scholarly journals Control of Vulval Cell Division Number in the Nematode Oscheius/Dolichorhabditis sp. CEW1

Genetics ◽  
2001 ◽  
Vol 157 (1) ◽  
pp. 183-197 ◽  
Author(s):  
Marie-Laure Dichtel ◽  
Sophie Louvet-Vallée ◽  
Mark E Viney ◽  
Marie-Anne Félix ◽  
Paul W Sternberg
Keyword(s):  
Cell Cycle ◽  
Precursor Cell ◽  
Spatial Patterning ◽  
Cell Fates ◽  
C Elegans ◽  
Induction Mechanism ◽  
Independent Mechanism ◽  
Genetic Mechanisms ◽  
Vulval Precursor Cell ◽  
Division Number

Abstract Spatial patterning of vulval precursor cell fates is achieved through a different two-stage induction mechanism in the nematode Oscheius/Dolichorhabditis sp. CEW1 compared with Caenorhabditis elegans. We therefore performed a genetic screen for vulva mutants in Oscheius sp. CEW1. Most mutants display phenotypes unknown in C. elegans. Here we present the largest mutant category, which affects division number of the vulva precursors P(4-8).p without changing their fate. Among these mutations, some reduce the number of divisions of P4.p and P8.p specifically. Two mutants omit the second cell cycle of all vulval lineages. A large subset of mutants undergo additional rounds of vulval divisions. We also found precocious and retarded heterochronic mutants. Whereas the C. elegans vulval lineage mutants can be interpreted as overall (homeotic) changes in precursor cell fates with concomitant cell cycle changes, the mutants described in Oscheius sp. CEW1 do not affect overall precursor fate and thereby dissociate the genetic mechanisms controlling vulval cell cycle and fate. Laser ablation experiments in these mutants reveal that the two first vulval divisions in Oscheius sp. CEW1 appear to be redundantly controlled by a gonad-independent mechanism and by a gonadal signal that operates partially independently of vulval fate induction.

Patterning of the C. elegans 1 degrees vulval lineage by RAS and Wnt pathways

Development ◽  
2000 ◽  
Vol 127 (23) ◽  
pp. 5047-5058 ◽  
Author(s):  
M. Wang ◽  
P.W. Sternberg
Keyword(s):  
Short Range ◽  
Precursor Cell ◽  
Ras Signaling ◽  
Cell Fates ◽  
C Elegans ◽  
Asymmetric Divisions ◽  
Anchor Cell ◽  
Wnt Pathways ◽  
Vulval Precursor Cell ◽  
Proper Orientation

In C. elegans, the descendants of the 1 degrees vulval precursor cell (VPC) establish a fixed spatial pattern of two different cell fates: E-F-F-E. The two inner granddaughters attach to the somatic gonadal anchor cell (AC) and generate four vulF cells, while the two outer granddaughters produce four vulE progeny. zmp-1::GFP, a molecular marker that distinguishes these two fates, is expressed in vulE cells, but not vulF cells. We demonstrate that a short-range AC signal is required to ensure that the pattern of vulE and vulF fates is properly established. In addition, signaling between the inner and outer 1 degrees VPC descendants, as well as intrinsic polarity of the 1 degrees VPC daughters, is involved in the asymmetric divisions of the 1 degrees VPC daughters and the proper orientation of the outcome. Finally, we provide evidence that RAS signaling is used during this new AC signaling event, while the Wnt receptor LIN-17 appears to mediate signaling between the inner and outer 1 degrees VPC descendants.

