Insect hormone prothoracicotropic hormone (PTTH) regulates lifespan through temporal and spatial activation of NF-κB signaling during Drosophila metamorphosis [1]
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ABSTRACT:
PROVIDER: PRJNA1130387 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29661002.fastq.gz | Fastqsanger.gz | |||
| SRR29661003.fastq.gz | Fastqsanger.gz | |||
| SRR29661004.fastq.gz | Fastqsanger.gz | |||
| SRR29661005.fastq.gz | Fastqsanger.gz | |||
| SRR29661006.fastq.gz | Fastqsanger.gz |
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Project description:The prothoracicotropic hormone (PTTH) is a well-known neuropeptide that regulates insect metamorphosis (the juvenile-to-adult transition) by inducing the biosynthesis of steroid hormones, similar to the hypothalamic-pituitary-gonadal control of mammalian puberty. However, the role of Ptth in adult physiology and longevity is largely unexplored. Here, we show that Ptth loss-of-function mutants are long-lived and exhibit increased resistance to oxidative stress in Drosophila. Intriguingly, we find that loss of Ptth blunt age-dependent upregulation of NF-κB signaling specifically in fly oenocytes, the homolog of mammalian hepatocytes. We further show that oenocyte-specific overexpression of NF-κB/Relish blocks the lifespan extension of Ptth mutants, suggesting that Ptth regulates lifespan through oenocyte-specific NF-κB signaling. Surprisingly, adult-specific knockdown of Ptth did not prolong lifespan, indicating that Ptth might control longevity through developmental programs. Our developmental transcriptomic analysis reveals an interesting activation of NF-κB signaling during fly metamorphosis, which is attenuated in Ptth mutants. Intriguingly, the knockdown of NF-κB/Relish, specifically in oenocytes during metamorphosis, significantly prolongs the lifespan of adult flies. Thus, our findings uncover an unexpected role of insect hormone PTTH in controlling adult lifespan through temporal and spatial activation of NF-κB signaling in developing hepatocytes.
2025-04-22 | GSE271166 | GEO
Project description:The prothoracicotropic hormone (PTTH) is a well-known neuropeptide that regulates insect metamorphosis (the juvenile-to-adult transition) by inducing the biosynthesis of steroid hormones, similar to the hypothalamic-pituitary-gonadal control of mammalian puberty. However, the role of Ptth in adult physiology and longevity is largely unexplored. Here, we show that Ptth loss-of-function mutants are long-lived and exhibit increased resistance to oxidative stress in Drosophila. Intriguingly, we find that loss of Ptth blunt age-dependent upregulation of NF-κB signaling specifically in fly oenocytes, the homolog of mammalian hepatocytes. We further show that oenocyte-specific overexpression of NF-κB/Relish blocks the lifespan extension of Ptth mutants, suggesting that Ptth regulates lifespan through oenocyte-specific NF-κB signaling. Surprisingly, adult-specific knockdown of Ptth did not prolong lifespan, indicating that Ptth might control longevity through developmental programs. Our developmental transcriptomic analysis reveals an interesting activation of NF-κB signaling during fly metamorphosis, which is attenuated in Ptth mutants. Intriguingly, the knockdown of NF-κB/Relish, specifically in oenocytes during metamorphosis, significantly prolongs the lifespan of adult flies. Thus, our findings uncover an unexpected role of insect hormone PTTH in controlling adult lifespan through temporal and spatial activation of NF-κB signaling in developing hepatocytes.
