Activation of Ftz-F1-responsive genes through Ftz/Ftz-F1 dependent enhancers
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE87342 | GEO | 2016/09/27
SECONDARY ACCESSION(S): PRJNA344461
REPOSITORIES: GEO
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Project description:Ftz-f1 (Fushi tarazu transcription factor 1) is an orphan member of the nuclear hormone receptor superfamily, with one of its transcriptional variant (βFtz-f) being homolog of the vertebrate SF1. Ftz-f1 gene is induced after a 20E pulse, and allows for the expression of down-stream genes in processes leading to major switching in development, like those of metamorphosis. In honeybees, the expression of some genes (e.g. vitellogenin, vg; pro-phenoloxidase, pro-Po; juvenile hormone esterase, jhe) during the last part of pharate-adult development is known to be under hormonal control [increasing juvenile hormone titers (JH) in the presence of declining levels of ecdysteroids], both, in queens and workers. However, despite the USP involvement in the gene expression cascade promoted by JH, it does not seem to be the unique mediator of its activity, and, thus, we are still ignorant of the molecular factors regulating the expression of these genes, at least, during the critical period of pharate-adult development. Here, we show that Amftz-f1 has caste-specific transcription profile in fat bodies during this developmental stage, peaking just at the moment of the resuming of JH titers increase in the presence of low levels of ecdysteroids. Knock-down experiments (by RNAi) showed that the expression of genes essential to adult development (e.g. vg, and cuticular protein genes) depends on ftz-f1. Our results suggest that Amftz-f1 can also be considered a competence factor to the expression of several genes during pharate-adult development, and, thus, as a key actor in one of the last developmental processes leading to caste differentiation in A. mellifera.
2018-12-13 | GSE90037 | GEO
Project description:The schistosome homolog of ftz-f1 is a nuclear receptor. In order to understand the function of Smftz-f1, we performed RNAseq with samples taken on two days, Day 5 and Day 9, on either control (RNAi) or Smftz-f1 (RNAi) parasites to see the transcriptional consequences of Smftz-f1 RNAi and to find potential transcriptional targets.
2021-11-15 | GSE188736 | GEO
Project description:Cancer represents a complex family of diseases, characterized by the uncontrolled malignant growth of a particular cell type and by metastatic dissemination of these transformed cells to secondary sites. The hallmark tumor features emerge as a result of aberrant cellular signaling and pathological gene expression driven by cooperating genetic lesions. Being the convergence points of signaling pathways, transcription factors play crucial roles in cancer. Here, we define a transcription factor network that triggers an abnormal gene expression program promoting malignancy of clonal tumors, generated in Drosophila imaginal disc epithelium by overexpressing oncogenic Ras (RasV12) in a background lacking the tumor suppressor gene scribble (scrib1). We show that the nuclear receptor Ftz-F1 and the ETS-domain transcription factor Ets21c are upregulated in the rasV12scrib1 tumors in response to activated Jun-N-terminal kinase (JNK) signaling. Depletion of either Ftz-F1 or Ets21c improves viability of Drosophila larvae suffering from tumors, and this effect can be further enhanced by simultaneous removal of the Jun-dimerizing partner Fos. We identified Fos as a key mediator of JNK-induced differentiation defects and further show that Ftz-F1 and Fos are required for tumor invasiveness. However, only Ets21c can efficiently substitute for JNK and cooperate with RasV12 to induce invasive tumors that recapitulate hallmarks of malignant rasV12scrib1 tumors including elevated matrix metalloprotease (MMP1) and insulin-like peptide 8 (Dilp8) expression. In conclusion, our study provides functional evidence for a network of cooperating transcription factor that dictates target gene expression and promotes tumor phenotypes in response to aberrant JNK signaling.
