scholarly journals The multivulva phenotype of certain Caenorhabditis elegans mutants results from defects in two functionally redundant pathways.

Genetics ◽  
1989 ◽  
Vol 123 (1) ◽  
pp. 109-121 ◽  
Author(s):  
E L Ferguson ◽  
H R Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Lineage ◽  
Gene Families ◽  
Precursor Cells ◽  
Wild Type ◽  
Vulval Development ◽  
Vulval Precursor Cells ◽  
New Mutations ◽  
Intercellular Signal

Abstract We previously identified Caenorhabditis elegans mutants in which certain of the six vulval precursor cells adopt fates normally expressed by other vulval precursor cells. These mutants define genes that appear to function in the response to an intercellular signal that induces vulval development. The multivulva (Muv) phenotype of one such mutant, CB1322, results from an interaction between two unlinked mutations, lin-8(n111) II and lin-9(n112) III. In this paper, we identify 18 new mutations, which are alleles of eight genes, that interact with either lin-8(n111) or lin-9(n112) to generate a Muv phenotype. None of these 20 mutations alone causes any vulval cell lineage defects. The "silent Muv" mutations fall into two classes; hermaphrodites carrying a mutation of each class are Muv, while hermaphrodites carrying two mutations of the same class have a wild-type vulval phenotype. Our results indicate that the Muv phenotype of these mutants results from defects in two functionally-redundant pathways, thereby demonstrating that redundancy can occur at the level of gene pathways as well as at the level of gene families.

scholarly journals Caenorhabditis elegans lin-13, a Member of the LIN-35 Rb Class of Genes Involved in Vulval Development, Encodes a Protein With Zinc Fingers and an LXCXE Motif

Genetics ◽  
2000 ◽  
Vol 155 (3) ◽  
pp. 1127-1137 ◽  
Author(s):  
Alicia Meléndez ◽  
Iva Greenwald
Keyword(s):  
Caenorhabditis Elegans ◽  
Zinc Fingers ◽  
Null Alleles ◽  
Temperature Sensitive ◽  
Wild Type ◽  
Vulval Development ◽  
Vulval Precursor Cells ◽  
Class B ◽  
Genes Encoding ◽  
Lxcxe Motif

Abstract The SynMuv genes appear to be involved in providing a signal that inhibits vulval precursor cells from adopting vulval fates in Caenorhabditis elegans. One group of SynMuv genes, termed class B, includes genes encoding proteins related to the tumor suppressor Rb and RbAp48, a protein that binds Rb. Here, we provide genetic evidence that lin-13 behaves as a class B SynMuv gene. We show that null alleles of lin-13 are temperature sensitive and maternally rescued, resulting in phenotypes ranging in severity from L2 arrest (when both maternal and zygotic activities are removed at 25°), to sterile Multivulva (when only zygotic activity is removed at 25°), to sterile non-Multivulva (when both maternal and zygotic activities are removed at 15°), to wild-type/class B SynMuv (when only zygotic activity is removed at 15°). We also show that LIN-13 is a nuclear protein that contains multiple zinc fingers and a motif, LXCXE, that has been implicated in Rb binding. These results together suggest a role for LIN-13 in Rb-mediated repression of vulval fates.

Reversal of cell fate determination in Caenorhabditis elegans vulval development

Development ◽  
1996 ◽  
Vol 122 (8) ◽  
pp. 2507-2515 ◽  
Author(s):  
S. Euling ◽  
V. Ambros
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Larval Stage ◽  
Cell Types ◽  
Wild Type ◽  
Vulval Development ◽  
Fate Determination ◽  
Developmental Arrest ◽  
Dauer Larva ◽  
Vulval Precursor Cells

In Caenorhabditis elegans, the fates of the multipotent vulval precursor cells (VPCs) are specified by intercellular signals. The VPCs divide in the third larval stage (L3) of the wild type, producing progeny of determined cell types. In lin-28 mutants, vulva development is similar to wild-type vulva development except that it occurs precociously, in the second larval stage (L2). Consequently, when lin-28 hermaphrodites temporarily arrest development at the end of L2 in the dauer larva stage, they have partially developed vulvae consisting of VPC progeny. During post-dauer development, these otherwise determined VPC progeny become reprogrammed back to the multipotent, signal-sensitive state of VPCs. Our results indicate that VPC fate determination by intercellular signals is reversible by dauer larva developmental arrest and post-dauer development.

The terminal differentiation factor LIN-29 is required for proper vulval morphogenesis and egg laying in Caenorhabditis elegans

Development ◽  
1997 ◽  
Vol 124 (21) ◽  
pp. 4333-4342 ◽  
Author(s):  
J.C. Bettinger ◽  
S. Euling ◽  
A.E. Rougvie
Keyword(s):  
Caenorhabditis Elegans ◽  
Terminal Differentiation ◽  
Egg Laying ◽  
Small Subset ◽  
Wild Type ◽  
Vulval Development ◽  
Genetic Mosaics ◽  
Hypodermal Cell ◽  
Heterochronic Gene ◽  
Final Molt

Caenorhabditis elegans vulval development culminates during exit from the L4-to-adult molt with the formation of an opening through the adult hypodermis and cuticle that is used for egg laying and mating. Vulva formation requires the heterochronic gene lin-29, which triggers hypodermal cell terminal differentiation during the final molt. lin-29 mutants are unable to lay eggs or mate because no vulval opening forms; instead, a protrusion forms at the site of the vulva. We demonstrate through analysis of genetic mosaics that lin-29 is absolutely required in a small subset of lateral hypodermal seam cells, adjacent to the vulva, for wild-type vulva formation and egg laying. However, lin-29 function is not strictly limited to the lateral hypodermis. First, LIN-29 accumulates in many non-hypodermal cells with known roles in vulva formation or egg laying. Second, animals homozygous for one lin-29 allele, ga94, have the vulval defect and cannot lay eggs, despite having a terminally differentiated adult lateral hypodermis. Finally, vulval morphogenesis and egg laying requires lin-29 activity within the EMS lineage, a lineage that does not generate hypodermal cells.

