C. elegans PlexinA PLX-1 mediates a cell contact-dependent stop signal in 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.

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Establishment of gut fate in the E lineage of C. elegans: the roles of lineage-dependent mechanisms and cell interactions

Development ◽

10.1242/dev.118.4.1267 ◽

1993 ◽

Vol 118 (4) ◽

pp. 1267-1277 ◽

Cited By ~ 14

Author(s):

B. Goldstein

Keyword(s):

Cell Interactions ◽

The Other ◽

Cell Contact ◽

Cell Stage ◽

C Elegans ◽

Daughter Cells ◽

Intact Embryo ◽

A Cell ◽

Random Position ◽

Recombination Experiments

The gut of C. elegans derives from all the progeny of the E blastomere, a cell of the eight cell stage. Previous work has shown that gut specification requires an induction during the four cell stage (Goldstein, B. (1992) Nature 357, 255–257). Blastomere isolation and recombination experiments were done to determine which parts of the embryo can respond to gut induction. Normally only the posterior side of the EMS blastomere contacts the inducing cell, P2. When P2 was instead placed in a random position on an isolated EMS, gut consistently differentiated from the daughter of EMS contacting P2, indicating that any side of EMS can respond to gut induction. Additionally, moving P2 around to the opposite side of EMS in an otherwise intact embryo caused EMS's two daughter cells to switch lineage timings, and gut to differentiate from the descendents of what normally would be the MS blastomere. The other cells of the four cell stage, ABa, ABp, and P2, did not form gut when placed in contact with the inducer. To determine whether any other inductions are involved in gut specification, timed blastomere isolations were done at the two and eight cell stages. In the absence of cell contact at the two cell stage, segregation of gut fate proceeded normally at both the two and four cell stages. Gut fate also segregated properly in the absence of cell contact at the eight cell stage. A model is presented for the roles of lineage-dependent mechanisms and cell interactions in establishing gut fate in the E lineage.

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

Nematology ◽

10.1163/156854100508809 ◽

2000 ◽

Vol 2 (1) ◽

pp. 89-98 ◽

Cited By ~ 13

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.

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

Development ◽

10.1242/dev.120.9.2359 ◽

1994 ◽

Vol 120 (9) ◽

pp. 2359-2368 ◽

Cited By ~ 8

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.

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Cell fate patterning during C. elegans vulval development

Development ◽

10.1242/dev.119.supplement.9 ◽

1993 ◽

Vol 119 (Supplement) ◽

pp. 9-18 ◽

Cited By ~ 3

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.

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Novel cell-cell interactions during vulva development in Pristionchus pacificus

Development ◽

10.1242/dev.127.15.3295 ◽

2000 ◽

Vol 127 (15) ◽

pp. 3295-3303 ◽

Cited By ~ 1

Author(s):

B. Jungblut ◽

R.J. Sommer

Keyword(s):

Precursor Cells ◽

Cell Interactions ◽

Developmental Competence ◽

Specific Response ◽

Pristionchus Pacificus ◽

C Elegans ◽

Vulval Precursor Cells ◽

Continuous Interaction ◽

One Step ◽

Cell Cell

Vulva development differs between Caenorhabditis elegans and Pristionchus pacificus in several ways. Seven of 12 ventral epidermal cells in P. pacificus die of apoptosis, whereas homologous cells in C. elegans fuse with the hypodermal syncytium. Vulva induction is a one-step process in C. elegans, but requires a continuous interaction between the gonad and the epidermis in P. pacificus. Here we describe several novel cell-cell interactions in P. pacificus, focusing on the vulva precursor cell P8.p and the mesoblast M. P8.p in P. pacificus, unlike its homologous cell in C. elegans, is incompetent to respond to gonadal signaling in the absence of other vulva precursor cells, but can respond to lateral signaling from a neighboring vulval precursor. P8.p provides an inhibitory signal that determines the developmental competence of P(5,7).p. This lateral inhibition acts via the mesoblast M and is regulated by the homeotic gene Ppa-mab-5. In Ppa-mab-5 mutants, M is misspecified and provides inductive signaling to the vulval precursor cells, including P8.p. Taken together, vulva development in P. pacificus displays novel cell-cell interactions involving the mesoblast M and P8.p. In particular, P8.p represents a new ventral epidermal cell type, which is characterized by novel interactions and a specific response to gonadal signaling.

