scholarly journals The Function of the Broad-Complex During Drosophila melanogaster Oogenesis

Genetics ◽  
1999 ◽  
Vol 153 (3) ◽  
pp. 1371-1383
Author(s):  
George Tzolovsky ◽  
Wu-Min Deng ◽  
Thomas Schlitt ◽  
Mary Bownes
Keyword(s):  
Gene Expression ◽  
Dna Replication ◽  
Zinc Finger ◽  
Target Genes ◽  
Ectopic Expression ◽  
Follicle Cells ◽  
Chorion Genes ◽  
Broad Complex ◽  
Late Expression

Abstract The Broad-Complex (BR-C) is an early ecdysone response gene that functions during metamorphosis and encodes a family of zinc-finger transcription factors. It is expressed in a dynamic pattern during oogenesis. Its late expression in the lateral-dorsal-anterior follicle cells is related to the morphogenesis of the chorionic appendages. All four zinc-finger isoforms are expressed in oogenesis, which is consistent with the abnormal appendage phenotypes resulting from their ectopic expression. We investigated the mechanism by which the BR-C affects chorion deposition by using BrdU to follow the effects of BR-C misexpression on DNA replication and in situ hybridization to ovarian mRNA to evaluate chorion gene expression. Ectopic BR-C expression leads to prolonged endoreplication and to additional amplification of genes, besides the chorion genes, at other sites in the genome. The pattern of chorion gene expression is not affected along the anterior-posterior axis, but the follicle cells at the anterior of the oocyte fail to migrate correctly in an anterior direction when BR-C is misexpressed. We conclude that the target genes of the BR-C in oogenesis include a protein essential for endoreplication and chorion gene amplification. This may provide a link between steroid hormones and the control of DNA replication during oogenesis.

Sonic hedgehog is not required for polarising activity in the Doublefoot mutant mouse limb bud

Development ◽  
1998 ◽  
Vol 125 (3) ◽  
pp. 351-357 ◽  
Author(s):  
C. Hayes ◽  
J.M. Brown ◽  
M.F. Lyon ◽  
G.M. Morriss-Kay
Keyword(s):  
Gene Expression ◽  
Limb Development ◽  
Target Genes ◽  
Anterior Part ◽  
Expression Patterns ◽  
Ectopic Expression ◽  
Mutant Gene ◽  
Limb Bud ◽  
Active Constituent ◽  
Limb Buds

The mouse mutant Doublefoot (Dbf) shows preaxial polydactyly of all four limbs. We have analysed limb development in this mutant with respect to morphogenesis, gene expression patterns and ectopic polarising activity. The results reveal a gain-of-function mutation at a locus that mediates pattern formation in the developing limb. Shh expression is identical with that of wild-type embryos, i.e. there is no ectopic expression. However, mesenchyme from the anterior aspects of Dbf/+ mutant limb buds, when transplanted to the anterior side of chick wing buds, induces duplication of the distal skeletal elements. Mid-distal mesenchymal transplants from early, but not later, Dbf/+ limb buds are also able to induce duplication. This demonstration of polarising activity in the absence of Shh expression identifies the gene at the Dbf locus as a new genetic component of the Shh signalling pathway, which (at least in its mutated form) is able to activate signal transduction independently of Shh. The mutant gene product is sufficient to fulfil the signalling properties of Shh including upregulation of the direct Shh target genes Ptc and Gli, and induction of the downstream target genes Bmp2, Fgf4 and Hoxd13. The expression domains of all these genes extend from their normal posterior domains into the anterior part of the limb bud without being focused on a discrete ectopic site. These observations dissociate polarising activity from Shh gene expression in the Dbf/+ limb bud. We suggest that the product of the normal Dbf gene is a key active constituent of the polarising region, possibly acting in the extracellular compartment.