The beta-catenin homolog BAR-1 and LET-60 Ras coordinately regulate the Hox gene lin-39 during Caenorhabditis elegans vulval development

Development ◽  
1998 ◽  
Vol 125 (18) ◽  
pp. 3667-3680 ◽  
Author(s):  
D.M. Eisenmann ◽  
J.N. Maloof ◽  
J.S. Simske ◽  
C. Kenyon ◽  
S.K. Kim
Keyword(s):  
Signaling Pathway ◽  
Cell Fate ◽  
Precursor Cell ◽  
Ras Signaling ◽  
Beta Catenin ◽  
Cell Fates ◽  
Vulval Development ◽  
Hox Gene ◽  
C Elegans ◽  
Vulval Precursor Cell

In C. elegans, the epithelial Pn.p cells adopt either a vulval precursor cell fate or fuse with the surrounding hypodermis (the F fate). Our results suggest that a Wnt signal transduced through a pathway involving the beta-catenin homolog BAR-1 controls whether P3.p through P8.p adopt the vulval precursor cell fate. In bar-1 mutants, P3.p through P8.p can adopt F fates instead of vulval precursor cell fates. The Wnt/bar-1 signaling pathway acts by regulating the expression of the Hox gene lin-39, since bar-1 is required for LIN-39 expression and forced lin-39 expression rescues the bar-1 mutant phenotype. LIN-39 activity is also regulated by the anchor cell signal/let-23 receptor tyrosine kinase/let-60 Ras signaling pathway. Our genetic and molecular experiments show that the vulval precursor cells can integrate the input from the BAR-1 and LET-60 Ras signaling pathways by coordinately regulating activity of the common target LIN-39 Hox.

scholarly journals Anchor cell signaling and vulval precursor cell positioning establish a reproducible spatial context during C. elegans vulval induction

2016 ◽  
Vol 416 (1) ◽  
pp. 123-135 ◽  
Author(s):  
Stéphanie Grimbert ◽  
Kyria Tietze ◽  
Michalis Barkoulas ◽  
Paul W. Sternberg ◽  
Marie-Anne Félix ◽  
...  
Keyword(s):  
Cell Signaling ◽  
Precursor Cell ◽  
Spatial Context ◽  
C Elegans ◽  
Anchor Cell ◽  
Cell Positioning ◽  
Vulval Precursor Cell

The evolution of cell lineage in nematodes

Development ◽  
1994 ◽  
Vol 1994 (Supplement) ◽  
pp. 85-95
Author(s):  
Ralf J. Sommer ◽  
Lynn K. Carta ◽  
Paul W. Sternberg
Keyword(s):  
Cell Lineage ◽  
Experimental System ◽  
Nematode Species ◽  
Cell Fates ◽  
Equivalence Group ◽  
Vulval Development ◽  
C Elegans ◽  
Somatic Gonad ◽  
Vulval Precursor Cell ◽  
P Cells

The invariant development of free-living nematodes combined with the extensive knowledge of Caenorhabditis elegans developmental biology provides an experimental system for an analysis of the evolution of developmental mechanisms. We have collected a number of new nematode species from soil samples. Most are easily cultured and their development can be analyzed at the level of individual cells using techniques standard to Caenorhabditis. So far, we have focused on differences in the development of the vulva among species of the families Rhabditidae and Panagrolaimidae. Preceding vulval development, twelve Pn cells migrate into the ventral cord and divide to produce posterior daughters [Pn.p cells] whose fates vary in a position specific manner [from P1.p anterior to P12.p posterior]. In C. elegans hermaphrodites, P(3-8).p are tripotent and form an equivalence group. These cells can express either of two vulval fates (1° or 2°) in response to a signal from the anchor cell of the somatic gonad, or a non-vulval fate (3°), resulting in a 3°-3°-2°-1°-2°-3° pattern of cell fates. Evolutionary differences in vulval development include the number of cells in the vulval equivalence group, the number of 1° cells, the number of progeny generated by each vulval precursor cell, and the position of VPCs before morphogenesis. Examples of three Rhabditidae genera have a posterior vulva in the position of P9-P11 ectoblasts. In Cruznema tripartitum, P(5-7).p form the vulva as in Caenorhabditis, but they migrate posteriorly before dividing. Induction occurs after the gonad grows posteriorly to the position of P(5-7).p cells. In two other species, Mesorhabditis sp. PS 1179 and Teratorhabditis palmarum, we have found changes in induction and competence with respect to their presumably more C. elegans-like ancestor. In Mesorhabditis, P(5-7).p form the vulva after migrating to a posterior position. However, the gonad is not required to specify the pattern of cell fates 3°-2°-1°-2°-3°. Moreover, the Pn.p cells are not equivalent in their potentials to form the vulva. A regulatory constraint in this family thus forces the same set of precursors to generate the vulva, rather than more appropriately positioned Pn.p cells.

