Ontology highlight
ABSTRACT:
PROVIDER: PRJNA549687 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR11831580.fastq.gz | Fastqsanger.gz | |||
| SRR11831581.fastq.gz | Fastqsanger.gz | |||
| SRR11831582.fastq.gz | Fastqsanger.gz | |||
| SRR11831583.fastq.gz | Fastqsanger.gz |
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Project description:Childhood obesity traces its roots to the parental lifestyle and eating habits. Familial clustering of obesity indicates that children’s feeding behavior is a result of a complex interplay between cultural inheritance, genetics, and epigenetics. In the current study, we asked a question if epigenetic factors, such as ancestral diet, could program offspring feeding behavior in a fruit fly model. Here we show that ancestral caloric overload produces a generational shift in the offspring’s feeding behavior, with a concomitant alteration in activity, triglycerides, and brain mitochondrial density. Mechanistically, we find the generational changes to be associated with alterations in brain mitochondrial proteome and miRNAs. The findings identify ancestral nutrition as a critical factor in the generational programming of feeding behavior.
2023-04-22 | PXD033363 | JPOST Repository
Project description:CRIF1 is a mitochondrial protein essential for the synthesis and formation of the OxPhos complex in the inner mitochondrial membrane. Beta cell specific Crif1 haploinsufficiency resulted in defect of first phase insulin secretion, and caused islet cell composition change as well as proliferation of beta cell for a compensation to maintain metabolic homeostasis. These results suggest that mitochondrial OxPhos function of beta cell has roles for beta cell compensation as well as insulin secretion.
2022-07-21 | GSE151708 | GEO
Project description:Developmental and homeostatic remodeling of cellular organelles is mediated by a complex process termed autophagy. The cohort of proteins that constitute the autophagy machinery function in a multistep biochemical pathway. Though components of the autophagy machinery are broadly expressed, autophagy can occur in specialized cellular contexts, and mechanisms underlying cell type-specific autophagy are poorly understood. We demonstrate that the master regulator of hematopoiesis GATA-1 directly activates transcription of genes encoding the essential autophagy component Microtubule Associated Protein 1 Light Chain 3B (LC3B) and its homologs (MAP1LC3A, GABARAP, GABARAPL1, GATE-16). In addition, GATA-1 directly activates genes involved in the biogenesis/function of lysosomes, which mediate autophagic protein turnover. We demonstrate that GATA-1 utilizes the forkhead protein FoxO3 to activate select autophagy genes. GATA-1-dependent LC3B induction is tightly coupled to accumulation of the active form of LC3B and autophagosomes, which mediate mitochondrial clearance as a critical step in erythropoiesis. These results illustrate a novel mechanism by which a master regulator of development establishes a genetic network to instigate cell type-specific autophagy. Genome-wide maps of GATA1 factor occupancy in primary human PBMC derived erythroblasts
2011-09-30 | E-GEOD-32491 | biostudies-arrayexpress
Project description:We examine how different transcriptional network structures can evolve from an ancestral network. We show that regulatory protein modularity, conversion of one cis-regulatory sequence to another, distribution of binding energy among protein-protein and protein-DNA interactions, and exploitation of ancestral network features all contribute to the evolution of a novel mode of regulation at a conserved gene set. The formation of this derived mode of regulation did not disrupt the ancestral mode and thereby created a hybrid regulatory state where both means of transcription regulation (ancestral and derived) contribute to the conserved expression pattern of the network. Finally, we show how this hybrid regulatory state has resolved in different ways in different lineages to generate the diversity of regulatory network structures observed in modern species.
2012-06-26 | GSE38919 | GEO
Project description:This experiment was conducted to identify novel XBP-1 targets involved in liver metabolism. The following abstract from the submitted manuscript describes the major findings of this work. The IRE1a-XBP1s axis regulates the COPII-mediated secretory program in response to nutrient availability. Lin Liu, Jie Cai, Xijun Liang, Qian Zhou, Huimin Wang, Chenyun Ding, Yuangang Zhu, Liwei Xiao, Tingting Fu, Zhisheng Xu, Jing Liu, Yujing Yin, Lei Fang, Bin Xue, Yan Wang, Aibin He, Yong Liu, Xiao-Wei Chen, and Zhenji Gan The cytoplasmic coat protein complex-II (COPII) is an evolutionarily conserved machinery that is essential for efficient trafficking of protein and lipid cargos. How the COPII machinery is regulated to meet the metabolic demand in response to alterations of nutritional state remains largely unexplored, however. Here, we show that dynamic changes of COPII-mediated secretion parallel the activation of XBP1s, the critical transcription factor in handling cellular ER stress, in both live cells and mouse liver upon physiological fluctuations of nutrient availability. Using live-cell imaging approaches, we demonstrate that XBP1s is sufficient to promote COPII-dependent secretion, mediating the nutrient stimulatory effects. ChIP-seq and RNA-seq analyses reveal that nutritional signals induce dynamic XBP1s occupancy of promoters of COPII secretion-related genes, thereby driving COPII-directed secretory process. Liver-specific disruption of the IRE1a-XBP1s signaling branch results in diminished COPII-mediated secretion. Reactivation of XBP1s in mice lacking hepatic IRE1a restores COPII-mediated lipoprotein secretion, and reverses the fatty liver and hypolipidemia phenotypes. Thus, our results demonstrate a previously unappreciated mechanism in the metabolic control of liver protein and lipid secretion: the IRE1a-XBP1s axis functions as a nutrient-sensing regulatory nexus that integrates nutritional states and the COPII secretory program.
