scholarly journals A role of polycomb group genes in the regulation of gap gene expression in Drosophila.

Genetics ◽  
1994 ◽  
Vol 136 (4) ◽  
pp. 1341-1353 ◽  
Author(s):  
F Pelegri ◽  
R Lehmann
Keyword(s):  
Gene Expression ◽  
Small Region ◽  
Early Embryo ◽  
Polycomb Group ◽  
Drosophila Embryo ◽  
Polycomb Group Genes ◽  
Gap Gene ◽  
Anteroposterior Polarity

Abstract Anteroposterior polarity of the Drosophila embryo is initiated by the localized activities of the maternal genes, bicoid and nanos, which establish a gradient of the hunchback (hb) morphogen. nanos determines the distribution of the maternal Hb protein by regulating its translation. To identify further components of this pathway we isolated suppressors of nanos. In the absence of nanos high levels of Hb protein repress the abdomen-specific genes knirps and giant. In suppressor-of-nanos mutants, knirps and giant are expressed in spite of high Hb levels. The suppressors are alleles of Enhancer of zeste (E(z)) a member of the Polycomb group (Pc-G) of genes. We show that E(z), and likely other Pc-G genes, are required for maintaining the expression domains of knirps and giant initiated by the maternal Hb protein gradient. We have identified a small region of the knirps promoter that mediates the regulation by E(z) and hb. Because Pc-G genes are thought to control gene expression by regulating chromatin, we propose that imprinting at the chromatin level underlies the determination of anteroposterior polarity in the early embryo.

Mutually repressive interactions between the gap genes giant and Kruppel define middle body regions of the Drosophila embryo

Development ◽  
1991 ◽  
Vol 111 (2) ◽  
pp. 611-621 ◽  
Author(s):  
R. Kraut ◽  
M. Levine
Keyword(s):  
Gene Expression ◽  
Weak Interactions ◽  
Ectopic Expression ◽  
Early Embryo ◽  
Drosophila Embryo ◽  
Regulatory Interactions ◽  
Gap Gene ◽  
Gap Genes ◽  
Body Regions ◽  
Bona Fide

The gap genes play a key role in establishing pair-rule and homeotic stripes of gene expression in the Drosophila embryo. There is mounting evidence that overlapping gradients of gap gene expression are crucial for this process. Here we present evidence that the segmentation gene giant is a bona fide gap gene that is likely to act in concert with hunchback, Kruppel and knirps to initiate stripes of gene expression. We show that Kruppel and giant are expressed in complementary, non-overlapping sets of cells in the early embryo. These complementary patterns depend on mutually repressive interactions between the two genes. Ectopic expression of giant in early embryos results in the selective repression of Kruppel, and advanced-stage embryos show cuticular defects similar to those observed in Kruppel- mutants. This result and others suggest that the strongest regulatory interactions occur among those gap genes expressed in nonadjacent domains. We propose that the precisely balanced overlapping gradients of gap gene expression depend on these strong regulatory interactions, coupled with weak interactions between neighboring genes.

Two distinct mechanisms for differential positioning of gene expression borders involving the Drosophila gap protein giant

Development ◽  
1998 ◽  
Vol 125 (19) ◽  
pp. 3765-3774 ◽  
Author(s):  
X. Wu ◽  
R. Vakani ◽  
S. Small
Keyword(s):  
Target Genes ◽  
Early Embryo ◽  
Drosophila Embryo ◽  
Anterior Border ◽  
Gap Gene ◽  
Gap Genes ◽  
Pair Rule Gene ◽  
Differential Positioning ◽  
Pair Rule

