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Drosophila melanogaster

ABSTRACT: Tissue overgrowth induced by coexpression of the progenitor genes hth/MEIS1 and tsh/TSHZ results from an imbalance in the estrogen response pathway in Drosophila [RNA-Seq]

PROVIDER: PRJNA273498 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1771533.fastq.gz	Fastqsanger.gz
	SRR1771534.fastq.gz	Fastqsanger.gz
	SRR1771535.fastq.gz	Fastqsanger.gz
	SRR1771536.fastq.gz	Fastqsanger.gz
	SRR1771537.fastq.gz	Fastqsanger.gz

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Tissue overgrowth induced by coexpression of the progenitor genes hth/MEIS1 and tsh/TSHZ results from an imbalance in the estrogen response pathway in Drosophila

Project description:Tissue overgrowth induced by coexpression of the progenitor genes hth/MEIS1 and tsh/TSHZ results from an imbalance in the estrogen response pathway in Drosophila

| PRJNA273496 | ENA

Drosophila melanogaster

Project description:Tissue overgrowth induced by coexpression of the progenitor genes hth/MEIS1 and tsh/TSHZ results from an imbalance in the estrogen response pathway in Drosophila [FAIRE-Seq]

| PRJNA273499 | ENA

Tissue overgrowth induced by coexpression of the progenitor genes hth/MEIS1 and tsh/TSHZ results from an imbalance in the estrogen response pathway in Drosophila [RNA-Seq]

Project description:Analysis of third instar eye-antennal Drosophila imaginal discs with forced expression of hth, tsh or hth+tsh in the eye using an eye-specific GAL4 driver (optix2.3-GAL4). Forced maintenance of hth+tsh expression (but not of any of the two alone) results in overgrowth and aberrant cell differentiation. Results provide insight into new targets of hth+tsh.

2017-08-31 | GSE65251 | GEO

Tissue overgrowth induced by coexpression of the progenitor genes hth/MEIS1 and tsh/TSHZ results from an imbalance in the estrogen response pathway in Drosophila [FAIRE-Seq]

2017-08-31 | GSE65250 | GEO

Hoxa9 and Meis1 cooperatively induce addiction to Syk signaling by suppressing miR-146a in acute myeloid leukemia

Project description:The transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overexpression but is currently considered undruggable. We therefore investigated whether myeloid progenitor cells transformed by Hoxa9 and Meis1 become addicted to targetable signaling pathways. A comprehensive (phospho)proteomic analysis revealed that Meis1 increased Syk protein expression and activity. Syk upregulation occurs through a Meis1-dependent feed-forward loop. By dissecting this loop, we show that Syk is a direct target of miR-146a, whose expression is indirectly regulated by Meis1 through the transcription factor PU.1. In the context of Hoxa9 overexpression, Syk induces Meis1, recapitulating several leukemogenic features of Hoxa9/Meis1-driven leukemia. Finally, we show that Syk inhibition disrupts the identified regulatory loop, prolonging survival of mice with Hoxa9/Meis1-driven leukemia.

2017-06-14 | PXD004192 | Pride

Transcriptomic Landscape of Hyperthyroidism in Mice Overexpressing Thyroid Stimulating Hormone

Project description:Activation of thyroid stimulating hormone receptor (TSHR) fundamentally leads to hyperthyroidism. To elucidate TSHR signaling, we conducted transcriptome analyses for hyperthyroid mice that we generated by overexpressing TSH. TSH overexpression drastically changed their thyroid transcriptome. In particular, enrichment analyses identified the cell cycle, phosphatidylinositol-3 kinase/Akt pathway, and Ras-related protein 1 pathway as possibly associated with goiter development. Regarding hyperthyroidism, Slc26a4 was exclusively upregulated with TSH overexpression among genes crucial to thyroid hormone secretion. To verify its significance, we overexpressed TSH in Slc26a4 knockout mice. TSH overexpression caused hyperthyroidism in Slc26a4 knockout mice, equivalent to that in control mice. Thus, we did not observe significant changes in known genes and pathways involved in thyroid hormone secretion with TSH overexpression. Our datasets might include candidate genes that have not yet been identified as regulators of thyroid function. Our transcriptome datasets regarding hyperthyroidism can contribute to future research on TSHR signaling.

