Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA171930 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Skeletal muscle senescence influences whole organism aging, yet little is known on the relay of pro-longevity signals from muscles to other tissues. We performed an RNAi screen in Drosophila for muscle-released cytokines ('myokines') regulating lifespan and identified Myoglianin, the homolog of human Myostatin. Myoglianin is induced in skeletal muscles by the transcription factor Mnt and together they constitute an inter-organ signaling module that regulates lifespan, age-related muscle dysfunction, and protein synthesis across aging tissues. Both Mnt and Myoglianin activate already in young age the protective decline in protein synthesis that is typical of old age, while knock-down of Myoglianin impairs this process. Mechanistically, Mnt decreases the expression of nucleolar components in muscles while also decreasing nucleolar size in distant tissues via Myostatin/p38 MAPK signaling. Our results highlight a myokine-dependent inter-organ longevity pathway that coordinates nucleolar function and protein synthesis across aging tissues. Affymetrix microarrays were used to evaluate genome-wide expression in skeletal muscles of flies with muscle-specific overexpression of FOXO or Mnt (Affymetrix Drosophila Genome 2.0 Array). This design allowed us to identify genes and pathways induced by overexpression of FOXO and/or Mnt, and enabled us to address the degree to which FOXO-induced pathways were independent of those induced by Mnt. Three independent biological replicates from each of three groups (control, UAS-Foxo and UAS-Mnt)
2014-07-02 | E-GEOD-39877 | biostudies-arrayexpress
Project description:Skeletal muscle senescence influences whole organism aging, yet little is known on the relay of pro-longevity signals from muscles to other tissues. We performed an RNAi screen in Drosophila for muscle-released cytokines (?myokines?) regulating lifespan and identified Myoglianin, the homolog of human Myostatin. Myoglianin is induced in skeletal muscles by the transcription factor Mnt and together they constitute an inter-organ signaling module that regulates lifespan, age-related muscle dysfunction, and protein synthesis across aging tissues. Both Mnt and Myoglianin activate already in young age the protective decline in protein synthesis that is typical of old age, while knock-down of Myoglianin impairs this process. Mechanistically, Mnt decreases the expression of nucleolar components in muscles while also decreasing nucleolar size in distant tissues via Myostatin/p38 MAPK signaling. Our results highlight a myokine-dependent inter-organ longevity pathway that coordinates nucleolar function and protein synthesis across aging tissues. Affymetrix microarrays were used to evaluate genome-wide expression in skeletal muscles of flies with muscle-specific overexpression of FOXO or Mnt (Affymetrix Drosophila Genome 2.0 Array). This design allowed us to identify genes and pathways induced by overexpression of FOXO and/or Mnt, and enabled us to address the degree to which FOXO-induced pathways were independent of those induced by Mnt.
2014-07-02 | GSE39877 | GEO
Project description:Transcription profiling by array of skeletal muscles of flies with muscle-specific overexpression of Foxo or Mnt
2014-07-30 | E-GEOD-39877 | ExpressionAtlas
Project description:Purpose: REPTOR and FoxO are two transcription factors that regulate muscle metabolism. However, these transcription factors share around 40% of target genes. Furthermore, the thorax of adult flies is composed of several tissues including muscle and fat body, making it difficult to discover direct target genes of REPTOR and FoxO specifically in muscle tissue. This experimental approach allows the identification of REPTOR-specific and FoxO-specific target genes in muscle clusters Methods: snRNA-seq analysis of dissected adult fly thoraces, when an active allele of REPTOR or an active allele of FoxO are overexpressed using a muscle-specific driver (dMef2-Gal4) Results: Identification of the transcriptional signature of each tissue present in the thorax of adult flies when REPTOR or FoxO are overexpressed in muscle. Discovery of potential direct target genes of REPTOR and FoxO in muscle tissue, as well as metabolic pathways regulated by each transcription factor. Conclusions: REPTOR and FoxO modulate distinct gene signatures in muscle tissue to regulate metabolism in adult flies.
