C. elegans LPIN-1 moderates lifespan-shortening effects of dietary glucose via maintaining ω-6 polyunsaturated fatty acids
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ABSTRACT:
PROVIDER: PRJNA574273 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10189234_1.fastq.gz | Fastqsanger.gz | |||
| SRR10189234_2.fastq.gz | Fastqsanger.gz | |||
| SRR10189235_1.fastq.gz | Fastqsanger.gz | |||
| SRR10189235_2.fastq.gz | Fastqsanger.gz | |||
| SRR10189236_1.fastq.gz | Fastqsanger.gz |
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Project description:A glucose-rich diet shortens lifespan via altering lipid metabolism in many organisms, including Caenorhabditis elegans. However, it remains incompletely understood how glucose and lipid metabolism regulates lifespan. Here, we show that Lipin 1/LPIN-1, a phosphatidic acid phosphatase and a putative transcription co-regulator that mediates glucose-to-triacylglyceride synthesis, prevents the life-shortening effects of glucose-rich diets on C. elegans. We showed that the expression levels of many genes related to lipid metabolism were differentially regulated by lpin-1 RNAi and glucose treatment.
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Project description:Excessive glucose causes various diseases and decreases lifespan by altering metabolic processes, but underlying mechanisms remain incompletely understood. Here, we show that Lipin 1/LPIN-1, a phosphatidic acid phosphatase and a putative transcriptional coregulator, prevents life-shortening effects of dietary glucose on Caenorhabditis elegans. We found that depletion of lpin-1 decreased overall lipid levels, despite increasing the expression of genes that promote fat synthesis and desaturation, and downregulation of lipolysis. We then showed that knockdown of lpin-1 altered the composition of various fatty acids in the opposite direction of dietary glucose. In particular, the levels of two ω-6 polyunsaturated fatty acids (PUFAs), linoleic acid and arachidonic acid, were increased by knockdown of lpin-1 but decreased by glucose feeding. Importantly, these ω-6 PUFAs attenuated the short lifespan of glucose-fed lpin-1-inhibited animals. Thus, the production of ω-6 PUFAs is crucial for protecting animals from living very short under glucose-rich conditions.
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Project description:The optimal ratio of omega-6 to omega-3 polyunsaturated fatty acids (PUFAs) is important for keeping homeostasis of biological processes and metabolism, yet the underlying biological mechanism is poorly understood. The objective of this study was to identify changes in the pig liver transcriptome induced by a diet enriched with omega-6 and omega-3 fatty acids, and to characterize the biological mechanisms related to PUFA metabolism. Polish Landrace pigs (n =12) were fed diet enriched with linoleic acid (LA, omega-6) and alpha-linolenic acid (ALA, omega-3 family) or standard diet as a control. The fatty acids profiling was assayed in order to verify how feeding influenced the fatty acids content in liver, and subsequently next-generation sequencing (NGS) was used to identify differentially expressed genes (DEG) between transcriptomes between dietary groups. The biological mechanisms and pathway interaction networks were identified by analysis in DAVID and Cytoscape tools. Fatty acids profile analysis indicated a higher contribution of PUFAs in liver for LA and ALA-enriched diet group, particularly for the omega-3 fatty acids family, but not omega-6. Next-generation sequencing identified 3,565 DEG, 1,484 of which were induced and 2,081 were suppressed by PUFA supplemenation. Low ratio of omega-6/-3 fatty acids resulted in modulation of fatty acids metabolism pathways and over-representation of genes involved in membrane composition, signal transduction and immune response pathways. In conclusion, a diet enriched with omega-6 and omega-3 fatty acids altered the transcriptomic profile of the pig liver and affected a set of genes involved in metabolic pathways important to animal health status. Hepatic mRNA profiles of Polish Landrace pig breed fed two different diets, were generated by deep sequencing, using Illumina MiSeq. Experimental diet was enriched with polyunsaturated fatty acids (omega-6 and omega-3), while standard diet remain as a cotrol. 2 pooled samples each containing RNA extracts from 6 individuals livers were analyzed.