2025-04-22 | GSE271165 | GEO
Project description:Insect hormone prothoracicotropic hormone (PTTH) regulates lifespan through temporal and spatial activation of NF-κB signaling during Drosophila metamorphosis [2]
| PRJNA1130386 | ENA
Project description:Transcriptional profiling of human control and Néstor-Guillermo Progeria Syndrome (NGPS) fibroblasts and induced pluripotent stem cells (iPSCs). Somatic cell reprogramming involves rejuvenation of adult cells and relies on the ability to erase age-associated molecular marks. Accordingly, reprogramming efficiency declines with ageing, and age-associated features such as genetic instability, cell senescence or telomere shortening negatively affect this process. However, the regulatory mechanisms that constitute age-associated barriers for cell reprogramming remain largely unknown. Here, by using cells from patients with premature ageing, we demonstrate that NF-κB activation is a critical barrier for the generation of induced pluripotent stem cells (iPSCs) in ageing. We show that NF-κB repression occurs during cell reprogramming towards a pluripotent state. Conversely, ageing-associated NF-κB hyperactivation impairs generation of iPSCs by eliciting reprogramming repressors DOT1L and YY1, reinforcing cell senescence signals and down-regulating pluripotency genes. We also show that genetic and pharmacological NF-κB inhibitory strategies significantly increase the reprogramming efficiency of fibroblasts from Néstor-Guillermo Progeria Syndrome (NGPS) and Hutchinson-Gilford Progeria Syndrome (HGPS) patients, as well as from normal aged donors. Finally, we demonstrate that DOT1L inhibition in vivo ameliorates the accelerated ageing phenotype and extends lifespan in a progeroid animal model. Collectively, our results provide evidence for a novel role of NF-κB in the control of cell fate transitions and reinforce the interest of studying age-associated molecular impairments to implement cell reprogramming methodologies, and to identify new targets of rejuvenation strategies. Control and NGPS fibroblasts were reprogrammed. RNA was extracted and transcriptional profiling was obtained with GeneChip Human Exon 1.0 ST Arrays.
2015-07-01 | E-GEOD-65170 | biostudies-arrayexpress
Project description:Transcriptional profiling of human control and Néstor-Guillermo Progeria Syndrome (NGPS) mesenchymal stem cells (MSCs). Somatic cell reprogramming involves rejuvenation of adult cells and relies on the ability to erase age-associated molecular marks. Accordingly, reprogramming efficiency declines with ageing, and age-associated features such as genetic instability, cell senescence or telomere shortening negatively affect this process. However, the regulatory mechanisms that constitute age-associated barriers for cell reprogramming remain largely unknown. Here, by using cells from patients with premature ageing, we demonstrate that NF-κB activation is a critical barrier for the generation of induced pluripotent stem cells (iPSCs) in ageing. We show that NF-κB repression occurs during cell reprogramming towards a pluripotent state. Conversely, ageing-associated NF-κB hyperactivation impairs generation of iPSCs by eliciting reprogramming repressors DOT1L and YY1, reinforcing cell senescence signals and down-regulating pluripotency genes. We also show that genetic and pharmacological NF-κB inhibitory strategies significantly increase the reprogramming efficiency of fibroblasts from Néstor-Guillermo Progeria Syndrome (NGPS) and Hutchinson-Gilford Progeria Syndrome (HGPS) patients, as well as from normal aged donors. Finally, we demonstrate that DOT1L inhibition in vivo ameliorates the accelerated ageing phenotype and extends lifespan in a progeroid animal model. Collectively, our results provide evidence for a novel role of NF-κB in the control of cell fate transitions and reinforce the interest of studying age-associated molecular impairments to implement cell reprogramming methodologies, and to identify new targets of rejuvenation strategies. Control and NGPS MSCs were differentiated into bone in the presence or absence of sodium salicylate. Total RNA was extracted and global gene expression was analyzed.
2015-07-01 | E-GEOD-65172 | biostudies-arrayexpress
Project description:Amphibian metamorphosis involves thyroid hormone (TH)-dependent postembryonic remodeling of differentiated tissues as a tadpole transforms into a frog. Rana [Lithobates] catesbeiana (American bullfrog) metamorphosis can be precociously induced in premetamorphic tadpoles by treatment with exogenous TH. However, metamorphosis is temperature-dependent and does not occur at 5°C, even with TH treatment. Remarkably, exposure to TH at 5°C establishes a molecular memory that primes the tadpole for an accelerated metamorphosis when shifted to a permissive temperature (24°C). Previous research suggests that histone post-translational modifications (PTMs) and the incorporation of histone variants are altered upon cold temperature exposure in the presence and absence of TH. Herein, we use mass spectrometry to analyze the histone composition of premetamorphic R. catesbeiana blood, liver, and tailfin following TH injection at a permissive temperature (24°C), a non-permissive temperature (5°C), and a shifted condition (5 to 24°C). We identify changes in histone and non-histone chromatin associated protein abundance and putative PTMs, suggesting that epigenetic variations may contribute to early TH signaling events and to molecular memory.