2015-11-04 | GSE65261 | GEO
Project description:Cancer represents a complex family of diseases, characterized by the uncontrolled malignant growth of a particular cell type and by metastatic dissemination of these transformed cells to secondary sites. The hallmark tumor features emerge as a result of aberrant cellular signaling and pathological gene expression driven by cooperating genetic lesions. Being the convergence points of signaling pathways, transcription factors play crucial roles in cancer. Here, we define a transcription factor network that triggers an abnormal gene expression program promoting malignancy of clonal tumors, generated in Drosophila imaginal disc epithelium by overexpressing oncogenic Ras (RasV12) in a background lacking the tumor suppressor gene scribble (scrib1). We show that the nuclear receptor Ftz-F1 and the ETS-domain transcription factor Ets21c are upregulated in the rasV12scrib1 tumors in response to activated Jun-N-terminal kinase (JNK) signaling. Depletion of either Ftz-F1 or Ets21c improves viability of Drosophila larvae suffering from tumors, and this effect can be further enhanced by simultaneous removal of the Jun-dimerizing partner Fos. We identified Fos as a key mediator of JNK-induced differentiation defects and further show that Ftz-F1 and Fos are required for tumor invasiveness. However, only Ets21c can efficiently substitute for JNK and cooperate with RasV12 to induce invasive tumors that recapitulate hallmarks of malignant rasV12scrib1 tumors including elevated matrix metalloprotease (MMP1) and insulin-like peptide 8 (Dilp8) expression. In conclusion, our study provides functional evidence for a network of cooperating transcription factor that dictates target gene expression and promotes tumor phenotypes in response to aberrant JNK signaling. 20 samples analyzed, 4 control samples
2015-11-04 | E-GEOD-65261 | biostudies-arrayexpress
Project description:Genome wide mapping of Ftz and Eve transcription factor binding sites in early Drosophila embryos
2009-04-02 | GSE14289 | GEO
Project description:Genome wide mapping of Ftz and Eve transcription factor binding sites in early Drosophila embryos Ftz has one replicate and dyes swapping Eve has two replicates with one dye swap Mock IPs were used as controls Slides were hybridized with two color samples, but individual channels were uploaded seperately to GEO
2010-06-20 | E-GEOD-14289 | biostudies-arrayexpress
Project description:The orphan nuclear receptor Ftz-F1 is expressed in all somatic nuclei in Drosophila embryos, but mutations result in a pair-rule phenotype. This was explained by the interaction of Ftz-F1 with the homeodomain protein Ftz that is expressed in stripes in the primordia of segments missing in either ftz-f1 or ftz mutants. Ftz-F1 and Ftz were shown to physically interact and coordinately activate the expression of ftz itself and engrailed by synergistic binding to composite Ftz-F1/Ftz binding sites. However, attempts to identify additional target genes on the basis of Ftz-F1/ Ftz binding alone has met with only limited success. To discern rules for Ftz-F1 target site selection in vivo and to identify additional target genes, a microarray analysis was performed comparing wildtype and ftz-f1 mutant embryos. Ftz-F1-responsive genes most highly regulated included engrailed and nine additional genes expressed in patterns dependent on both ftz and ftz-f1. Candidate enhancers for these genes were identified by combining BDTNP Ftz ChIP-chip data with a computational search for Ftz-F1 binding sites. Of eight enhancer reporter genes tested in transgenic embryos, six generated expression patterns similar to the corresponding endogenous gene and expression was lost in ftz mutants. These studies identified a new set of Ftz-F1 targets, all of which are co-regulated by Ftz. Comparative analysis of enhancers containing Ftz/Ftz-F1 binding sites that were or were not bona fide targets in vivo suggested that GAF negatively regulates enhancers that contain Ftz/Ftz-F1 binding sites but are not actually utilized. These targets include other regulatory factors as well as genes involved directly in morphogenesis, providing insight into how pair-rule genes establish the body pattern.
| S-EPMC5056698 | biostudies-literature
Project description:During development, cascades of regulatory genes act in a hierarchical fashion to subdivide the embryo into increasingly specified body regions. This has been best characterized in Drosophila, where genes encoding regulatory transcription factors form a network to direct the development of the basic segmented body plan. The pair-rule genes are pivotal in this process as they are responsible for the first subdivision of the embryo into repeated metameric units. The Drosophila pair-rule gene fushi tarazu (ftz) is a derived Hox gene expressed in and required for the development of alternate parasegments. Previous studies suggested that Ftz achieves its distinct regulatory specificity as a segmentation protein by interacting with a ubiquitously expressed cofactor, the nuclear receptor Ftz-F1. However, the downstream target genes regulated by Ftz and other pair-rule genes to direct segment formation are not known. In this study, we selected candidate Ftz targets by virtue of their early expression in Ftz-like stripes. This identified two new Ftz target genes, drumstick (drm) and no ocelli (noc), and confirmed that Ftz regulates a serotonin receptor (5-HT2). These are the earliest Ftz targets identified to date and all are coordinately regulated by Ftz-F1. Engrailed (En), the best-characterized Ftz/Ftz-F1 downstream target, is not an intermediate in regulation. The drm genomic region harbors two separate seven-stripe enhancers, identified by virtue of predicted Ftz-F1 binding sites, and these sites are necessary for stripe expression in vivo. We propose that pair-rule genes, exemplified by Ftz/Ftz-F1, promote segmentation by acting at different hierarchical levels, regulating first, other segmentation genes; second, other regulatory genes that in turn control specific cellular processes such as tissue differentiation; and, third, 'segmentation realizator genes' that are directly involved in morphogenesis.
| S-EPMC2784225 | biostudies-literature
Project description:Francisella tularensis strain:FTZ Genome sequencing and assembly
| PRJNA244566 | ENA
Project description:Activation of Ftz-F1-responsive genes through Ftz/Ftz-F1 dependent enhancers
| PRJNA344461 | ENA