scholarly journals The Caenorhabditis elegans lin-12 gene mediates induction of ventral uterine specialization by the anchor cell

Development ◽  
1995 ◽  
Vol 121 (2) ◽  
pp. 263-271 ◽  
Author(s):  
A.P. Newman ◽  
J.G. White ◽  
P.W. Sternberg
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Lateral Inhibition ◽  
Critical Role ◽  
Egg Laying ◽  
Cell Interactions ◽  
The Other ◽  
Cell Type ◽  
Specialized Cell ◽  
Anchor Cell

The anchor cell (AC) of the Caenorhabditis elegans gonad has a critical role in the development of a functional egg-laying system, which is accomplished through cell-cell interactions. Lateral inhibitory lin-12-mediated signaling among two bipotential cells causes one to adopt the ventral uterine precursor (VU) cell fate while the other becomes the AC. The AC then induces formation of vulval tissue. We find that the AC also induces a particular ventral uterine intermediate precursor fate (pi) by a mechanism that is genetically and temporally distinct from vulval induction. This process requires lin-12, but unlike previously described lin-12-mediated decisions, signaling is unidirectional, is between dissimilar cells and does not involve lateral inhibition. The pi fates are necessary for egg laying and appear to produce a distinct specialized cell type. Thus, patterning of the ventral uterus by the AC is crucial to the development of a functional egg-laying system.

Cell interactions involved in development of the bilaterally symmetrical intestinal valve cells during embryogenesis in Caenorhabditis elegans

Development ◽  
1992 ◽  
Vol 116 (4) ◽  
pp. 1113-1122 ◽  
Author(s):  
B. Bowerman ◽  
F.E. Tax ◽  
J.H. Thomas ◽  
J.R. Priess
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Cell Interaction ◽  
Cell Interactions ◽  
Cell Type ◽  
Cell Stage ◽  
Development Potential ◽  
Symmetrical Pattern ◽  
A Cell ◽  
Symmetrical Cell

We describe two different cell interactions that appear to be required for the proper development of a pair of bilaterally symmetrical cells in Caenorhabditis elegans called the intestinal valve cells. Previous experiments have shown that at the beginning of the 4-cell stage of embryogenesis, two sister blastomeres called ABa and ABp are equivalent in development potential. We show that cell interactions between ABp and a neighboring 4-cell-stage blastomere called P2 distinguish the fates of ABa and ABp by inducing descendants of ABp to produce the intestinal valve cells, a cell type not made by ABa. A second cell interaction appears to occur later in embryogenesis when two bilaterally symmetrical descendants of ABp, which both have the potential to produce valve cells, contact each other; production of the valve cells subsequently becomes limited to only one of the two descendants. This second interaction does not occur properly if the two symmetrical descendants of ABp are prevented from contacting each other. Thus the development of the intestinal valve cells appears to require both an early cell interaction that establishes a bilaterally symmetrical pattern of cell fate and a later interaction that breaks the symmetrical cell fate pattern by restricting to only one of two cells the ability to produce a pair of valve cells.

scholarly journals On the role of lateral stabilization during early patterning in the pancreas

2013 ◽  
Vol 10 (79) ◽  
pp. 20120766 ◽  
Author(s):  
Walter de Back ◽  
Joseph Xu Zhou ◽  
Lutz Brusch
Keyword(s):  
Progenitor Cells ◽  
Cell Fate ◽  
Lateral Inhibition ◽  
Endocrine Cells ◽  
Cell Interaction ◽  
Simultaneous Occurrence ◽  
Cell Type ◽  
Pancreatic Progenitor ◽  
Cell Cell

The cell fate decision of multi-potent pancreatic progenitor cells between the exocrine and endocrine lineages is regulated by Notch signalling, mediated by cell–cell interactions. However, canonical models of Notch-mediated lateral inhibition cannot explain the scattered spatial distribution of endocrine cells and the cell-type ratio in the developing pancreas. Based on evidence from acinar-to-islet cell transdifferentiation in vitro , we propose that lateral stabilization, i.e. positive feedback between adjacent progenitor cells, acts in parallel with lateral inhibition to regulate pattern formation in the pancreas. A simple mathematical model of transcriptional regulation and cell–cell interaction reveals the existence of multi-stability of spatial patterns whose simultaneous occurrence causes scattering of endocrine cells in the presence of noise. The scattering pattern allows for control of the endocrine-to-exocrine cell-type ratio by modulation of lateral stabilization strength. These theoretical results suggest a previously unrecognized role for lateral stabilization in lineage specification, spatial patterning and cell-type ratio control in organ development.

