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Gene expression profiling of dMyc null Drosophila larvae

ABSTRACT: Myc oncoproteins are essential regulators of the growth and proliferation of mammalian cells. In Drosophila the single ortholog of Myc (dMyc), encoded by the dm gene, influences organismal size and the growth of both mitotic and endoreplicating cells. A null mutation in dm (dm4) results in attenuated endoreplication and growth arrest early in larval development. Gene expression analysis indicates that loss of dMyc leads to decreased expression of genes required for ribosome biogenesis and protein synthesis. Keywords: cDNA expression microarray, mutant analysis

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE9729 | GEO | 2008/01/22

SECONDARY ACCESSION(S): PRJNA103647

REPOSITORIES: GEO

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Gene expression profiling of dMyc null Drosophila larvae

Project description:Myc oncoproteins are essential regulators of the growth and proliferation of mammalian cells. In Drosophila the single ortholog of Myc (dMyc), encoded by the dm gene, influences organismal size and the growth of both mitotic and endoreplicating cells. A null mutation in dm (dm4) results in attenuated endoreplication and growth arrest early in larval development. Gene expression analysis indicates that loss of dMyc leads to decreased expression of genes required for ribosome biogenesis and protein synthesis. Drosophila larvae were collected 24 hours after egg deposition. Sample comparisons were performed using 3 biological independent experimental replicates of dm4 that were each compared to a common reference (wild type larvae of the same genetic background as dm4). For each comparison, a dye-swapped technical replicate was also performed and the paired results were averaged and used as a single observation.

2010-05-26 | E-GEOD-9729 | biostudies-arrayexpress

Expression data from Drosophila embryos, control vs. dMyc+

Project description:dMyc is a conserved transcription factor that controls growth and proliferation by regulating its target genes. We used Affymetrix microarray to identify and classify targets of dMyc during Drosophila embryogenesis. RNA was extracted from 0-24 hour old Drosophila embryos in control (Gal 4 expressing animals) and Myc+ (flies over-expressing dMyc under UAS enhancer) to identify genomic targets od dMyc during embryogenesis

2012-09-15 | E-GEOD-38529 | biostudies-arrayexpress

Expression data from Drosophila embryos, control vs. dMyc+

2012-09-15 | GSE38529 | GEO

RNA-seq on Drosophila wing imaginal discs after Myc RNAi or overexpression

Project description:RNA-seq was performed to confirm the effect of dMyc overexpression or RNAi repression on conserved Myc targets in the Drosophila wing disc.

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dSirt6 Regulates Lifespan in Drosophila

Project description:Sirt6 is a multifunctional enzyme that regulates diverse cellular processes such as metabolism, DNA repair, and aging. Overexpressing Sirt6 extends lifespan in mice, but the underlying cellular mechanisms are unclear. Drosophila melanogaster are an excellent model to study genetic regulation of lifespan; however, despite extensive study in mammals, very little is known about Sirt6 function in flies. Here, we characterized the Drosophila ortholog of Sirt6, dSirt6, and examined its role in regulating longevity. dSirt6 is a nuclear and chromatin-associated protein with NAD+-dependent histone deacetylase activity. dSirt6 overexpression in flies produces robust lifespan extension in both sexes, while reducing dSirt6 levels shortens lifespan. dSirt6 OE flies have normal food consumption and fertility, but increased resistance to oxidative stress and reduced protein synthesis rates. Transcriptomic analyses reveal that dSirt6 OE reduces expression of genes involved in ribosome biogenesis, including many dMyc target genes. dSirt6 OE partially rescues many effects of dMyc OE, including increased nuclear size, up-regulation of ribosome biogenesis genes, and lifespan shortening. Lastly, dMyc haploinsufficiency does not convey additional lifespan extension to dSirt6 OE flies, suggesting dSirt6 OE is upstream of dMyc in regulating lifespan. Our results provide new insight into the mechanisms by which Sirt6 overexpression leads to longer lifespan.

