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RNA-seq of whole female drosophila wounded and/or infected with Pseudomonas entomophila

ABSTRACT: RNA-seq of whole female drosophila wounded and/or infected with Pseudomonas entomophila

PROVIDER: PRJEB19660 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1856410.fastq.gz	Fastqsanger.gz
	ERR1856420.fastq.gz	Fastqsanger.gz
	ERR1856411.fastq.gz	Fastqsanger.gz
	ERR1856421.fastq.gz	Fastqsanger.gz
	ERR1856412.fastq.gz	Fastqsanger.gz

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RNA-seq of whole female drosophila wounded and/or infected with Pseudomonas entomophila

Project description:Combination of both sterile wounding and infection may lead to severe health defects, revealing the importance of the balance between the intensity and resolution of the inflammatory response for the organisms fitness. Underlying mechanisms remain however elusive. Using Drosophila, we analyzed the very first steps of the process by comparing the transcriptome landscape of infected (simple hit flies, SH), wounded and infected (double hit flies, DH) and wounded (control) flies. Our objective was to identify the molecular mechanisms underlying the susceptibility of wounded flies to combined trauma and bacterial infection.

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Project description:Purpose: The goal of this RNA-Seq is to analyze the whole-body transcriptomes from mock-infected bvs oral P.e. infected flies to identify differentially expressed genes Abstract from associated manuscript: When infected by intestinal pathogenic bacteria, animals initiate both local and systemic defence responses. These responses are required to reduce pathogen burden but also to alter host physiology and behaviour to promote infection tolerance, and they are mediated through alterations in host gene expression. Here, we have used transcriptome profiling to examine gene expression changes induced by enteric infection with the gram-negative bacteria Pseudomonas entomophila (P.e) in adult female Drosophila. We find that infection induces a strong upregulation of metabolic gene expression, including gut and fat body-enriched genes involved in lipid transport, lipolysis, and beta-oxidation, as well as glucose and amino acid metabolism genes. Furthermore, we find that the classic innate immune deficiency (Imd)/Relish/NF-KappaB pathway is not required for, and in some cases limits, these infection-mediated increase in metabolic gene expression. We also see that enteric infection with P.e. down regulates the expression of many transcription factors and cell-cell signaling molecules, particularly those previously shown to be involved in gut-to-brain and neuronal signaling. Moreover, as with the metabolic genes, these changes occurred largely independent of the Imd pathway. Together, our study identifies many metabolic, signaling and transcription factor gene expression changes that may contribute to organismal physiological and behavioural responses to enteric pathogen infection. Results: RNA Seq differential expression analysis identified a significant (p<0.05,> 1.5 fold expression) change in 2835transcripts, with 1602 transcripts showing reduced expression levels and 1233 transcripts with elevated expression levels.

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