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Leptin mutation and mycobacterial infection lead non-synergistically to a similar metabolic syndrome

ABSTRACT: Leptin mutation and mycobacterial infection lead non-synergistically to a similar metabolic syndrome

PROVIDER: PRJNA873086 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21228018_1.fastq.gz	Fastqsanger.gz
	SRR21228018_2.fastq.gz	Fastqsanger.gz
	SRR21228019_1.fastq.gz	Fastqsanger.gz
	SRR21228019_2.fastq.gz	Fastqsanger.gz
	SRR21228020_1.fastq.gz	Fastqsanger.gz

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Leptin mutation and mycobacterial infection lead non-synergistically to a similar metabolic syndrome

Project description:The leptin signaling pathway plays an important role as a key regulator of glucose homeostasis, metabolism control and systemic inflammatory responses. However, the metabolic effects of leptin on infectious diseases, for example tuberculosis, is still little known. For transcriptome studies of zebrafish larvae, deep RNA sequencing was used. Mycobacteria induced a very distinct transcriptome signature in the lepbibl54 mutant zebrafish compared to wild type sibling control larvae.

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Genome-wide analysis of gene expression in response to leptin and IL-1β in gingival fibroblasts

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Defining the Transcriptional Targets of Leptin Reveals a Role for Atf3 in Leptin Action

Project description:We employed translating ribosome affinity purification followed by RNA sequencing to isolate and analyze mRNA from the hypothalamic LepRb neurons of wild-type or leptin-deficient (Lepob/ob) mice treated with vehicle or exogenous leptin. Although the expression of most of the genes encoding the neuropeptides commonly considered to represent the main targets of leptin action were altered only following chronic leptin deprivation, our analysis revealed other transcripts that were coordinately regulated by leptin under multiple treatment conditions. Among these, acute leptin treatment increased expression of the transcription factor Atf3 in LepRb neurons.

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Project description:Genome wide association studies (GWAS) in obesity have identified a large number of noncoding loci located near genes expressed in the central nervous system. However, due to the difficulties in isolating and characterizing specific neuronal subpopulations, very few obesity-associated SNPs have been functionally characterized. Leptin responsive neurons in the hypothalamus are essential in controlling energy homeostasis and body weight. Here, we show that by combining FACS-sorting of leptin-responsive hypothalamic neuron nuclei with genomic approaches (RNA-seq, ChIP-seq, ATAC-seq), we can provide a comprehensive map of leptin-response specific regulatory elements, several of which overlap obesity-associated GWAS variants. Further demonstrating the robustness of our leptin-response neuron regulome, we functionally characterize a novel enhancer near Socs3, a leptin response-associated transcription factor. Combined, our results provide a comprehensive map of active genomic regions in leptin-responsive neurons and present a blueprint for functionally characterizing obesity-associated SNPs in the hypothalamus.

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Project description:Obesity induces profound transcriptome changes in adipocytes; recent evidence suggests that lncRNAs play key roles in this process. Here, we performed a comprehensive transcriptome study by RNA-Seq in adipocytes isolated from interscapular brown, inguinal and epididymal white adipose tissues in diet-induced obese mice. Our analysis reveals a set of obesity-dysregulated lncRNAs, many of which exhibit dynamic changes in fed vs. fasted state, potentially serving as novel molecular markers reflecting adipose energy status. Among the most prominent ones is Lnc-leptin, an lncRNA transcribed from an enhancer region upstream of Leptin. Expression of Lnc-leptin is sensitive to insulin and closely correlates to Leptin expression across diverse pathophysiological conditions. Functionally, induction of Lnc-leptin is essential for adipogenesis, and its presence is required for a loop formation between exon2 of Lnc-leptin and promoter of Leptin in mature adipocytes and the maintenance of Leptin expression in vitro and in vivo. Our study establishes Lnc-leptin as a new regulator of Leptin.

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2019-07-12 | PXD013466 | Pride

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