Sequential activation of the EGF receptor pathway during Drosophila oogenesis establishes the dorsoventral axis

Development ◽  
1998 ◽  
Vol 125 (2) ◽  
pp. 191-200 ◽  
Author(s):  
A. Sapir ◽  
R. Schweitzer ◽  
B.Z. Shilo
Keyword(s):  
Target Genes ◽  
Egf Receptor ◽  
Ectopic Expression ◽  
Follicle Cell ◽  
Follicle Cells ◽  
Cell Fates ◽  
Dorsoventral Axis ◽  
Spatial Coordinates ◽  
Sequential Activation

Previous work has demonstrated a role for the Drosophila EGF receptor (Torpedo/DER) and its ligand, Gurken, in the determination of anterioposterior and dorsoventral axes of the follicle cells and oocyte. The roles of DER in establishing the polarity of the follicle cells were examined further, by following the expression of DER-target genes. One class of genes (e.g. kekon) is induced by the DER pathway at all stages. Broad expression of kekon at the stage in which the follicle cells migrate posteriorly over the oocyte, demonstrates the capacity of the pathway to pattern all follicle cells except the ventral-most rows. This may provide the spatial coordinates for the ventral-most follicle cell fates. A second group of target genes (e.g. rhomboid (rho)) is induced only at later stages of oogenesis, and may require additional inputs by signals emanating from the anterior, stretch follicle cells. The function of Rho was analyzed by ectopic expression in the stretch follicle cells, and shown to induce a non-autonomous dorsalizing activity that is independent of Gurken. Rho thus appears to be involved in processing a DER ligand in the follicle cells, to pattern the egg chamber and allow persistent activation of the DER pathway during formation of the dorsal appendages.

scholarly journals A plethora of plant serine/arginine-rich proteins: redundancy or evolution of novel gene functions?

2004 ◽  
Vol 32 (4) ◽  
pp. 561-564 ◽  
Author(s):  
M. Kalyna ◽  
A. Barta
Keyword(s):  
Gene Expression ◽  
Target Genes ◽  
Environmental Control ◽  
Expression Patterns ◽  
Ectopic Expression ◽  
Sr Proteins ◽  
Sr Protein ◽  
Duplication Events ◽  
Intron Recognition ◽  
Alternatively Spliced

Precursor-mRNA (pre-mRNA) processing is an important step in gene expression and its regulation leads to the expansion of the gene product repertoire. SR (serine-arginine)-rich proteins are key players in intron recognition and spliceosome assembly and significantly contribute to the alternative splicing process. Due to several duplication events, at least 19 SR proteins are present in the Arabidopsis genome, which is almost twice as many as in humans. They fall into seven different subfamilies, three of them homologous with metazoan splicing factors, whereas the other four seem to be specific for plants. The current results show that most of the duplicated genes have different spatiotemporal expression patterns indicating functional diversification. Interestingly, most of the SR protein genes are alternatively spliced and in some cases this process was shown to be under developmental and/or environmental control. This might greatly influence gene expression of target genes as also exemplified by ectopic expression studies of particular SR proteins.

scholarly journals DUX4 expressing immortalized FSHD lymphoblastoid cells express genes elevated in FSHD muscle biopsies, correlating with the early stages of inflammation

2020 ◽  
Vol 29 (14) ◽  
pp. 2285-2299 ◽  
Author(s):  
Christopher R S Banerji ◽  
Maryna Panamarova ◽  
Peter S Zammit
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Target Gene ◽  
Target Genes ◽  
Ectopic Expression ◽  
Lymphoblastoid Cell Lines ◽  
Immune Gene ◽  
Target Gene Expression ◽  
Early Stages ◽  
Muscle Biopsies

Abstract Facioscapulohumeral muscular dystrophy (FSHD) is an incurable disorder linked to ectopic expression of DUX4. However, DUX4 is notoriously difficult to detect in FSHD muscle cells, while DUX4 target gene expression is an inconsistent biomarker for FSHD skeletal muscle biopsies, displaying efficacy only on pathologically inflamed samples. Immune gene misregulation occurs in FSHD muscle, with DUX4 target genes enriched for those associated with inflammatory processes. However, there lacks an assessment of the FSHD immune cell transcriptome, and its contribution to gene expression in FSHD muscle biopsies. Here, we show that EBV-immortalized FSHD lymphoblastoid cell lines express DUX4 and both early and late DUX4 target genes. Moreover, a biomarker of 237 up-regulated genes derived from FSHD lymphoblastoid cell lines is elevated in FSHD muscle biopsies compared to controls. The FSHD Lymphoblast score is unaltered between FSHD myoblasts/myotubes and their controls however, implying a non-myogenic cell source in muscle biopsies. Indeed, the FSHD Lymphoblast score correlates with the early stages of muscle inflammation identified by histological analysis on muscle biopsies, while our two late DUX4 target gene expression biomarkers associate with macroscopic inflammation detectable via MRI. Thus, FSHD lymphoblastoid cell lines express DUX4 and early and late DUX4 target genes, therefore, muscle-infiltrated immune cells may contribute the molecular landscape of FSHD muscle biopsies.