We have combined genetic experiments and a targeted misexpression approach to examine the role of the gap gene giant (gt) in patterning anterior regions of the Drosophila embryo. Our results suggest that gt functions in the repression of three target genes, the gap genes Kruppel (Kr) and hunchback (hb), and the pair-rule gene even-skipped (eve). The anterior border of Kr, which lies 4–5 nucleus diameters posterior to nuclei that express gt mRNA, is set by a threshold repression mechanism involving very low levels of gt protein. In contrast, gt activity is required, but not sufficient for formation of the anterior border of eve stripe 2, which lies adjacent to nuclei that express gt mRNA. We propose that gt's role in forming this border is to potentiate repressive interaction(s) mediated by other factor(s) that are also localized to anterior regions of the early embryo. Finally, gt is required for repression of zygotic hb expression in more anterior regions of the embryo. The differential responses of these target genes to gt repression are critical for the correct positioning and maintenance of segmentation stripes, and normal anterior development.

Determination of spatial domains of zygotic gene expression in the Drosophila embryo by the affinity of binding sites for the bicoid morphogen

Nature ◽  
1989 ◽  
Vol 340 (6232) ◽  
pp. 363-367 ◽  
Author(s):  
Wolfgang Driever ◽  
Gudrun Thoma ◽  
Christiane Nüsslein-Volhard
Keyword(s):  
Gene Expression ◽  
Binding Sites ◽  
Drosophila Embryo ◽  
Zygotic Gene ◽  
Spatial Domains

Targeting gene expression to the head: the Drosophila orthodenticle gene is a direct target of the Bicoid morphogen

Development ◽  
1998 ◽  
Vol 125 (21) ◽  
pp. 4185-4193 ◽  
Author(s):  
Q. Gao ◽  
R. Finkelstein
Keyword(s):  
Gene Expression ◽  
Target Genes ◽  
Regulatory Element ◽  
Regulatory Region ◽  
Repeated Sequence ◽  
Drosophila Embryo ◽  
Sequence Motif ◽  
Specific Expression ◽  
Gap Gene

The Bicoid (Bcd) morphogen establishes the head and thorax of the Drosophila embryo. Bcd activates the transcription of identified target genes in the thoracic segments, but its mechanism of action in the head remains poorly understood. It has been proposed that Bcd directly activates the cephalic gap genes, which are the first zygotic genes to be expressed in the head primordium. It has also been suggested that the affinity of Bcd-binding sites in the promoters of Bcd target genes determines the posterior extent of their expression (the Gene X model). However, both these hypotheses remain untested. Here, we show that a small regulatory region upstream of the cephalic gap gene orthodenticle (otd) is sufficient to recapitulate early otd expression in the head primordium. This region contains two control elements, each capable of driving otd-like expression. The first element has consensus Bcd target sites that bind Bcd in vitro and are necessary for head-specific expression. As predicted by the Gene X model, this element has a relatively low affinity for Bcd. Surprisingly, the second regulatory element has no Bcd sites. Instead, it contains a repeated sequence motif similar to a regulatory element found in the promoters of otd-related genes in vertebrates. Our study is the first demonstration that a cephalic gap gene is directly regulated by Bcd. However, it also shows that zygotic gene expression can be targeted to the head primordium without direct Bcd regulation.

scholarly journals Gene expression profile of a selection of Polycomb Group genes during zebrafish embryonic and germ line development

PLoS ONE ◽  
2018 ◽  
Vol 13 (7) ◽  
pp. e0200316 ◽  
Author(s):  
Naomi D. Chrispijn ◽  
Karolina M. Andralojc ◽  
Charlotte Castenmiller ◽  
Leonie M. Kamminga
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Germ Line ◽  
Polycomb Group ◽  
Polycomb Group Genes ◽  
Selection Of

P–181 Morphine regulates BMP4 growth factor and is involved in in-vitro early embryo development and PGCs formation

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
I Muñoa ◽  
M Araolaza-Lasa ◽  
I Urizar-Arenaza ◽  
M Gianzo Citores ◽  
N Subiran Ciudad
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Environmental Factors ◽  
Embryo Development ◽  
Early Embryo ◽  
Epigenetic Changes ◽  
Morphine Treatment ◽  
Early Embryo Development

