Comparative developmental studies using Oscheius/Dolichorhabditis sp. CEW1 (Rhabditidae)

Nematology ◽  
2000 ◽  
Vol 2 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Marie Delattre ◽  
Marie-Laure Dichtel ◽  
Marie-Anne Félix
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Analysis ◽  
Precursor Cells ◽  
Developmental Studies ◽  
Morphological Markers ◽  
Molecular Tools ◽  
Ras Gene ◽  
C Elegans ◽  
Vulval Precursor Cells ◽  
Anchor Cell

AbstractIn order to study the evolution of nematode vulva development, we focus on Oscheius/Dolichorhabditis sp. CEW1 (Rhabditidae) in comparison with Caenorhabditis elegans. In this species, the fates of the vulval precursor cells are determined by two successive nested inductions by the uterine anchor cell (instead of a single one in C. elegans). This hermaphroditic species can be cultured and handled like C. elegans. We review vulva development in this species. We present some molecular tools and the sequence of the Ras gene. This species is amenable to genetic analysis and we discuss the isolation of morphological markers. Afin d’étudier l’évolution du développement de la vulve des nématodes, nous nous concentrons sur l’espèce Oscheius/Dolichorhabditis sp. CEW1 (Rhabditidae) en la comparant à Caenorhabditis elegans. Dans cette espèce, les destinées des cellules précurseurs de la vulve sont déterminées par deux inductions emboîtées provenant de la cellule ancre de l’utérus (au lieu d’une seule chez C. elegans). Cette espèce hermaphrodite peut être élévée et manipulée comme C. elegans. Nous décrivons le développement de la vulve dans cette espèce. Nous présentons des outils moléculaires et la séquence du gène Ras. Les analyses génétiques sont possibles dans cette espèce et nous discutons l’isolement de marqueurs morphologiques.

The Caenorhabditis elegans gene lin-26 is required to specify the fates of hypodermal cells and encodes a presumptive zinc-finger transcription factor

Development ◽  
1994 ◽  
Vol 120 (9) ◽  
pp. 2359-2368 ◽  
Author(s):  
M. Labouesse ◽  
S. Sookhareea ◽  
H.R. Horvitz
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Zinc Finger ◽  
Precursor Cells ◽  
Embryonic Lethality ◽  
Zinc Finger Transcription Factor ◽  
C Elegans ◽  
Neural Fate ◽  
Vulval Precursor Cells

The mutation lin-26(n156) prevents vulva formation in C. elegans by transforming the vulval precursor cells into neurons or neuroblasts. We have isolated and characterized three new lin-26 alleles, which result in embryonic lethality. These mutations cause a few other hypodermal cells to express a neural fate and most hypodermal cells to degenerate. lin-26 encodes a presumptive zinc-finger transcription factor. Our data indicate that lin-26 is required for cells to acquire the hypodermal fate.

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.

scholarly journals Cell fate patterning during C. elegans vulval development

Development ◽  
1993 ◽  
Vol 119 (Supplement) ◽  
pp. 9-18 ◽  
Author(s):  
Russell J. Hill ◽  
Paul W. Sternberg
Keyword(s):  
Cell Fate ◽  
Short Range ◽  
Precursor Cells ◽  
Cell Fates ◽  
Vulval Development ◽  
C Elegans ◽  
Vulval Precursor Cells ◽  
Combined Action ◽  
Anchor Cell ◽  
Inductive Signal

Precursor cells of the vulva of the C. elegans hermaphrodite choose between two vulval cell fates (1° and 2°) and a non-vulval epidermal fate (3°) in response to three intercellular signals. An inductive signal produced by the anchor cell induces the vulval precursors to assume the 1° and 2° vulval fates. This inductive signal is an EGF-like growth factor encoded by the gene lin-3. An inhibitory signal mediated by lin-15, and which may originate from the surrounding epidermis, prevents the vulval precursors from assuming vulval fates in the absence of the inductive signal. A short range lateral signal, which acts through the gene lin-12, regulates the pattern of 1° and 2° fates assumed by the induced vulval precursors. The combined action of the three signals precisely directs the six vulval precursors to adopt a 3° 3° 2° 1° 2 ° 3° pattern of fates. The amount of inductive signal produced by the anchor cell appears to determine the number or vulval precursors that assume vulval fates. The three induced vulval precursors most proximal to the anchor cell are proposed to adopt the 2° 1° 2° pattern of fates in response to a gradient of the inductive signal and also in response to lateral signalling that inhibits adjacent vulval precursor cells from both assuming the 1° fate.

scholarly journals Forces drive basement membrane invasion inCaenorhabditis elegans