2019-06-03 | GSE101202 | GEO
Project description:Tafazzin is a transacylase which causes the content and molecular structure of cardiolipin (CL) to be altered in the inner mitochondrial membrane. The enzymatic machinery responsible for oxidative respiration are localized to the inner mitochondrial membrane and require CL for activity. As a result, tafazzin is critical for maintaining mitochondrial function. In beta-cells, which are the insulin secreting cells in pancreatic islets, mitochondrial function is linked to insulin secretion. We previously established that tafazzin knock-down mice were lean and maintained insulin sensitivity compared to the obese insulin resistant control litter mates. However, it was unknown whether tafazzin deficiency also influenced insulin secretion in the establishment of the lean phenotype. Using X week-old mice, we ascertained that the number of beta-cells was similar between genotypes. Ex vivo insulin secretion under low glucose conditions was reduced (52%) from islets isolated from tafazzin knock-down mice. Consistent with this tafazzin knock-down mice exhibited reduced fasting insulin plasma insulin levels. Measurement of mitochondrial oxygen consumption revealed that basal oxygen consumption was reduced (58%) in islets from tafazzin-deficient animals. The addition of etomoxir, an inhibitor of mitochondrial fatty acid translocation, significantly elevated basal mitochondrial respiration (5-fold) in islets from tafazzin knockdown mice, indicating a significant fatty acid-mediated inhibitory effect. In contrast, etomoxir lacked any measurable effect on control wild-type islets. The altered mitochondrial function identified in taffazin knock-down islets was not associated with reduced CL content or elevated oxyCL species. Our experiments indicate that tafazzin plays a key role in regulating normal islet beta-cell function.
2021-07-31 | GSE136242 | GEO
Project description:We examine how different transcriptional network structures can evolve from a common, ancestral network. We show that regulatory protein modularity, conversion of one cis-regulatory sequence to another, distribution of binding energy among protein-protein and protein-DNA interactions, and exploitation of ancestral network features all contribute to the evolution of a novel mode of regulation at a conserved gene set. The formation of this derived mode of regulation did not disrupt the ancestral mode and thereby created a hybrid regulatory state where both means of transcription regulation (ancestral and derived) contribute to the conserved expression pattern of the network. Finally, we show how this hybrid regulatory state has resolved in different ways in different lineages to generate the diversity of regulatory network structures observed in modern species.
2012-06-29 | GSE39007 | GEO
Project description:Abstract: Secretion occurs in all cells, with relatively low levels in most cells and extremely high levels in specialized secretory cells, such as those of the pancreas, salivary and mammary glands. Here, we report that the CrebA/Creb3-like family of bZip transcription factors functions to upregulate expression of both the general protein machinery required in all cells for secretion and of cell-type specific secreted proteins. Drosophila CrebA directly binds the enhancers of secretory pathway genes and is both necessary and sufficient to activate expression of every secretory pathway component gene examined thus far. Microarray profiling reveals that CrebA also upregulates expression of genes encoding cell type specific secreted components. Finally, we find that the human CrebA orthologues, Creb3L1 and Creb3L2, have the ability to upregulate the secretory pathway in non-secretory cell types. Goals: The goals of the microarray experiments were to identify additional targets of the CrebA transcription factor to learn the range of genes regulated by this transcription factor during embryogenesis. Previous work had indicated that CrebA upregulates the protein machinery of the early secretory pathway. Our new data now shows that in addition to the protein machinery, CrebA also upregulates genes encoding the protein cargo that is secreted from specialized secretory organs. RNA was isolated from stage 11-15 wild type Drosophila embryos and compared to RNA from CrebA null mutant embryos of the same age; all samples were hybridized to the Drosophila Genome 2.0 Affymetrix array. Three individual replicates were obtained for each sample.
2010-10-18 | E-GEOD-23346 | biostudies-arrayexpress
Project description:The formation of mitochondria has enabled eukaryotes to thrive and evolve into multitude of unicellular and multicellular species. The nature of the early mitochondria and its relationship to the ancestral host cell is still unknown. Using a phylogenomic approach we have discovered the presence of core subunits of type II secretion pathway (T2SS) in several unicellular eukaryotes (protists) belonging to jakobids, hetereloboseans and malawimonads. We show that the proteins carry mitochondrial signal sequences and are localized in the protist mitochondria.The mitochondria of Nagleria gruberi were isolated by differential centrifugation and analysed by mass spectrometry. The data analyses revealed about 1000 proteins enriched in the mitochondrial fraction including the components of T2SS.
2021-05-19 | PXD007764 | Pride
Project description:T-cell receptor-induced Ca2+ signals are essential for proper T-cell activation and function. In this context, mitochondria play an important role and take up Ca2+ to support elevated bioenergetic demands. The protein machinery that regulates mitochondrial Ca2+ (mCa2+) uptake; the mitochondrial calcium uniporter (MCU) complex, could be thus implicated in T-cell immunity. However, the exact role of MCU in T-cells is not understood. Here, we show that upon activation of naïve T-cells, the MCU complex undergoes a compositional rearrangement that causes elevated mCa2+ uptake and increased bioenergetic output. Transcriptome and proteome analyses reveal molecular determinants involved in mitochondrial functional reprograming and identify signaling pathways controlled by MCU. MCUa knockdown diminishes mCa2+ uptake, mitochondrial respiration and ATP production as well as T-cell invasion and cytokine secretion. In vivo, downregulation of MCUa in rat CD4+ T-cells suppresses autoimmune responses in a multiple sclerosis model of inflammatory experimental autoimmune encephalomyelitis. In summary, Ca2+ uptake through MCU is essential for proper T-cell function and is involved in autoimmunity. T-cell specific MCU inhibition is a potential tool for treating autoimmune disorders.
2024-10-23 | GSE253049 | GEO