2021-12-23 | GSE191320 | GEO

EZH2 depletion potentiates MYC degradation inhibiting neuroblastoma and small cell carcinoma tumor formation

Project description:Efforts to therapeutically target EZH2 have generally focused on inhibition of its methyltransferase activity, although it remains less clear whether this is the central mechanism whereby EZH2 promotes cancer. We demonstrate that EZH2 directly interacts with both MYC family oncoproteins, MYC and MYCN, and promotes their stabilization in a methyltransferase-independent manner. By competing against the SCFFBW7 ubiquitin ligase to bind MYC and MYCN, EZH2 counteracted FBW7-mediated MYC(N) polyubiquitination and proteasomal degradation. Depletion, but not enzymatic inhibition, of EZH2 induced robust MYC(N) degradation and inhibited tumor cell growth in MYC(N) driven neuroblastoma and small cell lung cancer. These findings unveil the MYC family proteins as global EZH2 oncogenic effectors and EZH2 pharmacologic degraders as potential MYC(N) targeted cancer therapeutics, pointing out that MYC(N) driven cancers may develop inherent resistance to the canonical EZH2 enzymatic inhibitors currently in clinical development.

2022-02-17 | PXD029652 | Pride

The Myc binding partner Spt5 is essential for brain tumor growth in Drosophila

Project description:The transcription factor SPT5 physically interacts with MYC oncoproteins and is essential for the full transcriptional activation of MYC targets in cultured cells. Here, we use Drosophila to show that SPT5 is also required for MYC-dependent processes in vivo. Depletion of SPT5 strongly impairs the growth of a model neuronal tumor and substantially extends survival of tumor-bearing animals. This beneficial effect is also observed when SPT5 is knocked down systemically after tumor initiation, highlighting SPT5 is a potential drug target in human oncology.

2023-10-23 | GSE220110 | GEO

P493-6 treated with KJ-Pyr-9 and/or Doxycycline

Project description:In a fluorescence polarization screen for MYC-MAX interaction, we have identified a novel small molecule inhibitor of MYC, KJ-Pyr-9, from a Kröhnke pyridine library. The Kd of KJ-Pyr-9 for MYC in vitro is 6.5 ± 1.0 nM as determined by backscattering interferometry; KJ-Pyr-9 also interferes with MYC-MAX complex formation in the cell as shown in a protein fragment complementation assay. KJ-Pyr-9 specifically inhibits MYC-induced oncogenic transformation in cell culture; it has no or only weak effects on the oncogenic activity of several unrelated oncoproteins. KJ-Pyr-9 preferentially interferes with the proliferation of MYC-overexpressing human and avian cells and specifically reduces the MYC-driven transcriptional signature. In vivo, KJ-Pyr-9 effectively blocks the growth of a xenotransplant of MYC-overexpressing human cancer cells. 4 treatment groups analyzed in triplicate: no treatment(control), 20uM KJ-Pyr-9, 0.1ug/mL doxycycline and KJ-Pyr-9 in combination with doxycycline

2014-08-25 | E-GEOD-58168 | biostudies-arrayexpress

Il-17 p53 Developmental Series

Project description:Here, we show that the activity of the tumor suppressor p53 in the metazoan C. elegans switches organismal development between reproductive growth and dormancy by responding to nutrient availability signaled by the cytokine, ILC-17.1. ILC-17.1-dependent repression of the C. elegans p53 ortholog CEP-1 is required for larval growth and development; ILC-17.1 deficiency activates CEP-1/p53 in post-embryonically dividing progenitor blast cells, decreases glucose utilization and cytochrome C levels, upregulates cell cycle inhibitors, and causes larvae to arrest as stress-resistant, quiescent dauers.

2024-01-30 | GSE229132 | GEO

P493-6 treated with KJ-Pyr-9 and/or Doxycycline

2014-08-25 | GSE58168 | GEO

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