2018 ◽  
Vol 115 (45) ◽  
pp. 11537-11542 ◽  
Author(s):  
Rodrigo Cáceres ◽  
Nagagireesh Bojanala ◽  
Laura C. Kelley ◽  
Jes Dreier ◽  
John Manzi ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Basement Membrane ◽  
Actin Filaments ◽  
Actin Polymerization ◽  
Force Production ◽  
Developmental Event ◽  
C Elegans ◽  
Anchor Cell

During invasion, cells breach basement membrane (BM) barriers with actin-rich protrusions. It remains unclear, however, whether actin polymerization applies pushing forces to help break through BM, or whether actin filaments play a passive role as scaffolding for targeting invasive machinery. Here, using the developmental event of anchor cell (AC) invasion inCaenorhabditis elegans, we observe that the AC deforms the BM and underlying tissue just before invasion, exerting forces in the tens of nanonewtons range. Deformation is driven by actin polymerization nucleated by the Arp2/3 complex and its activators, whereas formins and cross-linkers are dispensable. Delays in invasion upon actin regulator loss are not caused by defects in AC polarity, trafficking, or secretion, as appropriate markers are correctly localized in the AC even when actin is reduced and invasion is disrupted. Overall force production emerges from this study as one of the main tools that invading cells use to promote BM disruption inC. elegans.

The Pristionchus HOX gene Ppa-lin-39 inhibits programmed cell death to specify the vulva equivalence group and is not required during vulval induction

Development ◽  
1998 ◽  
Vol 125 (19) ◽  
pp. 3865-3873 ◽  
Author(s):  
R.J. Sommer ◽  
A. Eizinger ◽  
K.Z. Lee ◽  
B. Jungblut ◽  
A. Bubeck ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Nematode Species ◽  
Precursor Cells ◽  
Body Region ◽  
Ras Signaling ◽  
Equivalence Group ◽  
Hox Gene ◽  
C Elegans ◽  
Vulval Precursor Cells

In the two nematode species Caenorhabditis elegans and Pristionchus pacificus the vulva equivalence group in the central body region is specified by the Hox gene lin-39. C. elegans lin-39 mutants are vulvaless and the vulval precursor cells fuse with the surrounding hypodermis, whereas in P. pacificus lin-39 mutants the vulval precursor cells die by apoptosis. Mechanistically, LIN-39 might inhibit non-vulval fate (cell fusion in C. elegans, apoptosis in P. pacificus), promote vulval fate or do both. To study the mechanism of lin-39 function, we isolated P. pacificus cell death mutants and identified mutations in ced-3. Surprisingly, P. pacificus ced-3; lin-39 double mutants form a functional vulva in the absence of LIN-39 activity. Thus, in P. pacificus lin-39 specifies the vulva equivalence group by inhibiting programmed cell death. Furthermore, these data reveal an important difference in a later function of lin-39 between the two species. In C. elegans, LIN-39 specifies vulval cell fates in response to inductive RAS signaling, and in P. pacificus LIN-39 is not required for vulval induction. Thus, the comparative analysis indicates that lin-39 has distinct functions in both species although the gene is acting in a homologous developmental system.

scholarly journals C. elegans PlexinA PLX-1 mediates a cell contact-dependent stop signal in vulval precursor cells

2005 ◽  
Vol 282 (1) ◽  
pp. 138-151 ◽  
Author(s):  
Zhicen Liu ◽  
Takashi Fujii ◽  
Akira Nukazuka ◽  
Rie Kurokawa ◽  
Motoshi Suzuki ◽  
...  
Keyword(s):  
Precursor Cells ◽  
Stop Signal ◽  
Cell Contact ◽  
C Elegans ◽  
Vulval Precursor Cells ◽  
A Cell

scholarly journals Genetic Analysis of Adult-Specific Surface Antigenic Differences Between Varieties of the Nematode Caenorhabditis elegans

Genetics ◽  
1987 ◽  
Vol 117 (3) ◽  
pp. 467-476
Author(s):  
Samuel M Politz ◽  
Karl J Chin ◽  
Daniel L Herman
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Genetic Analysis ◽  
Surface Antigen ◽  
Single Gene ◽  
Surface Antigens ◽  
Nematode Caenorhabditis Elegans ◽  
Specific Antibodies ◽  
C Elegans ◽  
Stage Specificity

ABSTRACT We have studied developmental stage-specificity and genetic specification of surface antigens in the nematode Caenorhabditis elegans. Rabbit antisera directed against the adult C. elegans cuticle were used in conjunction with antiserum adsorption experiments to obtain antibody reagents with specificity for the adult surface. Adult-specific antibodies were used to identify several varietal strains of C. elegans that display antigen-negative phenotypes as adults. Genetic mapping results using the surface antigen phenotype as a marker indicated that a single gene (designated srf-1) or cluster of genes on linkage group II determines the adult surface antigen phenotype.