Abstract Study question To elucidate if morphine can alter embryo development. Summary answer Chronic morphine treatment regulates BMP4 growth factor, in terms of gene expression and H3K27me3 enrichment and promotes in-vitro blastocysts development and PGC formation. What is known already BMP4 is a member of the bone morphogenetic protein family, which acts mainly through SMAD dependent pathway, to play an important role in early embryo development. Indeed, BMP4 enhances pluripotency in mouse embryonic stem cells (mESCs) and, specifically, is involved in blastocysts formation and primordial germ cells (PGCs) generation. Although, external morphine influence has been previously reported on the early embryo development, focus on implantation and uterus function, there is a big concern in understanding how environmental factors can cause stable epigenetic changes, which could be maintained during development and lead to health problems. Study design, size, duration First, OCT4-reported mESCs were chronically treated with morphine during 24h, 10–5mM. After morphine removal, mESCs were collected for RNA-seq and H3K27me3 ChIP-seq study. To elucidate the role of morphine in early embryo development, two cell- embryos stage were chronically treated with morphine for 24h and in-vitro cultured up to the blastocyst stage in the absence of morphine. Furthermore, after morphine treatment mESCs were differentiated to PGCs, to elucidate the role of morphine in PGC differentiation. Participants/materials, setting, methods Transcriptomic analyses and H3K27me3 genome wide distribution were carried out by RNA-Sequencing and Chip-Sequencing respectively. Validations were performed by RNA-RT-qPCR and Chip-RT-qPCR. Main results and the role of chance Dynamic transcriptional analyses identified a total of 932 differentially expressed genes (DEGs) after morphine treatment on mESCs, providing strong evidence of a transcriptional epigenetic effect induced by morphine. High-throughput screening approaches showed up Bmp4 as one of the main morphine targets on mESCs. Morphine caused an up-regulation of Bmp4 gene expression together with a decrease of H3K27me3 enrichment at promoter level. However, no significant differences were observed on gene expression and H3K27me3 enrichment on BMP4 signaling pathway components (such as Smad1, Smad4, Smad5, Smad7, Prdm1 and Prmd14) after morphine treatment. On the other hand, the Bmp4 gene expression was also up-regulated in in-vitro morphine treated blastocyst and in-vitro morphine treated PGCs. These results were consistent with the increase in blastocyst rate and PGC transformation rate observed after morphine chronic treatment. Limitations, reasons for caution To perform the in-vitro analysis. Further studies are needed to describe the whole signaling pathways underlying BMP4 epigenetic regulation after morphine treatment. Wider implications of the findings: Our findings confirmed that mESCs and two-cell embryos are able to memorize morphine exposure and promote both blastocyst development and PGCs formation through potentially BMP4 epigenetic regulation. These results provide insights understanding how environmental factors can cause epigenetic changes during the embryo development, leading to alterations and producing health problems/diseases Trial registration number Not applicable

The Expression of Polycomb Group Genes Products, Bmi1 and Mel-18, Regulate the Function of Murine Primitive Hematopoietic Cells.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 1261-1261
Author(s):  
Teruyuki Kajiume ◽  
Takashi Sato ◽  
Masao Kobayashi
Keyword(s):  
Gene Expression ◽  
Hematopoietic Cells ◽  
Inverse Function ◽  
Complex Form ◽  
Negative Control ◽  
Polycomb Group ◽  
Self Renewal ◽  
Hematopoietic Stem ◽  
Polycomb Group Genes ◽  
Marrow Cells

