The Schistosoma mansoni nuclear receptor FTZ-F1 maintains esophageal gland function via direct transcriptional regulation of meg-8.3
Ontology highlight
ABSTRACT:
ORGANISM(S): Schistosoma mansoni
PROVIDER: GSE188736 | GEO | 2021/11/15
REPOSITORIES: GEO
Similar Datasets
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. Previously characterized Ftz-F1 target genes were co-regulated by Ftz, which is expressed in stripes, consistent with the pair-rule phenotype observed for ftz-f1 and ftz mutants. However, attempts to identify new target genes on the basis of Ftz-F1 and Ftz binding sites alone has met with only limited success. To discern the 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.
2016-09-27 | GSE87342 | GEO
Project description:Schistosomes infect over 200 million of the world's poorest people, but unfortunately treatment relies on a single drug. Nuclear hormone receptors are ligand-activated transcription factors that regulate diverse processes in metazoans, yet few have been functionally characterized in schistosomes. During a systematic analysis of nuclear receptor function, we found that an FTZ-F1-like receptor was essential for parasite survival. Using a combination of transcriptional profiling and chromatin immunoprecipitation (ChIP), we discovered that the micro-exon gene meg-8.3 is a transcriptional target of SmFTZ-F1. We found that both Smftz-f1 and meg-8.3 are required for esophageal gland maintenance as well as integrity of the worm's head. Together, these studies define a new role for micro-exon gene function in the parasite and suggest that factors associated with the esophageal gland could represent viable therapeutic targets.
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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 Schistosoma mansoni nuclear receptor FTZ-F1 maintains esophageal gland function via direct transcriptional regulation of meg-8.3
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Project description:Transcriptome analysis of inhibitor-treated schistosome female
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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:Stem cells rejuvinate the schistosome host-parasite interface
| PRJNA305542 | ENA
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:The schistosome homolog of hnf4 is involved in parasite blood feeding and stem cell biology. In order to understand the function of hnf4, we performed RNAseq on either control(RNAi) or hnf4(RNAi) parasites to see the transcriptional consequences of hnf4 RNAi
2020-03-11 | GSE146735 | GEO
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