2023-06-01 | GSE227038 | GEO
Project description:FOXO1, a member of the FOXO forkhead type transcription factors, is markedly up-regulated in skeletal muscle during atrophy. Previously, we created transgenic mice specifically overexpressing FOXO1 in skeletal muscle (FOXO1 Tg mice). These mice weighed less than the wildtype control mice, had a reduced skeletal muscle mass. In this study, to better understand changes in skeletal muscle during atrophy, we performed a microarray analysis of skeletal muscle in wild-type control and FOXO1 Tg mice. The microarray data shows that in the skeletal muscles of FOXO1 Tg mice, gene expression of PGC-1β, a transcriptional regulator whose increased expression activates energy-expenditure-related genes in skeletal muscles, is decreased.
2020-07-07 | GSE146919 | GEO
Project description:Forkhead BoxO (FoxO) transcription factors expressed in adult skeletal muscle promote muscle atrophy during various catabolic conditions. We have identified the genome wide target genes and biological networks regulated by FoxO in skeletal muscle during Colon-26 (C-26) cancer cachexia. In this dataset, we include the expression data obtained from the tibialis anterior muscles of control and severely cachectic Colon-26 mice in which FoxO-dependent transcription was either intact (AAV9-EV) or inhibited (AAV9-d.n.FoxO). These data were used to obtain 543 FoxO target genes during cancer. These target genes were identified as those genes whose expression was both differentially regulated in skeletal muscle in response to cancer (control AAV9-EV vs. C26 AAV9-EV), and differentially regulated in the presence of d.n.FoxO (C26 AAV9-EV vs. C26 AAV9-d.n.FoxO).
2014-12-31 | GSE56555 | GEO
Project description:dFOXO targets in adult Drosophila melanogaster females, and the effect of insulin signalling and stress on binding. The experimets determined the binding locations of dFOXO in the whole adult female fly using ChIP-chip. The protocol was validated using mock conditions: pre-immune serum or IP on chromatin from foxo null flies. The response of this binding to stress induced by treatment of flies with paraquat or by their exposure to starvation, as well as the response to an insulin-signalling-reducing genetic manipulation (over-expression of dominant negative form of the insulin receptor), was determined.
2011-06-18 | E-TABM-751 | biostudies-arrayexpress
Project description:FOXO transcription factors control numerous pathways involving metabolism, stress response, and longevity. Although direct targets of FOXO have been reported in various long-lived mutants and under stress conditions, no studies have investigated how normal aging impacts the cellular activity of FOXO. In this study, we compared genome wide dFOXO-bound sites in young and aged wild-type flies kept under normal feeding conditions to evaluate the dynamics of FOXO gene targeting during aging. Our results provide a new insight into FOXO chromatin targeting under a normal aging model and highlight the diverse regulatory mechanisms for FOXO transcriptional activity that are currently less understood.
2019-04-25 | GSE121102 | GEO
Project description:Notch signaling plays essential roles in maintenance of muscle stem cell pool. We found that Notch2, but not Notch1 and Notch3, is expressed in fully differentiated myofibers. To study the specific role of Notch2 in adult myofibers, we generated muscle-specific Notch2-knockout mice. Here, we showed that muscle-specific Notch2 deficiency prevented muscle atrophy induced by hindlimb unloading and diabetes millitus. RNA sequencing analysis revealed that the loss of Notch2 gene in myofibers inhibited gene responses to unloading and diabetes. Especially, several FoxO-target genes and atrogenes were upregulated in wildtype muscles but not in Notch2-deficient muscles by unloading and diabetes. Thus, our characterization of muscle-specific Notch2-knockout mice indicates that Notch2 acts as a regulatory factor of skeletal muscle plasticity and could be a therapeutic target of muscle atrophy.
2022-01-07 | GSE161693 | GEO
Project description:Gadd45a is a stress-induced protein that causes skeletal muscle atrophy. The goal of these studies was to determine the effects of Gadd45a overexpression on mRNA levels in mouse skeletal muscle. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12, 2012. Tibialis anterior (TA) muscles from muscle-specfic ATF4 knockout mice (ATF4 mKO) were transfected with either 20 mg empty plasmid (pcDNA3) (left TA) or 20 mg pCMV-FLAG-Gadd45a (right TA) and harvested 7 days later. mRNA levels in Gadd45a-transfected muscles were normalized to levels in control transfected muscles.
2012-09-15 | E-GEOD-39196 | biostudies-arrayexpress