Abstract The Polycomb group (PcG) genes (bmi1 and mel-18) known as negative control factors of the Hox gene is thought to regulate the differentiation and self-renewal of hematopoietic stem cells (HSCs). The loss of mel-18 results in the promotion of HSC self-renewal, and the increase of mel-18 expression inversely leads to the differentiation of HSCs. On the other hand, the loss of bmi1 does not lead to self-renewal activity of HSCs. In this study we examined the effect of expression of bmi1 and mel-18 on the role of function in murine HSCs. Lineage-negative, Sca1-positive, and cKit-positive primitive hematopoietic cells were purified and the expression of PcG protein was evaluated from the intra-nuclear distribution of PcG proteins. The Bmi1-positive hematopoietic cells barely contained Mel-18, and the Mel-18-positive cells barely contained Bmi1. the frequency of positive cells for both Bmi1 and Mel-18 was less than 0.5% of purified primitive hematopoietic cells. The expression levels of the PcG genes, bmi1 and mel-18, in HSCs were knocked down by siRNA and then gene expression was assessed by quantitative real-time PCR. The introduction of siRNA against bmi1 or mell-18 resulted in approximate 50 to 60% decrease of each gene expression without affecting another gene expression. Primary colony-forming activity of knocked down cells in response to stem cell factor, thrombopoietin and the ligand for flt3 was not affected by the induction of siRNA. However, secondary colony-forming activity from primary colony-forming cells in bmi1-knockdown cells was significantly decreased when compared with that of control cells. Conversely, the mel-18-knockdown cells significantly increased, suggesting that mel-18-knockdown cells are capable of proliferating activity. Finally, bone marrow reconstitutive activity was examined by using Ly5.1 and Ly5.2 system. While the bmi1-knockdown marrow cells decreased the reconstitutive activity, the mel-18-knockdown marrow cells showed the increase of engraftment activity after 6 months of transplantation. From these results, we consider that mel-18 and bmi1 have reciprocal functions in HSCs. Mammalian PcG protein complexes can be classified into two distinct types, Polycomb repressive complexes 1 and 2 (PRC1 and PRC2). The Mel-18 protein is a constituent of mammalian PRC1 together with M33, Bmi1 or rae28, and Scmh1. The Mel-18 protein is composed of 342 amino acids and the N-terminal region of the 102 amino acid, which includes the RING finger motif, shares 93% homology with Bmi1 protein. In addition, its secondary structure shows high homology with the Mel-18 and Bmi1 proteins. We hypothesized that the opposite function is expressed in HSCs because Mel-18 and Bmi1 share the same structure and compete when in the complex form. These results suggest that mel-18 and bmi1 have inverse function in HSCs and that the balance of Bmi1 and Mel-18 may regulate the fate of self-renewal and differentiation in HSCs.

scholarly journals Molecular characterisation of the Polycomblike gene of Drosophila melanogaster, a trans-acting negative regulator of homeotic gene expression

Development ◽  
1994 ◽  
Vol 120 (9) ◽  
pp. 2629-2636 ◽  
Author(s):  
A. Lonie ◽  
R. D'Andrea ◽  
R. Paro ◽  
R. Saint
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Polycomb Group ◽  
Negative Regulator ◽  
Homeotic Gene ◽  
Homeotic Genes ◽  
Molecular Characterisation ◽  
Polycomb Group Proteins ◽  
Polycomb Group Genes ◽  
Homeotic Gene Expression

The Polycomblike gene of Drosophila melanogaster, a member of the Polycomb Group of genes, is required for the correct spatial expression of the homeotic genes of the Antennapaedia and Bithorax Complexes. Mutations in Polycomb Group genes result in ectopic homeotic gene expression, indicating that Polycomb Group proteins maintain the transcriptional repression of specific homeotic genes in specific tissues during development. We report here the isolation and molecular characterisation of the Polycomblike gene. The Polycomblike transcript encodes an 857 amino acid protein with no significant homology to other proteins. Antibodies raised against the product of this open reading frame were used to show that the Polycomblike protein is found in all nuclei during embryonic development. Antibody staining also revealed that the Polycomblike protein is found on larval salivary gland polytene chromosomes at about 100 specific loci, the same loci to which the Polycomb and polyhomeotic proteins, two other Polycomb Group proteins, are found. These data add further support for a model in which Polycomb Group proteins form multimeric protein complexes at specific chromosomal loci to repress transcription at those loci.

Sign in / Sign up

Export Citation Format

Share Document