LIN-12 protein expression and localization during vulval development in C. elegans

Development ◽  
1998 ◽  
Vol 125 (16) ◽  
pp. 3101-3109 ◽  
Author(s):  
D. Levitan ◽  
I. Greenwald
Keyword(s):  
Cell Fate ◽  
Feedback Mechanism ◽  
Precursor Cell ◽  
Vulval Development ◽  
Ras Pathway ◽  
Cell Fate Decisions ◽  
C Elegans ◽  
Somatic Gonad ◽  
Multiple Cell ◽  
Vulval Precursor Cell

We have used a LIN-12::GFP fusion protein to examine LIN-12 accumulation during cell fate decisions important for vulval development. During the naturally variable anchor cell (AC)/ventral uterine precursor cell (VU) decision of the somatic gonad, a transcription-based feedback mechanism biases two equivalent cells so that one becomes the AC while the other becomes a VU. LIN-12::GFP accumulation reflects lin-12 transcription: LIN-12::GFP is initially present in both cells, but disappears from the presumptive AC and becomes restricted to the presumptive VU. During vulval precursor cell (VPC) fate determination, six equipotential cells uniformly transcribe lin-12 and have invariant fates that are specified by multiple cell-cell interactions. The pattern of LIN-12::GFP accumulation in VPCs and in the VPC lineages is dynamic and does not always reflect lin-12 transcription. In particular, LIN-12::GFP is expressed initially in all six VPCs, but appears to be reduced specifically in P6.p as a consequence of the activation of the Ras pathway by an EGF-like inductive signal from the AC. We propose that downregulation of LIN-12 stability or translation in response to inductive signalling helps impose a bias on lateral signalling and contributes to the invariant pattern of VPC fates.

scholarly journals Necessity and contingency in developmental genetic screens: LIN-3, Wnt and semaphorin pathways in vulval induction of the nematode Oscheius tipulae

2018 ◽  
Author(s):  
Amhed M. Vargas-Velazquez ◽  
Fabrice Besnard ◽  
Marie-Anne Félix
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Wnt Pathway ◽  
Precursor Cell ◽  
Genetic Screens ◽  
C Elegans ◽  
Forward Genetic Screens ◽  
Anchor Cell ◽  
Notch Pathways ◽  
Vulval Precursor Cell

AbstractGenetic screens in the nematode Caenorhabditis elegans identified the EGF/Ras and Notch pathways as central for vulval precursor cell fate patterning. Schematically, the anchor cell secretes EGF, inducing the P6.p cell to a 1° vulval fate; P6.p in turn induces its neighbors to a 2° fate through Delta-Notch signaling and represses Ras signaling. In the nematode Oscheius tipulae, the anchor cell successively induces 2° then 1° vulval fates. Here we report on the molecular identification of mutations affecting vulval induction in O. tipulae. A single Induction Vulvaless mutation was found, which we identify as a cis-regulatory deletion in a tissue-specific enhancer of the O. tipulae lin-3 homolog, confirmed by CRISPR/Cas9 mutation. In contrast to this predictable Vulvaless mutation, mutations resulting in an excess of 2° fates unexpectedly correspond to the plexin/semaphorin pathway, which was not implicated in vulval fate induction in C. elegans. Hyperinduction of P4.p and P8.p in these mutants likely results from mispositioning of these cells due to a lack of contact inhibition. The third signaling pathway found by forward genetics in O. tipulae is the Wnt pathway: decrease in Wnt pathway activity results in loss of vulval precursor competence and induction, and 1° fate miscentering on P5.p. Our results suggest that the EGF and Wnt pathways have qualitatively similar activities in vulval induction in C. elegans and O. tipulae, albeit with quantitative differences in the effects of mutation. This study highlights both necessity and contingency in forward genetic screens.100-word summaryGenetic screens in the nematode Caenorhabditis elegans identified EGF and Notch pathways as key for vulval precursor cell fate patterning. Here we report on the molecular identification of mutations affecting vulval induction in another nematode, Oscheius tipulae. The single mutation with reduced induction is identified as a cis-regulatory deletion in the O. tipulae lin-3 homolog, confirmed by CRISPR/Cas9 mutation. In contrast to this predictable Vulvaless mutation, mutations resulting in an excess of 2° vulval fates unexpectedly correspond to the plexin/semaphorin pathway, not implicated in vulval induction in C. elegans. This study highlights both necessity and contingency in forward genetic screens.