Drosophila chorion gene amplification requires an upstream region regulating s18 transcription

1986 ◽  
Vol 6 (12) ◽  
pp. 4624-4633
Author(s):  
T L Orr-Weaver ◽  
A C Spradling
Keyword(s):  
Gene Expression ◽  
Ovarian Follicle ◽  
Follicle Cells ◽  
Upstream Region ◽  
Transcription Control ◽  
The Third ◽  
Chorion Genes ◽  
Specific Amplification ◽  
Essential Region ◽  
Per Se

A cluster of Drosophila melanogaster chorion genes at locus 66D on the third chromosome amplifies 60-fold in the ovarian follicle cells prior to the onset of gene expression. A 3.8-kilobase (kb) region of the gene cluster can induce tissue-specific amplification in transformants. Previous models postulated that amplification is activated in follicle cells by transcription of one of the two chorion genes (s15 and s18) located within the 3.8-kb essential region. In this study, we showed that neither s15 nor s18 chorion gene transcription was required for amplification. However, a 510-bp region upstream from s18 contained sequences essential for both amplification and s18 transcription. No other region within the 3.8-kb fragment was required for amplification. We propose that upstream transcription control elements rather than transcription per se are involved in controlling amplification during development.

Organization of regionally expressed silkmoth chorion genes

1986 ◽  
Vol 6 (9) ◽  
pp. 3215-3220
Author(s):  
A K Hatzopoulos ◽  
J C Regier
Keyword(s):  
Gene Expression ◽  
Follicle Cells ◽  
Gene Copy ◽  
Late Period ◽  
Chorion Genes ◽  
Copy Numbers ◽  
Total Dna ◽  
Dna Strand ◽  
Gene Copy Numbers ◽  
Silkmoth Chorion

We described the organization of two silkmoth chorion genes, called E1 and E2, whose expression is largely restricted in time to the very late period of choriogenesis and in space to one of two major subpopulations of follicle cells. Using E1 and E2 clone cDNAs as probes, we showed that gene copy numbers per haploid genome remain constant throughout silkmoth development despite major changes in total DNA content per nucleus. Furthermore, gene copy numbers are the same in both cellular regions of the choriogenic follicle despite differences in nuclear size and levels of E gene expression. Southern analysis indicated between two and four copies each for E1 and E2 genes. Analysis of chromosomal clones showed that single copies of E1 and E2 are separated by about 7.5 kilobases and are transcribed from the same DNA strand. Two distinct pairs of cloned E1 and E2 genes were characterized. No other chorion genes were in their immediate vicinity.

Blocking cell division does not remove the requirement for Polycomb function in Drosophila embryogenesis

Development ◽  
1990 ◽  
Vol 110 (4) ◽  
pp. 1319-1325 ◽  
Author(s):  
A.P. Gould ◽  
R.Y. Lai ◽  
M.J. Green ◽  
R.A. White
Keyword(s):  
Gene Expression ◽  
Cell Division ◽  
Dna Replication ◽  
Ectopic Expression ◽  
Homeotic Gene ◽  
Germ Band ◽  
Drosophila Embryogenesis ◽  
Stable Transmission ◽  
Homeotic Gene Expression