Developmental strategies during early embryogenesis of Caenorhabditis elegans

Development ◽  
1986 ◽  
Vol 97 (Supplement) ◽  
pp. 31-44
Author(s):  
Einhard Schierenberg
Keyword(s):  
Caenorhabditis Elegans ◽  
Parasitic Nematode ◽  
Soil Nematode ◽  
Developmental Studies ◽  
Central Question ◽  
Unique Combination ◽  
Nematode Caenorhabditis Elegans ◽  
Free Living ◽  
C Elegans ◽  
Multicellular Structure

How the complex, multicellular structure of an organism is generated from the information contained in the uncleaved egg is a central question in developmental studies. Nematodes are particularly suitable for studying this question. A unique combination of favourable properties, including transparent eggshell, normal embryogenesis under the microscope outside the mother, small number of cells and rapid, reproducible development made nematodes classic models for developmental biologists (for reviews see Chitwood & Chitwood, 1974; von Ehrenstein & Schierenberg, 1980). In addition to the attractive features mentioned above, the free-living soil nematode Caenorhabditis elegans (Fig. 1) is also well suited for analysis of the genetic control of development (Brenner, 1974) unlike the classically studied parasitic nematode Parascaris equorum (Ascaris megalocephala). Recently cellular (e.g. Sulston, Schierenberg, White & Thomson, 1983) and genetic (e.g. Sternberg & Horvitz, 1984) aspects of development have been studied extensively in C. elegans.

scholarly journals The lin-15 locus encodes two negative regulators of Caenorhabditis elegans vulval development.

1994 ◽  
Vol 5 (4) ◽  
pp. 395-411 ◽  
Author(s):  
L S Huang ◽  
P Tzou ◽  
P W Sternberg
Keyword(s):  
Caenorhabditis Elegans ◽  
Null Allele ◽  
Negative Regulator ◽  
Vulval Development ◽  
Genetic Studies ◽  
Vulval Precursor Cells ◽  
Complex Locus ◽  
Anchor Cell ◽  
Inductive Signal

During Caenorhabditis elegans vulval development, an inductive signal from the anchor cell stimulates three of the six vulval precursor cells (VPCs) to adopt vulval rather than nonvulval epidermal fates. Genes necessary for this induction include the lin-3 growth factor, the let-23 receptor tyrosine kinase, and let-60 ras. lin-15 is a negative regulator of this inductive pathway. In lin-15 mutant animals, all six VPCs adopt vulval fates, even in the absence of inductive signal. Previous genetic studies suggested that lin-15 is a complex locus with two independently mutable activities, A and B. We have cloned the lin-15 locus by germline transformation and find that it encodes two nonoverlapping transcripts that are transcribed in the same direction. The downstream transcript encodes the lin-15A function; the upstream transcript encodes the lin-15B function. The predicted lin-15A and lin-15B proteins are novel and hydrophilic. We have identified a molecular null allele of lin-15 and have used it to analyze the role of lin-15 in the signaling pathway. We find that lin-15 acts upstream of let-23 and in parallel to the inductive signal.

scholarly journals CSC-1

2003 ◽  
Vol 161 (2) ◽  
pp. 229-236 ◽  
Author(s):  
Alper Romano ◽  
Annika Guse ◽  
Ivica Krascenicova ◽  
Heinke Schnabel ◽  
Ralf Schnabel ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Analysis ◽  
Chromosome Segregation ◽  
Kinase Activity ◽  
Aurora B ◽  
Aurora B Kinase ◽  
C Elegans ◽  
The Individual

The Aurora B kinase complex is a critical regulator of chromosome segregation and cytokinesis. In Caenorhabditis elegans, AIR-2 (Aurora B) function requires ICP-1 (Incenp) and BIR-1 (Survivin). In various systems, Aurora B binds to orthologues of these proteins. Through genetic analysis, we have identified a new subunit of the Aurora B kinase complex, CSC-1. C. elegans embryos depleted of CSC-1, AIR-2, ICP-1, or BIR-1 have identical phenotypes. CSC-1, BIR-1, and ICP-1 are interdependent for their localization, and all are required for AIR-2 localization. In vitro, CSC-1 binds directly to BIR-1. The CSC-1/BIR-1 complex, but not the individual subunits, associates with ICP-1. CSC-1 associates with ICP-1, BIR-1, and AIR-2 in vivo. ICP-1 dramatically stimulates AIR-2 kinase activity. This activity is not stimulated by CSC-1/BIR-1, suggesting that these two subunits function as targeting subunits for AIR-2 kinase.

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