Dependence of position-effect variegation in Drosophila on dose of a gene encoding an unusual zinc-finger protein

Nature ◽  
1990 ◽  
Vol 344 (6263) ◽  
pp. 219-223 ◽  
Author(s):  
Gunter Reuter ◽  
Marianna Giarre ◽  
Joseph Farah ◽  
Janos Gausz ◽  
Anne Spierer ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Gene Encoding ◽  
Finger Protein ◽  
Effect Variegation

The heterochromatin-associated protein HP-1 is an essential protein in Drosophila with dosage-dependent effects on position-effect variegation.

Genetics ◽  
1992 ◽  
Vol 131 (2) ◽  
pp. 345-352 ◽  
Author(s):  
J C Eissenberg ◽  
G D Morris ◽  
G Reuter ◽  
T Hartnett
Keyword(s):  
Germ Line ◽  
Position Effect ◽  
Inducible Promoter ◽  
Specific Protein ◽  
P Element ◽  
Position Effect Variegation ◽  
Chromosomal Protein ◽  
Gene Encoding ◽  
Position Effects ◽  
Effect Variegation

Abstract Chromosome rearrangements which place euchromatic genes adjacent to a heterochromatic breakpoint frequently result in gene repression (position-effect variegation). This repression is thought to reflect the spreading of a heterochromatic structure into neighboring euchromatin. Two allelic dominant suppressors of position-effect variegation were found to contain mutations within the gene encoding the heterochromatin-specific chromosomal protein HP-1. The site of mutation for each allele is given: one converts Lys169 into a nonsense (ochre) codon, while the other is a frameshift after Ser10. In flies heterozygous for one of the mutant alleles (Su(var)2-504), a truncated HP-1 protein was detectable by Western blot analysis. An HP-1 minigene, consisting of HP-1 cDNA under the control of an Hsp70 heat-inducible promoter, was transduced into flies by P element-mediated germ line transformation. Heat-shock driven expression of this minigene results in elevated HP-1 protein level and enhancement of position-effect variegation. Levels of variegating gene expression thus appear to depend upon the level of expression of a heterochromatin-specific protein. The implications of these observations for mechanism of heterochromatic position effects and heterochromatin function are discussed.

scholarly journals Characterization of a Novel Gene Encoding a Putative Single Zinc-finger Protein,ZIM, Expressed during the Reproductive Phase inArabidopsis thaliana

2000 ◽  
Vol 64 (7) ◽  
pp. 1402-1409 ◽  
Author(s):  
Akiko NISHII ◽  
Miho TAKEMURA ◽  
Hidetomo FUJITA ◽  
Masahito SHIKATA ◽  
Akiho YOKOTA ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Gene Encoding ◽  
Novel Gene ◽  
Finger Protein ◽  
Reproductive Phase

scholarly journals Promoter Analysis ofZfp-36,the Mitogen-inducible Gene Encoding the Zinc Finger Protein Tristetraprolin

1995 ◽  
Vol 270 (42) ◽  
pp. 25266-25272 ◽  
Author(s):  
Wi S. Lai ◽  
Michael J. Thompson ◽  
Gregory A. Taylor ◽  
Yi Liu ◽  
Perry J. Blackshear
Keyword(s):  
Zinc Finger ◽  
Promoter Analysis ◽  
Zinc Finger Protein ◽  
Gene Encoding ◽  
Finger Protein ◽  
Inducible Gene

scholarly journals Requirement for the Murine Zinc Finger Protein ZFR in Perigastrulation Growth and Survival

2001 ◽  
Vol 21 (8) ◽  
pp. 2880-2890 ◽  
Author(s):  
Madeleine J. Meagher ◽  
Robert E. Braun
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Cellular Growth ◽  
Gene Encoding ◽  
Growth And Survival ◽  
Finger Protein ◽  
Development Delay ◽  
Cellular Phenotypes

ABSTRACT The transition from preimplantation to postimplantation development leads to the initiation of complex cellular differentiation and morphogenetic movements, a dramatic decrease in cell cycle length, and a commensurate increase in the size of the embryo. Accompanying these changes is the need for the transfer of nutrients from the mother to the embryo and the elaboration of sophisticated genetic networks that monitor genomic integrity and the homeostatic control of cellular growth, differentiation, and programmed cell death. To determine the function of the murine zinc finger protein ZFR in these events, we generated mice carrying a null mutation in the gene encoding it. Homozygous mutant embryos form normal-appearing blastocysts that implant and initiate the process of gastrulation. Mutant embryos form mesoderm but they are delayed in their development and fail to form normal anterior embryonic structures. Loss of ZFR function leads to both an increase in programmed cell death and a decrease in mitotic index, especially in the region of the distal tip of the embryonic ectoderm. Mutant embryos also have an apparent reduction in apical vacuoles in the columnar visceral endoderm cells in the extraembryonic region. Together, these cellular phenotypes lead to a dramatic development delay and embryonic death by 8 to 9 days of gestation, which are independent of p53 function.

Gene Encoding a Putative Zinc Finger Protein inSynechocystisPCC6803

1991 ◽  
Vol 55 (9) ◽  
pp. 2259-2264
Author(s):  
Yutaka Ogura ◽  
Tadashi Yoshida ◽  
Yasukazu Nakamura ◽  
Miho Takemura ◽  
Kenji Oda ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Gene Encoding ◽  
Finger Protein ◽  
Putative Zinc Finger
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