scholarly journals Mutations in cye-1, a Caenorhabditis elegans cyclin E homolog, reveal coordination between cell-cycle control and vulval development

Development ◽  
2000 ◽  
Vol 127 (18) ◽  
pp. 4049-4060 ◽  
Author(s):  
D.S. Fay ◽  
M. Han
Keyword(s):  
Cell Cycle ◽  
Cyclin E ◽  
Cell Cycle Control ◽  
Terminal Differentiation ◽  
Loss Of Function ◽  
Cell Fates ◽  
Vulval Development ◽  
C Elegans ◽  
Vulval Precursor Cells ◽  
Specific Number

We have identified strong loss-of-function mutations in the C. elegans cyclin E gene, cye-1. Mutations in cye-1 lead to the underproliferation of many postembryonic blast lineages as well as defects in fertility and gut-cell endoreduplication. In addition, cye-1 is required maternally, but not zygotically for embryonic development. Our analysis of vulval development in cye-1 mutants suggests that a timing mechanism may control the onset of vulval cell terminal differentiation: once induced, these cells appear to differentiate after a set amount of time, rather than a specific number of division cycles. cye-1 mutants also show an increase in the percentage of vulval precursor cells (VPCs) that adopt vulval cell fates, indicating that cell-cycle length can play a role in the proper patterning of vulval cells. By analyzing cul-1 mutants, we further demonstrate that vulval cell terminal differentiation can be uncoupled from associated changes in vulval cell division planes.

Clonal heterogeneity in the germinal zone of the developing rat telencephalon

Development ◽  
1993 ◽  
Vol 118 (1) ◽  
pp. 175-192 ◽  
Author(s):  
S.E. Acklin ◽  
D. van der Kooy
Keyword(s):  
Cell Cycle ◽  
Cell Lines ◽  
Spatial Organization ◽  
Precursor Cell ◽  
Clonal Heterogeneity ◽  
Double Labeling ◽  
Germinal Zone ◽  
Dividing Cells ◽  
Cellular Phenotypes ◽  
Developing Rat

A double-labeling technique, combining retroviral tagging of individual cell lines (one clone per brain hemisphere) with the simultaneous [3H]thymidine-labeling of dividing cells in S phase, was used to study proliferation characteristics of individual precursor cell lines in the germinal zone of the developing rat forebrain. The cortical germinal zone was found to be segregated into three spatially distinct horizontal populations of precursor cell lineages, which differed in cell cycle kinetics, amount of cell death, and synchronous versus asynchronous mode of proliferation. The striatal germinal zone demonstrated a similar heterogeneity in the cell cycle characteristics of proliferating clones, but did not show nearly as distinct a spatial segregation of these different populations. The results demonstrate the clonal heterogeneity among precursor populations in the telencephalon and the differential spatial organization of the cortical and the striatal germinal zones. This germinal zone heterogeneity may predict some of the differences found among cellular phenotypes in the adult forebrain.

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