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Project description:The optimal ratio of omega-6 to omega-3 polyunsaturated fatty acids (PUFAs) is important for keeping homeostasis of biological processes and metabolism, yet the underlying biological mechanism is poorly understood. The objective of this study was to identify changes in the pig liver transcriptome induced by a diet enriched with omega-6 and omega-3 fatty acids, and to characterize the biological mechanisms related to PUFA metabolism. Polish Landrace pigs (n =12) were fed diet enriched with linoleic acid (LA, omega-6) and alpha-linolenic acid (ALA, omega-3 family) or standard diet as a control. The fatty acids profiling was assayed in order to verify how feeding influenced the fatty acids content in liver, and subsequently next-generation sequencing (NGS) was used to identify differentially expressed genes (DEG) between transcriptomes between dietary groups. The biological mechanisms and pathway interaction networks were identified by analysis in DAVID and Cytoscape tools. Fatty acids profile analysis indicated a higher contribution of PUFAs in liver for LA and ALA-enriched diet group, particularly for the omega-3 fatty acids family, but not omega-6. Next-generation sequencing identified 3,565 DEG, 1,484 of which were induced and 2,081 were suppressed by PUFA supplemenation. Low ratio of omega-6/-3 fatty acids resulted in modulation of fatty acids metabolism pathways and over-representation of genes involved in membrane composition, signal transduction and immune response pathways. In conclusion, a diet enriched with omega-6 and omega-3 fatty acids altered the transcriptomic profile of the pig liver and affected a set of genes involved in metabolic pathways important to animal health status.
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2018-08-29 | GSE104338 | GEO
Project description:There is a gap in our understanding of the protective effect of the essential ω-3 long-chain polyunsaturated fatty acid (LCPUFA) docosahexaenoic acid (DHA) on proliferative retinopathies. In retinopathy of prematurity (ROP), DHA supplementation alone may not reduce the risk for severe disease. We found that in mouse neonates with hyperglycemia-associated retinopathy (HAR) with impaired retinal vessel growth modeling Phase I ROP versus controls, there was a strong metabolic shift in almost all types of retinal neuronal cells identified with single-cell transcriptomics. Loss of adiponectin (Apn-/-), modeling low APN seen in premature infants, caused a ω-3 and ω-6 LCPUFA imbalance in HAR mouse retinas. Dietary intake of ω-3 vs ω-6 LCPUFA promoted retinal vessel growth, associated with increased APN levels and increased retinal APN receptor AdipoR1 gene expression. Interestingly, we found that ω-6 vs. ω-3 LCPUFA was essential in maintaining retinal metabolism and neuronal development. Our findings suggest that both ω-3 and ω-6 LCPUFA are essential in protecting against retinal neurovascular dysfunction in Phase I ROP model. Maintaining adequate ω-6 LCPUFA levels is required while supplementing ω-3 LCPUFA to prevent retinopathy.
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Project description:Staphylococcus aureus is a major human pathogen that causes infection in a wide variety of sites within the human body. Its ability to adapt to the human host, and to produce a successful infection, requires precise orchestration of gene expression. While DNA-dependent RNA polymerase (RNAP) is generally well characterized, the role of several small accessory subunits within the complex has yet to be fully explored. This is particularly true for the omega (ω or RpoZ) subunit, which has been extensively studied in Gram-negative bacteria, but largely neglected in Gram-positive counterparts. In Escherichia coli, it has been shown that ppGpp binding, and thus control of the stringent response, is facilitated by ω. Interestingly, key residues that facilitate ppGpp binding by ω are not conserved in S. aureus, and consequently, survival under starvation conditions is unaffected by rpoZ deletion. Further to this, ω-lacking strains of S. aureus display structural changes in the RNAP complex, which result from increased degradation and misfolding of the β’ subunit, alterations in δ and σ-factor abundance, and a general dissociation of RNAP in the absence of ω. Through RNAseq analysis we detected a variety of transcriptional changes in rpoZ-deficient strains, presumably as a response to the negative effects of ω-depletion on the transcription machinery. These transcriptional changes translated to an impaired ability of ΔrpoZ mutant strains to resist stress, and to fully form a biofilm. Collectively, our data underlines, for the first time, the importance of ω for RNAP stability, function and cellular physiology in S. aureus.
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