scholarly journals The Zinc Finger Protein DIE-1 Is Required for Late Events during Epithelial Cell Rearrangement in C. elegans

2001 ◽  
Vol 236 (1) ◽  
pp. 165-180 ◽  
Author(s):  
Paul J. Heid ◽  
William B. Raich ◽  
Ryan Smith ◽  
William A. Mohler ◽  
Kristin Simokat ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
C Elegans ◽  
Cell Rearrangement ◽  
Finger Protein

scholarly journals LIN-39 and the EGFR/RAS/MAPK pathway regulate C. elegans vulval morphogenesis via the VAB-23 zinc finger protein

Development ◽  
2011 ◽  
Vol 138 (21) ◽  
pp. 4649-4660 ◽  
Author(s):  
M. W. Pellegrino ◽  
S. Farooqui ◽  
E. Frohli ◽  
H. Rehrauer ◽  
S. Kaeser-Pebernard ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Mapk Pathway ◽  
C Elegans ◽  
Finger Protein

scholarly journals Molecular Cloning and Characterization of a Zinc Finger Protein Involved in Id-1-stimulated Mammary Epithelial Cell Growth

2001 ◽  
Vol 276 (15) ◽  
pp. 11852-11858 ◽  
Author(s):  
Jarnail Singh ◽  
Yoko Itahana ◽  
Simona Parrinello ◽  
Kenji Murata ◽  
Pierre-Yves Desprez
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Mammary Epithelial Cells ◽  
Constitutive Expression ◽  
Mammary Epithelial ◽  
Protein Fusion ◽  
Degenerate Primers ◽  
Finger Protein

Id proteins are dominant negative regulators of basic helix-loop-helix transcription factors. Previous work in our laboratory has shown that constitutive expression of Id-1 in SCp2 mouse mammary epithelial cells inhibits their differentiation and induces proliferation, invasion, and migration. Id-1 expression also correlates with the invasive and aggressive potential of human breast cancer cells. However, little is known about Id-1 target genes that are important for regulating normal and transformed breast epithelial cell phenotypes. Now we report the cloning of a novel zinc finger protein, Zfp289, using degenerate primers to specifically amplify cDNAs from Id-1-transfected SCp2 cells. Zfp289 has homology with a yeast zinc finger protein, the GTPase-activating protein Gcs-1, which was initially identified as a gene required for the re-entry of cells into the cell cycle after stationary phase growth. Zfp289 mRNA expression pattern correlates with Id-1 expression in SCp2 mammary epithelial cells under various experimental conditions as well as in the mouse mammary gland at different stages of development. It is predominantly present in the cytoplasm of the cells as evident from green fluorescent protein fusion protein localization. SCp2 mammary epithelial cells with constitutive expression of Zfp289 have a higher S-phase index, compared with control cells, when cultured in a serum-free medium. We conclude that the novel zinc finger protein Zfp289, which may represent the mammalian homologue of Gcs-1, is potentially an important mediator of the Id-1-induced proliferation pathway in mammary epithelial cells.

TRA-1A regulates transcription of fog-3, which controls germ cell fate in C. elegans

Development ◽  
2000 ◽  
Vol 127 (14) ◽  
pp. 3119-3129 ◽  
Author(s):  
P. Chen ◽  
R.E. Ellis
Keyword(s):  
Transcriptional Regulation ◽  
Sexual Identity ◽  
Cell Fate ◽  
Zinc Finger ◽  
Germ Cells ◽  
Zinc Finger Protein ◽  
Rt Pcr ◽  
C Elegans ◽  
Finger Protein

In C. elegans, the zinc-finger protein TRA-1A is thought to be the final arbiter of somatic sexual identity. We show that fog-3, which is required for germ cells to become sperm rather than oocytes, is a target of TRA-1A. First, northern analyses and RT-PCR experiments indicate that expression of fog-3 is controlled by tra-1. Second, studies of double mutants show that this control could be direct. Third, the fog-3 promoter contains multiple sites that bind TRA-1A in gel shift assays, and mutations in these sites alter activity of fog-3 in vivo. These results establish fog-3 as one of the first known targets of transcriptional regulation by TRA-1A. Furthermore, they show that tra-1 controls a terminal regulator of sexual fate in germ cells, just as it is thought to do in the soma.

scholarly journals The C. elegans HP1 homologue HPL-2 and the LIN-13 zinc finger protein form a complex implicated in vulval development

2006 ◽  
Vol 297 (2) ◽  
pp. 308-322 ◽  
Author(s):  
Vincent Coustham ◽  
Cécile Bedet ◽  
Karine Monier ◽  
Sonia Schott ◽  
Marianthi Karali ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Vulval Development ◽  
C Elegans ◽  
Finger Protein

scholarly journals C. elegans PAT-9 is a nuclear zinc finger protein critical for the assembly of muscle attachments

2012 ◽  
Vol 2 (1) ◽  
pp. 18 ◽  
Author(s):  
Qian Liu ◽  
Takako I Jones ◽  
Rebecca A Bachmann ◽  
Mitchell Meghpara ◽  
Lauren Rogowski ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
C Elegans ◽  
Finger Protein

scholarly journals The zinc-finger protein OEF-1 stabilizes histone modification patterns and promotes efficient splicing in the C. elegans germ line

2021 ◽  
Author(s):  
Catherine E McManus ◽  
Mariateresa Mazzetto ◽  
Guifeng Wei ◽  
Mei Han ◽  
Valerie Reinke
Keyword(s):  
Histone Modification ◽  
Zinc Finger ◽  
Germ Cells ◽  
Zinc Finger Protein ◽  
Germ Line ◽  
C Elegans ◽  
Finger Protein ◽  
Downstream Effects ◽  
Line Loss ◽  
Mutant Phenotypes

Abstract To ensure stable transmission of genetic information to the next generation, germ cells frequently silence sex chromosomes, as well as autosomal loci that promote inappropriate differentiation programs. In C. elegans, silenced and active genomic domains are established in germ cells by the histone modification complexes MES-2/3/6 and MES-4, which promote silent and active chromatin states, respectively. These states are generally mutually exclusive and modulation of one state influences the pattern of the other. Here we identify the zinc-finger protein OEF-1 as a novel modifier of this epigenetic balance in the C. elegans germ line. Loss of oef-1 genetically enhances mes mutant phenotypes. Moreover, OEF-1 binding correlates with the active modification H3K36me3 and sustains H3K36me3 levels in the absence of MES-4 activity. OEF-1 also promotes efficient mRNA splicing activity, a process that is influenced by H3K36me3 levels. Finally, OEF-1 limits deposition of the silencing modification H3K27me3 on the X chromosome and at repressed autosomal loci. We propose that OEF-1 might act as an intermediary to mediate the downstream effects of H3K36me3 that promote transcript integrity, and indirectly affect gene silencing as a consequence.

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