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Cell contact regulates neuroblast formation in the Caenorhabditis elegans lateral epidermis

Development ◽

10.1242/dev.120.2.313 ◽

1994 ◽

Vol 120 (2) ◽

pp. 313-323 ◽

Cited By ~ 9

Author(s):

J. Austin ◽

C. Kenyon

Keyword(s):

Cell Adhesion ◽

Cell Division ◽

Direct Contact ◽

Normal Development ◽

Cell Contact ◽

Cell Recognition ◽

Sensory Structure ◽

C Elegans ◽

Seam Cell ◽

A Cell

A single line of epidermal seam cells lies along each side of the nematode C. elegans. During normal development, one of these cells, V5, produces a neuroblast that will give rise to a sensory structure, the postdeirid. If seam cells located either anterior or posterior to V5 are ablated however, this neuroblast formation is blocked. Because of this requirement for the presence of adjacent seam cells, we have asked whether V5's ability to produce a neuroblast depends on direct contact with its seam cell neighbors. We find that direct contact between seam cells is required for commitment to neuroblast production. Seam cells lose and reform their contacts with each other as they go through rounds of cell division during larval development. Signaling required for neuroblast formation occurs when the seam cells make contact after their first round of division. If this contact is prevented, no neuroblast is made; when it is delayed, the time of signaling is also delayed. The characteristics of these signals suggest that a seam cell must be part of a continuous epithelium in order to develop normally and that signaling may occur via a cell recognition/cell adhesion pathway. The effect of seam cell ablations on neuroblast formation is altered in mab-5(−) animals, suggesting that this HOM-C gene is part of the pathway by which seam cell signaling controls the decision to make a postdeirid neuroblast.

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High sensitivity of C. elegans vulval precursor cells to the dose of posterior Wnts

Developmental Biology ◽

10.1016/j.ydbio.2011.06.006 ◽

2011 ◽

Vol 357 (2) ◽

pp. 428-438 ◽

Cited By ~ 23

Author(s):

Jean-Baptiste Pénigault ◽

Marie-Anne Félix

Keyword(s):

High Sensitivity ◽

Precursor Cells ◽

C Elegans ◽

Vulval Precursor Cells

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Faculty Opinions recommendation of An instructive role for C. elegans E-cadherin in translating cell contact cues into cortical polarity.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.725465140.793509423 ◽

2015 ◽

Author(s):

Albert Reynolds

Keyword(s):

Cell Contact ◽

C Elegans ◽

E Cadherin

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Polymodal Functionality of C. elegans OLL Neurons in Mechanosensation and Thermosensation

Neuroscience Bulletin ◽

10.1007/s12264-021-00629-4 ◽

2021 ◽

Author(s):

Yuedan Fan ◽

Wenjuan Zou ◽

Jia Liu ◽

Umar Al-Sheikh ◽

Hankui Cheng ◽

...

Keyword(s):

Glutamate Receptor ◽

Sensory Neurons ◽

Molecular Mechanisms ◽

Temperature Sensitive ◽

Cold Sensation ◽

Cold Response ◽

C Elegans ◽

Sensory Modalities ◽

A Cell ◽

Bona Fide

AbstractSensory modalities are important for survival but the molecular mechanisms remain challenging due to the polymodal functionality of sensory neurons. Here, we report the C. elegans outer labial lateral (OLL) sensilla sensory neurons respond to touch and cold. Mechanosensation of OLL neurons resulted in cell-autonomous mechanically-evoked Ca2+ transients and rapidly-adapting mechanoreceptor currents with a very short latency. Mechanotransduction of OLL neurons might be carried by a novel Na+ conductance channel, which is insensitive to amiloride. The bona fide mechano-gated Na+-selective degenerin/epithelial Na+ channels, TRP-4, TMC, and Piezo proteins are not involved in this mechanosensation. Interestingly, OLL neurons also mediated cold but not warm responses in a cell-autonomous manner. We further showed that the cold response of OLL neurons is not mediated by the cold receptor TRPA-1 or the temperature-sensitive glutamate receptor GLR-3. Thus, we propose the polymodal functionality of OLL neurons in mechanosensation and cold sensation.

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