scholarly journals ELT-1, a GATA-like transcription factor, is required for epidermal cell fates in Caenorhabditis elegans embryos.

1997 ◽  
Vol 11 (13) ◽  
pp. 1651-1661 ◽  
Author(s):  
B D Page ◽  
W Zhang ◽  
K Steward ◽  
T Blumenthal ◽  
J R Priess
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Epidermal Cell ◽  
Cell Fates

scholarly journals Genetic Analysis of the Caenorhabditis elegans MAP Kinase Gene mpk-1

Genetics ◽  
1998 ◽  
Vol 150 (1) ◽  
pp. 103-117 ◽  
Author(s):  
Mark R Lackner ◽  
Stuart K Kim
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Double Mutant ◽  
Cell Fates ◽  
Gain Of Function ◽  
Kinase Gene ◽  
Epistasis Analysis ◽  
Anchor Cell ◽  
Ets Transcription Factor

Abstract The Caenorhabditis elegans mpk-1 gene encodes a MAP kinase protein that plays an important role in Ras-mediated induction of vulval cell fates. We show that mutations that eliminate mpk-1 activity result in a highly penetrant, vulvaless phenotype. A double mutant containing a gain-of-function mpk-1 mutation and a gain-of-function mek mutation (MEK phosphorylates and activates MPK-1) exhibits a multivulva phenotype. These results suggest that mpk-1 may transduce most or all of the anchor cell signal. Epistasis analysis suggests that mpk-1 acts downstream of mek-2 (encodes a MEK homolog) and upstream of lin-1 (encodes an Ets transcription factor) in the anchor cell signaling pathway. Finally, mpk-1 may act together with let-60 ras in multiple developmental processes, as mpk-1 mutants exhibit nearly the same range of developmental phenotypes as let-60 ras mutants.

scholarly journals The EGL-13 SOX Domain Transcription Factor Affects the Uterine Cell Lineages in Caenorhabditis elegans

Genetics ◽  
2003 ◽  
Vol 165 (3) ◽  
pp. 1623-1628
Author(s):  
Hediye Nese Cinar ◽  
Keri L Richards ◽  
Kavita S Oommen ◽  
Anna P Newman
Keyword(s):  
Transcription Factor ◽  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Cell Lineages

Abstract We isolated egl-13 mutants in which the cells of the Caenorhabditis elegans uterus initially appeared to develop normally but then underwent an extra round of cell division. The data suggest that egl-13 is required for maintenance of the cell fate.

In Caenorhabditis elegans, the RNA-Binding Domains of the Cytoplasmic Polyadenylation Element Binding Protein FOG-1 Are Needed to Regulate Germ Cell Fates

Genetics ◽  
2001 ◽  
Vol 159 (4) ◽  
pp. 1617-1630
Author(s):  
Suk-Won Jin ◽  
Nancy Arno ◽  
Adam Cohen ◽  
Amy Shah ◽  
Qijin Xu ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Rna Binding ◽  
Dominant Negative ◽  
Missense Mutations ◽  
Biochemical Tests ◽  
Cell Fates ◽  
Cytoplasmic Polyadenylation ◽  
Binding Domains ◽  
Rna Binding Domains

Abstract FOG-1 controls germ cell fates in the nematode Caenorhabditis elegans. Sequence analyses revealed that FOG-1 is a cytoplasmic polyadenylation element binding (CPEB) protein; similar proteins from other species have been shown to bind messenger RNAs and regulate their translation. Our analyses of fog-1 mutations indicate that each of the three RNA-binding domains of FOG-1 is essential for activity. In addition, biochemical tests show that FOG-1 is capable of binding RNA sequences in the 3′-untranslated region of its own message. Finally, genetic assays reveal that fog-1 functions zygotically, that the small fog-1 transcript has no detectable function, and that missense mutations in fog-1 cause a dominant negative phenotype. This last observation suggests that FOG-1 acts in a complex, or as a multimer, to regulate translation. On the basis of these data, we propose that FOG-1 binds RNA to regulate germ cell fates and that it does so by controlling the translation of its targets. One of these targets might be the fog-1 transcript itself.

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.

scholarly journals Converting cell fates: generating hematopoietic stem cellsde novovia transcription factor reprogramming

2016 ◽  
Vol 1370 (1) ◽  
pp. 24-35 ◽  
Author(s):  
Michael G. Daniel ◽  
Ihor R. Lemischka ◽  
Kateri Moore
Keyword(s):  
Transcription Factor ◽  
Cell Fates ◽  
Hematopoietic Stem

scholarly journals A MAP kinase homolog, mpk-1, is involved in ras-mediated induction of vulval cell fates in Caenorhabditis elegans.

1994 ◽  
Vol 8 (2) ◽  
pp. 160-173 ◽  
Author(s):  
M R Lackner ◽  
K Kornfeld ◽  
L M Miller ◽  
H R Horvitz ◽  
S K Kim
Keyword(s):  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Cell Fates

Knock-down of transcription factor skinhead-1 exacerbates arsenite-induced oxidative damage in Caenorhabditis elegans

BioMetals ◽  
2021 ◽  
Author(s):  
Yijie Mao ◽  
Ling Yao ◽  
Xuejun Jiang ◽  
Golamaully Sumayyah ◽  
Zhen Zou ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Knock Down

scholarly journals How affinity of the ELT-2 GATA factor binding to cis-acting regulatory sites controls Caenorhabditis elegans intestinal gene transcription

Development ◽  
2020 ◽  
Vol 147 (14) ◽  
pp. dev190330
Author(s):  
Brett R. Lancaster ◽  
James D. McGhee
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Binding Affinity ◽  
Experimental System ◽  
Quantitative Relationship ◽  
Gata Factor ◽  
Unknown Parameters ◽  
Cis Acting ◽  
Complicated Model

ABSTRACTWe define a quantitative relationship between the affinity with which the intestine-specific GATA factor ELT-2 binds to cis-acting regulatory motifs and the resulting transcription of asp-1, a target gene representative of genes involved in Caenorhabditis elegans intestine differentiation. By establishing an experimental system that allows unknown parameters (e.g. the influence of chromatin) to effectively cancel out, we show that levels of asp-1 transcripts increase monotonically with increasing binding affinity of ELT-2 to variant promoter TGATAA sites. The shape of the response curve reveals that the product of the unbound ELT-2 concentration in vivo [i.e. (ELT-2free) or ELT-2 ‘activity’] and the largest ELT-XXTGATAAXX association constant (Kmax) lies between five and ten. We suggest that this (unitless) product [Kmax×(ELT-2free) or the equivalent product for any other transcription factor] provides an important quantitative descriptor of transcription-factor/regulatory-motif interaction in development, evolution and genetic disease. A more complicated model than simple binding affinity is necessary to explain the fact that ELT-2 appears to discriminate in vivo against equal-affinity binding sites that contain AGATAA instead of TGATAA.

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