scholarly journals Drosophila small ovary encodes a zinc-finger repressor required for ovarian differentiation

2018 ◽  
Author(s):  
Leif Benner ◽  
Elias A. Castro ◽  
Cale Whitworth ◽  
Koen J.T. Venken ◽  
Haiwang Yang ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Position Effect ◽  
Specific Gene ◽  
Position Effect Variegation ◽  
Heterochromatin Protein 1 ◽  
Heterochromatin Protein ◽  
Tissue Degeneration ◽  
Cell Type Specific ◽  
Small Ovary

AbstractRepression is essential for coordinated cell type-specific gene regulation and controlling the expression of transposons. In the Drosophila ovary, stem cell regeneration and differentiation requires controlled gene expression, with derepression leading to tissue degeneration and ovarian tumors. Likewise, the ovary is acutely sensitive to deleterious consequences of transposon derepression. The small ovary (sov) locus was identified in a female sterile screen, and mutants show dramatic ovarian morphogenesis defects. We mapped the locus to the uncharacterized gene CG14438, which encodes a zinc-finger protein that colocalizes with the essential Heterochromatin Protein 1 (HP1a). We demonstrate that Sov functions to repress inappropriate cell signaling, silence transposons, and suppress position-effect variegation in the eye, suggesting a central role in heterochromatin stabilization.

Genetic factors controlling white gene expression of the transposon AR4-24 at a telomere in Drosophila melanogaster

Genome ◽  
2002 ◽  
Vol 45 (6) ◽  
pp. 1025-1034 ◽  
Author(s):  
M L Balasov
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Genetic Factors ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Heterochromatin Protein 1 ◽  
Heterochromatin Protein ◽  
Effect Variegation ◽  
Restricted Pattern

The position effect of the AR 4-24 P[white, rosy] transposon was studied at cytological position 60F. Three copies of the transposon (within ~50-kb region) resulted in a spatially restricted pattern of white variegation. This pattern was modified by temperature and by removal of the Y chromosome, suggesting that it was due to classical heterochromatin-induced position effect variegation (PEV). In contrast with classical PEV, extra dose of the heterochromatin protein 1 (HP1) suppressed white variegation and one dose enhanced it. The effect of Pc-G, trx-G, and other PEV suppressors was also tested. It was found that E(Pc)1, TrlR85, and mutations of Su(z)2C relieve AR 4-24- silencing and z1 enhances it. To explain the results obtained with these modifiers, it is proposed that PEV and telomeric position effect can counteract each other at this particular cytological site.Key words: position effect variegation, heterochromatin protein 1, Drosophila melanogaster.

Heterochromatin protein 1 is required for correct chromosome segregation in Drosophila embryos

1995 ◽  
Vol 108 (4) ◽  
pp. 1419-1431 ◽  
Author(s):  
R. Kellum ◽  
B.M. Alberts
Keyword(s):  
Chromosome Segregation ◽  
Position Effect ◽  
Chromosome Morphology ◽  
Chromosome Condensation ◽  
Centromeric Heterochromatin ◽  
Position Effect Variegation ◽  
Loss Of Function ◽  
Heterochromatin Protein 1 ◽  
Gene Encoding ◽  
Heterochromatin Protein

Heterochromatin protein 1 is associated with centromeric heterochromatin in Drosophila, mice, and humans. Loss of function mutations in the gene encoding heterochromatin protein 1 in Drosophila, Suppressor of variegation2-5, decrease the mosaic repression observed for euchromatic genes that have been juxtaposed to centromeric heterochromatin. These heterochromatin protein 1 mutations not only suppress this position-effect variegation, but also cause recessive embryonic lethality. In this study, we analyze the latter phenotype in the hope of gaining insight into heterochromatin function. In our analyses of four alleles of Suppressor of variegation2-5, the lethality was found to be associated with defects in chromosome morphology and segregation. While some of these defects are seen throughout embryonic development, both the frequency and severity of the defects are greatest between cycles 10 and 14 when zygotic transcription of the Suppressor of variegation2-5 gene apparently begins. By this time in development, heterochromatin protein 1 levels are diminished by four-fold in a quarter of the embryos produced by parents that are both heterozygous for a null allele (Suppressor of variegation2-5(05)). In a live analysis of the phenotype, we find prophase to be lengthened by more than two-fold in Suppressor of variegation2-5(05) mutant embryos with subsequent defects in chromosome segregation. The elongated prophase suggests that the segregation phenotype is a consequence of defects in events that occur during prophase, either in chromosome condensation or kinetochore assembly or function. Immunostaining with an antibody against a centromerespecific antigen indicates that the kinetochores of most chromosomes are functional. The immunostaining results are more consistent with defects in chromosome condensation being responsible for the segregation phenotype.