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.

CAENORHABDITIS ELEGANS DEFICIENCY MAPPING

Genetics ◽  
1984 ◽  
Vol 108 (2) ◽  
pp. 331-345
Author(s):  
D Christine Sigurdson ◽  
Gail J Spanier ◽  
Robert K Herman
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Ethyl Methanesulfonate ◽  
Single Site ◽  
Crossing Over ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
Recessive Lethal ◽  
X Ray ◽  
New Mutations

ABSTRACT Six schemes were used to identify 80 independent recessive lethal deficiencies of linkage group (LG) II following X-ray treatment of the nematode Caenorhabditis elegans. Complementation tests between the deficiencies and ethyl methanesulfonate-induced recessive visible, lethal and sterile mutations and between different deficiencies were used to characterize the extents of the deficiencies. Deficiency endpoints thus helped to order 36 sites within a region representing about half of the loci on LG II and extending over about 5 map units. New mutations occurring in this region can be assigned to particular segments of the map by complementation tests against a small number of deficiencies; this facilitates the assignment of single-site mutations to particular genes, as we illustrate. Five sperm-defective and five oocyte-defective LG II sterile mutants were identified and mapped. Certain deficiency-by-deficiency complementation tests allowed us to suggest that the phenotypes of null mutations at two loci represented by visible alleles are wild type and that null mutations at a third locus confer a visible phenotype. A segment of LG II that is about 12 map units long and largely devoid of identified loci seems to be greatly favored for crossing over.

A Test for Epistasis Among Induced Mutations in Caenorhabditis elegans

Genetics ◽  
2000 ◽  
Vol 156 (4) ◽  
pp. 1635-1647 ◽  
Author(s):  
Andrew D Peters ◽  
Peter D Keightley
Keyword(s):  
Caenorhabditis Elegans ◽  
Maximum Level ◽  
Soil Nematode ◽  
Deleterious Mutations ◽  
Wild Type ◽  
Induced Mutations ◽  
Large Numbers ◽  
Significant Difference ◽  
Sexual Production ◽  
New Mutations

Abstract Synergistic epistasis, in which deleterious mutations tend to magnify each other’s effects, is a necessary component of the mutational deterministic hypothesis for the maintenance of sexual production. We tested for epistasis for life-history traits in the soil nematode Caenorhabditis elegans by inducing mutations in two genetic backgrounds: a wild-type strain and a set of genetically loaded lines that contain large numbers of independent mildly detrimental mutations. There was no significant difference between the effect of new mutations on the wild-type background and the genetically loaded background for four out of five fitness correlates. In these four cases, the maximum level of epistasis compatible with the data was very low. The fifth trait, late productivity, is not likely to be an important component of fitness. This suggests either that specific environmental conditions are required to cause epistasis or that synergistic epistasis is not a general phenomenon. We also suggest a new mechanism by which deleterious mutations may provide an advantage to sexual reproduction under low selection coefficients.

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-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 The ncl-1 gene and genetic mosaics of Caenorhabditis elegans.

Genetics ◽  
1995 ◽  
Vol 141 (3) ◽  
pp. 989-1006 ◽  
Author(s):  
E M Hedgecock ◽  
R K Herman
Keyword(s):  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Embryonic Cell ◽  
Vulval Development ◽  
Genetic Mosaics ◽  
Cell Divisions ◽  
Mosaic Analysis ◽  
A Cell ◽  
Intercellular Signal

Abstract A ncl-1 mutation results in enlarged nucleoli, which can be detected in nearly all cells of living animals by Nomarski microscopy. Spontaneous mitotic loss of a ncl-1(+)-containing free duplication in an otherwise homozygous ncl-1 mutant animal results in mosaicism for ncl-1 expression, and the patterns of mosaicism lead us to conclude that ncl-1 acts cell autonomously. The probability of mitotic loss of the duplication sDp3 is approximately constant over many cell divisions. About 60% of the losses of sDp3 at the first embryonic cell division involve nondisjunction. Frequencies of mitotic loss of different ncl-1(+)-bearing free duplications varied over a 200-fold range. The frequencies of mitotic loss were enhanced by a chromosomal him-10 mutation. We have used ncl-1 as a cell autonomous marker in the mosaic analysis of dpy-1 and lin-37. The focus of action of dpy-1 is in hypodermis. A mutation in lin-37 combined with a mutation in another gene results in a synthetic multivulva phenotype. We show that lin-37 acts cell nonautonomously and propose that it plays a role, along with the previously studied gene lin-15, in the generation of an intercellular signal by hyp7 that represses vulval development.

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