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 Specific collagens maintain the cuticle permeability barrier in Caenorhabditis elegans

Genetics ◽  
2021 ◽  
Author(s):  
Anjali Sandhu ◽  
Divakar Badal ◽  
Riya Sheokand ◽  
Shalini Tyagi ◽  
Varsha Singh
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Barrier Function ◽  
Permeability Barrier ◽  
Nematode Caenorhabditis Elegans ◽  
Zinc Finger Transcription Factor ◽  
Outermost Layer ◽  
C Elegans ◽  
Receptor Mutant ◽  
Antioxidant Machinery

Abstract Collagen enriched cuticle forms the outermost layer of skin in nematode Caenorhabditis elegans. The nematode’s genome encodes 177 collagens, but little is known about their role in maintaining the structure or barrier function of the cuticle. In this study, we found six permeability determining (PD) collagens. Loss of any of these PD collagens- DPY-2, DPY-3, DPY-7, DPY-8, DPY-9, and DPY-10- led to enhanced susceptibility of nematodes to paraquat (PQ) and antihelminthic drugs levamisole and ivermectin. Upon exposure to paraquat, PD collagen mutants accumulated more PQ and incurred more damage and death despite the robust activation of antioxidant machinery. We find that BLMP-1, a zinc finger transcription factor, maintains the barrier function of the cuticle by regulating the expression of PD collagens. We show that the permeability barrier maintained by PD collagens acts in parallel to FOXO transcription factor DAF-16 to enhance survival of insulin-like receptor mutant, daf-2. In all, this study shows that PD collagens regulate cuticle permeability by maintaining the structure of C. elegans cuticle and thus provide protection against exogenous toxins.

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.

scholarly journals The Evolutionary Duplication and Probable Demise of an Endodermal GATA Factor in Caenorhabditis elegans

Genetics ◽  
2003 ◽  
Vol 165 (2) ◽  
pp. 575-588 ◽  
Author(s):  
Tetsunari Fukushige ◽  
Barbara Goszczynski ◽  
Helen Tian ◽  
James D McGhee
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Zinc Finger ◽  
Specific Binding ◽  
Ectopic Expression ◽  
Intestinal Development ◽  
Wild Type ◽  
C Elegans ◽  
Dna Binding Domains ◽  
Binding Domains

Abstract We describe the elt-4 gene from the nematode Caenorhabditis elegans. elt-4 is predicted to encode a very small (72 residues, 8.1 kD) GATA-type zinc finger transcription factor. The elt-4 gene is located ∼5 kb upstream of the C. elegans elt-2 gene, which also encodes a GATA-type transcription factor; the zinc finger DNA-binding domains are highly conserved (24/25 residues) between the two proteins. The elt-2 gene is expressed only in the intestine and is essential for normal intestinal development. This article explores whether elt-4 also has a role in intestinal development. Reporter fusions to the elt-4 promoter or reporter insertions into the elt-4 coding regions show that elt-4 is indeed expressed in the intestine, beginning at the 1.5-fold stage of embryogenesis and continuing into adulthood. elt-4 reporter fusions are also expressed in nine cells of the posterior pharynx. Ectopic expression of elt-4 cDNA within the embryo does not cause detectable ectopic expression of biochemical markers of gut differentiation; furthermore, ectopic elt-4 expression neither inhibits nor enhances the ectopic marker expression caused by ectopic elt-2 expression. A deletion allele of elt-4 was isolated but no obvious phenotype could be detected, either in the gut or elsewhere; brood sizes, hatching efficiencies, and growth rates were indistinguishable from wild type. We found no evidence that elt-4 provided backup functions for elt-2. We used microarray analysis to search for genes that might be differentially expressed between L1 larvae of the elt-4 deletion strain and wild-type worms. Paired hybridizations were repeated seven times, allowing us to conclude, with some confidence, that no candidate target transcript could be identified as significantly up- or downregulated by loss of elt-4 function. In vitro binding experiments could not detect specific binding of ELT-4 protein to candidate binding sites (double-stranded oligonucleotides containing single or multiple WGATAR sequences); ELT-4 protein neither enhanced nor inhibited the strong sequence-specific binding of the ELT-2 protein. Whereas ELT-2 protein is a strong transcriptional activator in yeast, ELT-4 protein has no such activity under similar conditions, nor does it influence the transcriptional activity of coexpressed ELT-2 protein. Although an elt-2 homolog was easily identified in the genomic sequence of the related nematode C. briggsae, no elt-4 homolog could be identified. Analysis of the changes in silent third codon positions within the DNA-binding domains indicates that elt-4 arose as a duplication of elt-2, some 25–55 MYA. Thus, elt-4 has survived far longer than the average duplicated gene in C. elegans, even though no obvious biological function could be detected. elt-4 provides an interesting example of a tandemly duplicated gene that may originally have been the same size as elt-2 but has gradually been whittled down to its present size of little more than a zinc finger. Although elt-4 must confer (or must have conferred) some selective advantage to C. elegans, we suggest that its ultimate evolutionary fate will be disappearance from the C. elegans genome.

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 Two distinct types of neuronal asymmetries are controlled by the Caenorhabditis elegans zinc finger transcription factor die-1

2013 ◽  
Vol 28 (1) ◽  
pp. 34-43 ◽  
Author(s):  
L. Cochella ◽  
B. Tursun ◽  
Y.-W. Hsieh ◽  
S. Galindo ◽  
R. J. Johnston ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Zinc Finger ◽  
Zinc Finger Transcription Factor
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