The fog-3 gene and regulation of cell fate in the germ line of Caenorhabditis elegans.

Genetics ◽  
1995 ◽  
Vol 139 (2) ◽  
pp. 561-577 ◽  
Author(s):  
R E Ellis ◽  
J Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Sexual Identity ◽  
Cell Fate ◽  
Germ Cells ◽  
Regulatory Network ◽  
Germ Line ◽  
The Other ◽  
Nematode Caenorhabditis Elegans ◽  
Inhibitory Interactions

Abstract In the nematode Caenorhabditis elegans, germ cells normally adopt one of three fates: mitosis, spermatogenesis or oogenesis. We have identified and characterized the gene fog-3, which is required for germ cells to differentiate as sperm rather than as oocytes. Analysis of double mutants suggests that fog-3 is absolutely required for spermatogenesis and acts at the end of the regulatory hierarchy controlling sex determination for the germ line. By contrast, mutations in fog-3 do not alter the sexual identity of other tissues. We also have characterized the null phenotype of fog-1, another gene required for spermatogenesis; we demonstrate that it too controls the sexual identity of germ cells but not of other tissues. Finally, we have studied the interaction of these two fog genes with gld-1, a gene required for germ cells to undergo oogenesis rather than mitosis. On the basis of these results, we propose that germ-cell fate might be controlled by a set of inhibitory interactions among genes that specify one of three fates: mitosis, spermatogenesis or oogenesis. Such a regulatory network would link the adoption of one germ-cell fate to the suppression of the other two.

scholarly journals Genetics of intercellular signalling in C. elegans

Development ◽  
1989 ◽  
Vol 107 (Supplement) ◽  
pp. 53-57
Author(s):  
Judith Austin ◽  
Eleanor M. Maine ◽  
Judith Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Molecular Level ◽  
Cell Interactions ◽  
Nematode Caenorhabditis Elegans ◽  
Developmental Potential ◽  
C Elegans ◽  
Intercellular Signalling ◽  
Mitotic Proliferation ◽  
Cell Cell

Cell–cell interactions play a significant role in controlling cell fate during development of the nematode Caenorhabditis elegans. It has been found that two genes, glp-1 and lin-12, are required for many of these decisions, glp-1 is required for induction of mitotic proliferation in the germline by the somatic distal tip cell and for induction of the anterior pharynx early in embryogenesis. lin-12 is required for the interactions between cells of equivalent developmental potential, which allow them to take on different fates. Comparison of these two genes on a molecular level indicates that they are similar in sequence and organization, suggesting that the mechanisms of these two different sets of cell–cell interactions are similar.

scholarly journals Caenorhabditis elegans mutants defective in the functioning of the motor neurons responsible for egg laying.

Genetics ◽  
1989 ◽  
Vol 121 (4) ◽  
pp. 703-721 ◽  
Author(s):  
C Desai ◽  
H R Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
Synaptic Transmission ◽  
Motor Neurons ◽  
Egg Laying ◽  
The Other ◽  
Single Type ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Sensitive Allele