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

scholarly journals Isolation of a gene encoding a functional zinc finger protein homologous to erythroid Krüppel-like factor: identification of a new multigene family.

1995 ◽  
Vol 15 (11) ◽  
pp. 5957-5965 ◽  
Author(s):  
K P Anderson ◽  
C B Kern ◽  
S C Crable ◽  
J B Lingrel
Keyword(s):  
Dna Binding ◽  
Binding Site ◽  
Zinc Finger ◽  
Reporter Gene ◽  
Zinc Finger Protein ◽  
Erythroid Cell ◽  
Specific Gene ◽  
Beta Globin ◽  
Gene Encoding ◽  
Hybridization Probe

We have identified and characterized the gene for a novel zinc finger transcription factor which we have termed lung Krüppel-like factor (LKLF). LKLF was isolated through the use of the zinc finger domain of erythroid Krüppel-like factor (ELKF) as a hybridization probe and is closely related to this erythroid cell-specific gene. LKLF is expressed in a limited number of tissues, with the predominant expression seen in the lungs and spleen. The gene is developmentally controlled, with expression noted in the 7-day embryo followed by a down-regulation at 11 days and subsequent reactivation. A high degree of similarity is noted in the zinc finger regions of LKLF and EKLF. Beyond this domain, the sequences diverge significantly, although the putative transactivation domains for both LKLF and EKLF are proline-rich regions. In the DNA-binding domain, the three zinc finger motifs are so closely conserved that the predicted DNA contact sites are identical, suggesting that both proteins may bind to the same core sequence. This was further suggested by transactivation assays in which mouse fibroblasts were transiently transfected with a human beta-globin reporter gene in the absence and presence of an LKLF cDNA construct. Expression of the LKLF gene activates this human beta-globin promoter containing the CACCC sequence previously shown to be a binding site for EKLF. Mutation of this potential binding site results in a significant reduction in the reporter gene expression. LKLF and EKLF can thus be grouped as members of a unique family of transcription factors which have discrete patterns of expression in different tissues and which appear to recognize the same DNA-binding site.

scholarly journals Identification of Zfp393, a germ cell-specific gene encoding a novel zinc finger protein

2002 ◽  
Vol 118 (1-2) ◽  
pp. 233-239 ◽  
Author(s):  
Wei Yan ◽  
Kathleen H Burns ◽  
Lang Ma ◽  
Martin M Matzuk
Keyword(s):  
Germ Cell ◽  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Specific Gene ◽  
Gene Encoding ◽  
Finger Protein

Dynamics and stability: epigenetic conversions in position effect variegation

2013 ◽  
Vol 91 (1) ◽  
pp. 6-13 ◽  
Author(s):  
Krassimir Yankulov
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Position Effect ◽  
Specific Gene ◽  
Position Effect Variegation ◽  
Human Pathogens ◽  
Dynamic Nature ◽  
Host Environment ◽  
Effect Variegation ◽  
Transcription And Replication