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Expression profiling of human CD34+ cells derived from mobilized peripheral blood samples after overexpression of MEIS1B or MEIS1D

Project description:MEIS1 is a transcription factor expressed in hematopoietic stem and progenitor cells (HSPC) and in mature megakaryocytes. In contrast to its role in leukemogenesis, the role of MEIS1 in normal hematopoiesis is largely unknown. We show that MEIS1 can direct human hematopoietic progenitors towards a megakaryocyte-erythroid progenitor (MEP) fate. Ectopoic expression of MEIS1 in CD34+ cells resulted in increased erythroid differentiation at the expense of granulocyte and monocyte (GM) differentiation. MEIS1 overexpression not only skewed differentiation of CMPs towards the erythroid lineage but also reprogrammed GM progenitors towards erythrocyte differentiation. Expression profiling was used to determine the transcriptional changes induced by MEIS1 that lead to the oberved phenotype. A transcriptional program enriched for erythrocytic and megakaryocytic genes was detected.

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Tin Sinh

Project description:TSH

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The BTB-zinc finger transcription factor Abrupt acts as an epithelial oncogene in Drosophila through maintaining a progenitor-like cell state

Project description:The capacity of tumor cells to maintain continual overgrowth potential has been linked to the commandeering of normal self-renewal pathways. Using an epithelial cancer model in Drosophila we carried out an overexpression screen for oncogenes capable of cooperating with the loss of the epithelial apico-basal cell polarity regulator, scribbled, and identified the cell fate regulator, Abrupt, a BTB-zinc finger protein. Abrupt overexpression alone is insufficient to transform cells, but in cooperation with scrib loss of function, Abrupt promotes the formation of massive tumors in the eye/antennal disc. The steroid hormone receptor coactivator, Taiman (SRC3/AIB1), is known to associate with Abrupt, and Taiman overexpression also drives tumor formation in cooperation with the loss of Scribbled. Expression arrays and ChIP-Seq indicates that Abrupt overexpression represses a large number of genes, including steroid hormone-response genes and multiple cell fate regulators, thereby maintaining cells within an epithelial progenitor-like state. The progenitor-like state is characterised by the failure to express the conserved Eyes absent/Dachshund regulatory complex in the eye disc, and in the antennal disc by the failure to express cell fate regulators that define the temporal elaboration of the appendage along the proximo-distal axis downstream of Distalless. Loss of scribbled promotes cooperation with Abrupt through impaired Hippo signaling, which is required and sufficient for cooperative overgrowth with Abrupt, and JNK signaling, which is required for tumor cell migration/invasion but not overgrowth. These results thus identify a novel cooperating oncogene, mammalian family members of which are also known oncogenes, and demonstrate that epithelial tumors in Drosophila can be characterised by the maintenance of a progenitor-like state. ChIP-Seq of Abrupt, ChIP-Seq of Abrupt (scrib-), Input, Input (scrib-)

2013-08-15 | E-GEOD-42928 | biostudies-arrayexpress

A double negative post-transcriptional regulatory circuit mediates the virgin behavioral state

Project description:The survival and reproductive success of animals depends on the ability to harmonize their external behaviors with their internal states. For example, females conduct numerous social programs that are distinctive to virgins compared to post-mated and/or pregnant individuals. In Drosophila, the fact that the post-mating switch is initiated by seminal factors implies the default state as virgin. Recently, we uncovered molecular and genetic control of the female virgin state. In particular, repression of the transcription factor Homothorax (Hth) by mir-iab-4/8 within the abdominal ventral nerve cord (VNC) is critical for unmated females to execute virgin behaviors. To elucidate new components of this regulatory circuit, we exploited mir-iab-4/8 deletion and hth-miRNA binding site mutants (hth[BSmut]) to elucidate doublesex (dsx) as a critical downstream factor. While Dsx has mostly been studied during sex-specific differentiation, its activities in neurons are little known. We find that accumulation of Dsx in the CNS is mutually exclusive with Hth, and downregulated in miRNA/hth[BSmut] mutants. Moreover, experimental suppression of Dsx in highly restricted sets of abdominal neurons abrogates female virgin conducts, in favor of mated behavioral programs. Thus, a double negative pathway in the VNC mediates the virgin behavioral state.

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