Abstract We have isolated and characterized 45 Caenorhabditis elegans mutants presumed to be defective in the functioning of the hermaphrodite-specific neurons (HSNs). Like hermaphrodites that lack the HSN motor neurons, these mutants are egg-laying defective and do not lay eggs in response to exogenous imipramine but do lay eggs in response to exogenous serotonin. Twenty of the 45 mutations define 10 new egl genes; the other 25 mutations are alleles of five previously defined genes, four of which are known to affect the HSNs. Seven mutations in three genes cause the HSNs to die in hermaphrodites, as they normally do in males. These genes appear to be involved in the determination of the sexual phenotype of the HSNs, and one of them (egl-41) is a newly identified gene that may function generally in sex determination. Five of the 15 genes are defined only by mutations that have dominant effects on egg laying. One gene egl(n1108), is defined by a temperature-sensitive allele that has a temperature-sensitive period after HSN development is complete, suggesting that egl(n1108) may be involved in HSN synaptic transmission. Four of the genes are defined by single alleles, which suggests that other such genes remain to be discovered. Mutations in no more than 4 of the 15 genes specifically affect the HSNs, indicating that there are few genes with functions needed only in this single type of nerve cell.

scholarly journals The lin-11 LIM domain transcription factor is necessary for morphogenesis of C. elegans uterine cells

Development ◽  
1999 ◽  
Vol 126 (23) ◽  
pp. 5319-5326 ◽  
Author(s):  
A.P. Newman ◽  
G.Z. Acton ◽  
E. Hartwieg ◽  
H.R. Horvitz ◽  
P.W. Sternberg
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Egg Laying ◽  
Wild Type ◽  
Lim Domain ◽  
C Elegans ◽  
Expression Studies ◽  
Vulval Precursor Cells ◽  
Cell Induction ◽  
Anchor Cell

The Caenorhabditis elegans hermaphrodite egg-laying system comprises several tissues, including the uterus and vulva. lin-11 encodes a LIM domain transcription factor needed for certain vulval precursor cells to divide asymmetrically. Based on lin-11 expression studies and the lin-11 mutant phenotype, we find that lin-11 is also required for C. elegans uterine morphogenesis. Specifically, lin-11 is expressed in the ventral uterine intermediate precursor (pi) cells and their progeny (the utse and uv1 cells), which connect the uterus to the vulva. Like (pi) cell induction, the uterine lin-11 expression responds to the uterine anchor cell and the lin-12-encoded receptor. In wild type animals, the utse, which forms the planar process at the uterine-vulval interface, fuses with the anchor cell. We found that, in lin-11 mutants, utse differentiation was abnormal, the utse failed to fuse with the anchor cell and a functional uterine-vulval connection was not made. These findings indicate that lin-11 is essential for uterine-vulval morphogenesis.

Suppressors of a lin-12 hypomorph define genes that interact with both lin-12 and glp-1 in Caenorhabditis elegans.

Genetics ◽  
1993 ◽  
Vol 135 (3) ◽  
pp. 765-783 ◽  
Author(s):  
M Sundaram ◽  
I Greenwald
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Gene Dosage ◽  
Egg Laying ◽  
Loss Of Function ◽  
Cell Fate Decision ◽  
Cell Fates ◽  
Cell Fate Decisions ◽  
Suppressor Mutations ◽  
Fate Decision

Abstract The lin-12 gene of Caenorhabditis elegans is thought to encode a receptor which mediates cell-cell interactions required to specify certain cell fates. Reversion of the egg-laying defective phenotype caused by a hypomorphic lin-12 allele identified rare extragenic suppressor mutations in five genes, sel-1, sel-9, sel-10, sel-11 and sel(ar40) (sel = suppressor and/or enhancer of lin-12). Mutations in each of these sel genes suppress defects associated with reduced lin-12 activity, and enhance at least one defect associated with elevated lin-12 activity. None of the sel mutations cause any obvious phenotype in a wild-type background. Gene dosage experiments suggest that sel-1 and sel(ar40) mutations are reduction-of-function mutations, while sel-9 and sel-11 mutations are gain-of-function mutations. sel-1, sel-9, sel-11 and sel(ar40) mutations do not suppress amorphic lin-12 alleles, while sel-10 mutations are able to bypass partially the requirement for lin-12 activity in at least one cell fate decision. sel-1, sel-9, sel-10, sel-11 and sel(ar40) mutations are also able to suppress the maternal-effect lethality caused by a partial loss-of-function allele of glp-1, a gene that is both structurally and functionally related to lin-12. These sel genes may therefore function in both lin-12 and glp-1 mediated cell fate decisions.