Position effect variegation (PEV) refers to quasi-stable patterns of gene expression that are observed at specific loci throughout the genomes of eukaryotes. The genes subjected to PEV can be completely silenced or fully active. Stochastic conversions between these 2 states are responsible for the variegated phenotypes. Positional variegation is used by human pathogens (Trypanosoma, Plasmodium, and Candida) to evade the immune system or adapt to the host environment. In the yeasts Saccharomyces cerevisiae and S accharomyces pombe, telomeric PEV aids the adaptation to a changing environment. In metazoans, similar epigenetic conversions are likely to accompany cell differentiation and the setting of tissue-specific gene expression programs. Surprisingly, we know very little about the mechanisms of epigenetic conversions. In this article, earlier models on the nature of PEV are revisited and recent advances on the dynamic nature of chromatin are reviewed. The normal dynamic histone turnover during transcription and DNA replication and its perturbation at transcription and replication pause sites are discussed. It is proposed that such perturbations play key roles in epigenetic conversions and in PEV.

scholarly journals On the relations of phase separation and Hi-C maps to epigenetics

2020 ◽  
Vol 7 (3) ◽  
pp. 191976 ◽  
Author(s):  
Prim B. Singh ◽  
Andrew G. Newman
Keyword(s):  
Phase Separation ◽  
Constitutive Heterochromatin ◽  
Position Effect ◽  
Embryonic Stem ◽  
Position Effect Variegation ◽  
Heterochromatin Protein 1 ◽  
Modified Dna ◽  
Contact Frequency ◽  
Evolutionarily Conserved ◽  
Pluripotent Embryonic Stem Cell

The relationship between compartmentalization of the genome and epigenetics is long and hoary. In 1928, Heitz defined heterochromatin as the largest differentiated chromatin compartment in eukaryotic nuclei. Müller's discovery of position-effect variegation in 1930 went on to show that heterochromatin is a cytologically visible state of heritable (epigenetic) gene repression. Current insights into compartmentalization have come from a high-throughput top-down approach where contact frequency (Hi-C) maps revealed the presence of compartmental domains that segregate the genome into heterochromatin and euchromatin. It has been argued that the compartmentalization seen in Hi-C maps is owing to the physiochemical process of phase separation. Oddly, the insights provided by these experimental and conceptual advances have remained largely silent on how Hi-C maps and phase separation relate to epigenetics. Addressing this issue directly in mammals, we have made use of a bottom-up approach starting with the hallmarks of constitutive heterochromatin, heterochromatin protein 1 (HP1) and its binding partner the H3K9me2/3 determinant of the histone code. They are key epigenetic regulators in eukaryotes. Both hallmarks are also found outside mammalian constitutive heterochromatin as constituents of larger (0.1–5 Mb) heterochromatin -like domains and smaller (less than 100 kb) complexes. The well-documented ability of HP1 proteins to function as bridges between H3K9me2/3-marked nucleosomes contributes to polymer–polymer phase separation that packages epigenetically heritable chromatin states during interphase. Contacts mediated by HP1 ‘bridging’ are likely to have been detected in Hi-C maps, as evidenced by the B4 heterochromatic subcompartment that emerges from contacts between large KRAB-ZNF heterochromatin -like domains. Further, mutational analyses have revealed a finer, innate, compartmentalization in Hi-C experiments that probably reflect contacts involving smaller domains/complexes. Proteins that bridge (modified) DNA and histones in nucleosomal fibres—where the HP1–H3K9me2/3 interaction represents the most evolutionarily conserved paradigm—could drive and generate the fundamental compartmentalization of the interphase nucleus. This has implications for the mechanism(s) that maintains cellular identity, be it a terminally differentiated fibroblast or a pluripotent embryonic stem cell.

scholarly journals A Krüppel-Associated Box-Zinc Finger Protein, NT2, Represses Cell-Type-Specific Promoter Activity of the α2(XI) Collage Gene

2006 ◽  
Vol 26 (21) ◽  
pp. 8215-8216
Author(s):  
Kazuhiro Tanaka ◽  
Noriyuki Tsumaki ◽  
Christine A. Kozak ◽  
Yoshihiro Matsumoto ◽  
Fumihiko Nakatani ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Promoter Activity ◽  
Zinc Finger Protein ◽  
Cell Type ◽  
Finger Protein ◽  
Cell Type Specific
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