2025-04-25 | PXD062623 | Pride
Project description:Thyroid hormone receptor alpha is required for thyroid hormone-dependent neural cell proliferation during tadpole metamorphosis
| PRJNA542536 | ENA
Project description:Transcriptional profiling of human control and Néstor-Guillermo Progeria Syndrome (NGPS) fibroblasts and induced pluripotent stem cells (iPSCs). Somatic cell reprogramming involves rejuvenation of adult cells and relies on the ability to erase age-associated molecular marks. Accordingly, reprogramming efficiency declines with ageing, and age-associated features such as genetic instability, cell senescence or telomere shortening negatively affect this process. However, the regulatory mechanisms that constitute age-associated barriers for cell reprogramming remain largely unknown. Here, by using cells from patients with premature ageing, we demonstrate that NF-κB activation is a critical barrier for the generation of induced pluripotent stem cells (iPSCs) in ageing. We show that NF-κB repression occurs during cell reprogramming towards a pluripotent state. Conversely, ageing-associated NF-κB hyperactivation impairs generation of iPSCs by eliciting reprogramming repressors DOT1L and YY1, reinforcing cell senescence signals and down-regulating pluripotency genes. We also show that genetic and pharmacological NF-κB inhibitory strategies significantly increase the reprogramming efficiency of fibroblasts from Néstor-Guillermo Progeria Syndrome (NGPS) and Hutchinson-Gilford Progeria Syndrome (HGPS) patients, as well as from normal aged donors. Finally, we demonstrate that DOT1L inhibition in vivo ameliorates the accelerated ageing phenotype and extends lifespan in a progeroid animal model. Collectively, our results provide evidence for a novel role of NF-κB in the control of cell fate transitions and reinforce the interest of studying age-associated molecular impairments to implement cell reprogramming methodologies, and to identify new targets of rejuvenation strategies.
2015-07-01 | GSE65170 | GEO
Project description:Transcriptional profiling of human control and Néstor-Guillermo Progeria Syndrome (NGPS) mesenchymal stem cells (MSCs). Somatic cell reprogramming involves rejuvenation of adult cells and relies on the ability to erase age-associated molecular marks. Accordingly, reprogramming efficiency declines with ageing, and age-associated features such as genetic instability, cell senescence or telomere shortening negatively affect this process. However, the regulatory mechanisms that constitute age-associated barriers for cell reprogramming remain largely unknown. Here, by using cells from patients with premature ageing, we demonstrate that NF-κB activation is a critical barrier for the generation of induced pluripotent stem cells (iPSCs) in ageing. We show that NF-κB repression occurs during cell reprogramming towards a pluripotent state. Conversely, ageing-associated NF-κB hyperactivation impairs generation of iPSCs by eliciting reprogramming repressors DOT1L and YY1, reinforcing cell senescence signals and down-regulating pluripotency genes. We also show that genetic and pharmacological NF-κB inhibitory strategies significantly increase the reprogramming efficiency of fibroblasts from Néstor-Guillermo Progeria Syndrome (NGPS) and Hutchinson-Gilford Progeria Syndrome (HGPS) patients, as well as from normal aged donors. Finally, we demonstrate that DOT1L inhibition in vivo ameliorates the accelerated ageing phenotype and extends lifespan in a progeroid animal model. Collectively, our results provide evidence for a novel role of NF-κB in the control of cell fate transitions and reinforce the interest of studying age-associated molecular impairments to implement cell reprogramming methodologies, and to identify new targets of rejuvenation strategies.
2015-07-01 | GSE65172 | GEO
Project description:The transcription factor NF-κB is the master regulator of the immune response but also regulates gene expression to influences cell survival, proliferation and differentiation. Inducible site-specific phosphorylation of NF-κB is critical for its activity and appears to be important in gene specific transcriptional control. Promyelocytic Leukemia (PML) is a nuclear protein that forms sub-nuclear structures termed nuclear bodies associated with transcriptionally active genomic regions. We demonstrate that PML promotes NF-κB- induced transcriptional responses by promoting the phosphorylation of NF-κB p65 at key regulatory sites. Our findings demonstrate a critical role for PML in promoting NF-κB transcriptional activity through signal induced post-translational modifications.
2016-06-01 | GSE47828 | GEO