Author(s):  
Lisa Friedman ◽  
Sonia Santa Anna-Arriola ◽  
Jonathan Hodgkin ◽  
Judith Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Lineage ◽  
A Cell

scholarly journals Enteroviruses infect human enteroids and induce antiviral signaling in a cell lineage-specific manner

2017 ◽  
Vol 114 (7) ◽  
pp. 1672-1677 ◽  
Author(s):  
Coyne G. Drummond ◽  
Alexa M. Bolock ◽  
Congrong Ma ◽  
Cliff J. Luke ◽  
Misty Good ◽  
...  
Keyword(s):  
Cell Lineage ◽  
Enterovirus 71 ◽  
Oral Route ◽  
Intestinal Cell ◽  
Specific Cell ◽  
Human Intestine ◽  
Intestinal Cell Line ◽  
Coxsackievirus B ◽  
Specific Manner ◽  
A Cell

Enteroviruses are among the most common viral infectious agents of humans and are primarily transmitted by the fecal–oral route. However, the events associated with enterovirus infections of the human gastrointestinal tract remain largely unknown. Here, we used stem cell-derived enteroids from human small intestines to study enterovirus infections of the intestinal epithelium. We found that enteroids were susceptible to infection by diverse enteroviruses, including echovirus 11 (E11), coxsackievirus B (CVB), and enterovirus 71 (EV71), and that contrary to an immortalized intestinal cell line, enteroids induced antiviral and inflammatory signaling pathways in response to infection in a virus-specific manner. Furthermore, using the Notch inhibitor dibenzazepine (DBZ) to drive cellular differentiation into secretory cell lineages, we show that although goblet cells resist E11 infection, enteroendocrine cells are permissive, suggesting that enteroviruses infect specific cell populations in the human intestine. Taken together, our studies provide insights into enterovirus infections of the human intestine, which could lead to the identification of novel therapeutic targets and/or strategies to prevent or treat infections by these highly clinically relevant viruses.

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