The Polycomb (Pc) gene is required from the extended germ band stage onwards, to maintain spatially restricted patterns of homeotic gene expression. It has been thought to be involved in the ‘stable inheritance of the determined state’. In this paper, we have tested the notion that the Pc gene is required specifically during or after DNA replication to enable the stable transmission of states of gene activity. We found that arresting cell division using the string mutation or blocking DNA replication with aphidicolin failed to prevent ectopic expression of the homeotic gene Ultrabithorax in Pc mutants. Thus, even in the absence of DNA replication, Pc is required to maintain spatially restricted patterns of homeotic gene expression. The role of the Pc gene product in the stable repression of homeotic gene transcription is discussed.

scholarly journals Ten-Eleven Translocation 1 (Tet1) Is Regulated by O-Linked N-Acetylglucosamine Transferase (Ogt) for Target Gene Repression in Mouse Embryonic Stem Cells

2013 ◽  
Vol 288 (29) ◽  
pp. 20776-20784 ◽  
Author(s):  
Feng-Tao Shi ◽  
Hyeung Kim ◽  
Weisi Lu ◽  
Quanyuan He ◽  
Dan Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Large Scale ◽  
Target Genes ◽  
Es Cells ◽  
Ectopic Expression ◽  
Embryonic Stem ◽  
Dna Demethylation ◽  
Mouse Es Cells ◽  
Chromatin Regulators ◽  
Glcnac Transferase

As a member of the Tet (Ten-eleven translocation) family proteins that can convert 5-methylcytosine (5mC) to 5-hydroxylmethylcytosine (5hmC), Tet1 has been implicated in regulating global DNA demethylation and gene expression. Tet1 is highly expressed in embryonic stem (ES) cells and appears primarily to repress developmental genes for maintaining pluripotency. To understand how Tet1 may regulate gene expression, we conducted large scale immunoprecipitation followed by mass spectrometry of endogenous Tet1 in mouse ES cells. We found that Tet1 could interact with multiple chromatin regulators, including Sin3A and NuRD complexes. In addition, we showed that Tet1 could also interact with the O-GlcNAc transferase (Ogt) and be O-GlcNAcylated. Depletion of Ogt led to reduced Tet1 and 5hmC levels on Tet1-target genes, whereas ectopic expression of wild-type but not enzymatically inactive Ogt increased Tet1 levels. Mutation of the putative O-GlcNAcylation site on Tet1 led to decreased O-GlcNAcylation and level of the Tet1 protein. Our results suggest that O-GlcNAcylation can positively regulate Tet1 protein concentration and indicate that Tet1-mediated 5hmC modification and target repression is controlled by Ogt.

scholarly journals Mutations in SIX1 associated with Branchio-oto-renal Syndrome (BOR) differentially affect otic expression of putative target genes

2021 ◽  
Author(s):  
Tanya Mehdizadeh ◽  
Himani Datta Majumdar ◽  
Sahra Ahsan ◽  
Andre Luiz Pasqua Tavares ◽  
Sally A Moody
Keyword(s):  
Gene Expression ◽  
Target Genes ◽  
Otic Vesicle ◽  
Wild Type ◽  
Single Nucleotide ◽  
Putative Target ◽  
Individual Effects ◽  
Factor Interactions ◽  
Ability To Drive

Single nucleotide mutations in SIX1 are causative in some individuals diagnosed with branchiootic/branchio-oto-renal (BOR) syndrome. To test whether these mutations have differential effects on otic gene expression, we engineered four BOR mutations in Xenopus six1 and targeted mutant protein expression to the neural crest and cranial placode precursor cells in wild-type embryos. Changes in the otic expression of putative Six1 targets and/or co-factors were monitored by qRT-PCR and in situ hybridization. We found that each mutant had a different combination of effects. The V17E mutant reduced eya2, tspan13, zbtb16 and pa2g4 otic vesicle expression at a frequency indistinguishable from wildtype Six1, but reduced prdm1 more and spry1 less compared to wild-type Six1. For most of these genes, the R110W, W122R and Y129C mutants were significantly less repressive compared to wild-type Six1. Their individual effects varied according to the level at which they were expressed. The R110W, W122R and Y129C mutants also often expanded prdm1 otic expression. Since previous studies showed that all four mutants are transcriptionally deficient and differ in their ability to interact with co-factors such as Eya1, we propose that altered co-factor interactions at the mutated sites differentially interfere with their ability to drive otic gene expression.

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