Interchangeability of Caenorhabditis elegans DSL proteins and intrinsic signalling activity of their extracellular domains in vivo

Development ◽  
1995 ◽  
Vol 121 (12) ◽  
pp. 4275-4282 ◽  
Author(s):  
K. Fitzgerald ◽  
I. Greenwald
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Cell Interactions ◽  
Regulatory Sequences ◽  
Cell Fate Decisions ◽  
C Elegans ◽  
Dsl Ligands ◽  
Mediate Cell ◽  
Intracellular Domains

Ligands of the Delta/Serrate/lag-2 (DSL) family and their receptors, members of the lin-12/Notch family, mediate cell-cell interactions that specify cell fate in invertebrates and vertebrates. In C. elegans, two DSL genes, lag-2 and apx-1, influence different cell fate decisions during development. Here we show that APX-1 can fully substitute for LAG-2 when expressed under the control of lag-2 regulatory sequences. In addition, we demonstrate that truncated forms lacking the transmembrane and intracellular domains of both LAG-2 and APX-1 can also substitute for endogenous lag-2 activity. Moreover, we provide evidence that these truncated forms are secreted and able to activate LIN-12 and GLP-1 ectopically. Finally, we show that expression of a secreted DSL domain alone may enhance endogenous LAG-2 signalling. Our data suggest ways that activated forms of DSL ligands in other systems may be created.

scholarly journals Super-Enhancers and CTCF in Early Embryonic Cell Fate Decisions

2021 ◽  
Vol 9 ◽  
Author(s):  
Puja Agrawal ◽  
Sridhar Rao
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Critical Role ◽  
Regulatory Elements ◽  
Specific Gene ◽  
Cell Type ◽  
Mammalian Development ◽  
Cell Fate Decisions ◽  
Cell Type Specific ◽  
Early Mammalian Development

Cell fate decisions are the backbone of many developmental and disease processes. In early mammalian development, precise gene expression changes underly the rapid division of a single cell that leads to the embryo and are critically dependent on autonomous cell changes in gene expression. To understand how these lineage specifications events are mediated, scientists have had to look past protein coding genes to the cis regulatory elements (CREs), including enhancers and insulators, that modulate gene expression. One class of enhancers, termed super-enhancers, is highly active and cell-type specific, implying their critical role in modulating cell-type specific gene expression. Deletion or mutations within these CREs adversely affect gene expression and development and can cause disease. In this mini-review we discuss recent studies describing the potential roles of two CREs, enhancers and binding sites for CTCF, in early mammalian development.

COG-2, a sox domain protein necessary for establishing a functional vulval-uterine connection in Caenorhabditis elegans

Development ◽  
1999 ◽  
Vol 126 (1) ◽  
pp. 169-179 ◽  
Author(s):  
W. Hanna-Rose ◽  
M. Han
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
Caenorhabditis Elegans ◽  
Late Stage ◽  
Egg Laying ◽  
Functional Connection ◽  
Seam Cell ◽  
Anchor Cell ◽  
Domain Protein ◽  
Lineage Analysis

In screens for mutants defective in vulval morphogenesis, multiple mutants were isolated in which the uterus and the vulva fail to make a proper connection. We describe five alleles that define the gene cog-2, for connection of gonad defective. To form a functional connection between the vulva and the uterus, the anchor cell must fuse with the multinucleate uterine seam cell, derived from uterine cells that adopt a (pi) lineage. In cog-2 mutants, the anchor cell does not fuse to the uterine seam cell and, instead, remains at the apex of the vulva, blocking the connection between the vulval and uterine lumens, resulting in an egg-laying defective phenotype. According to lineage analysis and expression assays for two (pi)-cell-specific markers, induction of the (pi) fate occurs normally in cog-2 mutants. We have cloned cog-2 and shown that it encodes a Sox family transcription factor that is expressed in the (pi) lineage. Thus, it appears that COG-2 is a transcription factor that regulates a late-stage aspect of uterine seam cell differentiation that specifically affects anchor cell-uterine seam cell fusion.

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