Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1111600 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29139649_1.fastq.gz | Fastqsanger.gz |
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Project description:Understanding how dietary nutrients alter lipid metabolism in the host is important in deciphering the physiological mechanisms that regulate organismal health. Using the nematode Caenorhabditis elegans as a model organism, I found that a novel gram-positive monomethyl branched-chain fatty acid (mmBCFA) rich bacteria, Microbacterium sp., isolated from C. elegans natural habit can induce supersized lipid droplets (LDs) up to 30 μm in diameter in older animals and adversely affect their lifespan, development rate and brood size. Lipidomic analysis indicated that Microbacterium sp.-fed worms primarily accumulate dietary mmBCFAs in the triacylglycerides stored within LDs. Transcriptomic analysis discovered that the mmBCFA-rich bacteria diet would enhance fatty acid desaturase fat-7 expression and therefore polyunsaturated fatty acids (PUFAs) production to support LD biosynthesis and fusion processes. Additionally, the diet from Microbacterium sp. significantly inhibits creatine kinase argk-1, which results in the suppression of the AMP-activated protein kinase pathway, leading to a halt in mitochondrial beta-oxidation, enhanced lipid de novo synthesis and activation of a mitochondrial unfolded protein response (UPRmt) in C. elegans. Furthermore, using this enlarged LD-inducing bacteria diet, a gain-of-function missense mutation in scav-4 is identified to exacerbate the LD expansion phenotype while the loss of scav-4 results in diminished lipid storage in the worms. Lipidomic analysis showed that the L462F missense mutation nearly doubles the uptake of dietary mmBCFAs, whereas deletion mutants exhibit a reduced proportion of dietary mmBCFAs in total lipids. The localization of SCAV-4 on the intestinal apical membrane and its phylogenetic similarity to the human CD36 fatty acid transporter suggest that SCAV-4 is a homolog of CD36. Structural analysis indicates that the missense mutation is likely located within the transport tunnel, potentially affecting lipid transport. Among the six SCAV family members in C. elegans, SCAV-6 appears to be a less critical paralog compared to SCAV-4, sharing similar expression patterns and showing reduced lipid storage upon deletion. Notably, the transcriptomic analysis reveals that the SCAV-4 missense mutation does not cause much transcriptomic changes under the E. coli OP50 diet but affects over 3,000 genes in response to the Microbacterium sp. diet, suggesting that animals with SCAV-4(L462F) mutation is much more sensitive to the mmBCFAs-rich diet than the wild-type animals. This finding highlights the influence of host genetic variations in the interactions with dietary nutrients, which has strong impact on host metabolism.
2024-12-12 | GSE282709 | GEO
Project description:The project aimed to characterize the collagen type I (COL1) sequences from Pleistocene Macrauchenia sp. and Toxodon sp. bone samples, and by comparison with existing COL1 sequences available from genomic sources establish the phylogenetic position of both extinct species. In order to resolve their phylogenetic position, COL1 was extracted from two Toxodon (samples MLP201204, MACN201212, York12, York13) and two Macrauchenia (samples MLP201212, MACN201202, York14, York15). In addition, modern and Pleistocene COL1 was extracted from additional species currently not present in available databases (Mylodon darwinii, Cyclopes didactylus, Hippopotamus amphibius, Tapirus terrestris) or from species for which COL1 sequences are available (Equus sp., Oryceropus afer). All extractions were performed at BioArCh, University of York (UK). Analyses took place on Bruker maXis HD (Macrauchenia sp., Toxodon sp., Equus sp.) and Thermo Scientific Hybrid Quadruopole-Orbitrap (Macrauchenia sp., Toxodon sp., Mylodon darwinii, Cyclopes didactylus, Hippopotamus amphibius, Tapirus terrestris, Oryceropus afer) platforms.
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Project description:Human solid tumors contain rare cancer side population (SP) cells, which expel the fluorescencent dye H33342 and display cancer stem cell characteristics. Transcriptional profiling of cancer SP cells isolated by H33342 fluorescence analysis is a newly emerging approach to discover cancer stem cell markers and aberrant differentiation pathways. Using Affymetrix expression microarrays this study investigated differential gene expression between SP and non-SP (NSP) cells isolated from the CAL-51 human mammary carcinoma cell line. Keywords: cell type comparison
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Project description:Chronic obstructive pulmonary disease (COPD) is a heterogenous respiratory disease mainly caused by smoking. Respiratory infections constitute a major risk factor for acute worsening of COPD symptoms or COPD exacerbation. Mitochondrial functionality, which is crucial for the execution of physiologic functions of metabolically active cells, is impaired in airway epithelial cells (AECs) of COPD patients as well as smokers. However, the potential contribution of mitochondrial dysfunction in AECs to progression of COPD, infection-triggered exacerbations in AECs and a potential mechanistic link between mitochondrial and epithelial barrier dysfunction is unknown to date. In this study, we used an in vitro COPD exacerbation model based on AECs exposed to cigarette smoke extract (CSE) followed by infection with Streptococcus pneumoniae (Sp). The levels of oxidative stress, as an indicator of mitochondrial stress were quantified upon CSE and Sp. The expression of proteins associated with mitophagy, mitochondrial content and biogenesis as well as mitochondrial fission and fusion was quantified upon CSE and Sp. Transcriptional AEC profiling was performed to identify the potential changes in innate immune pathways and correlate them with mitochondrial function. We found that CSE exposure substantially altered mitochondrial function in AECs by suppressing mitochondrial complex protein levels, reducing mitochondrial membrane potential and increasing mitochondrial stress and mitophagy. Moreover, CSE-induced mitochondrial dysfunction correlated with reduced enrichment of genes involved in apical junctions and innate immune responses to Sp, particularly type I interferon responses. Together, our results demonstrated that CSE-induced mitochondrial dysfunction may contribute to impaired innate immune responses to Sp and may thus trigger COPD exacerbation.
2022-05-27 | GSE197751 | GEO