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Age-specific variation in immune response in Drosophila melanogaster has a genetic basis.

ABSTRACT: Immunosenescence, the age-related decline in immune system function, is a general hallmark of aging. While much is known about the cellular and physiological changes that accompany immunosenescence, we know very little about the genetic influences on this phenomenon. We used microarrays to determine genome-wide expression profiles in twelve inbred D. melanogaster lines that varied in their ability to to clear an E. coli infection at one and four weeks of age. Bacterially infected and sham-injected flies from each of the lines were frozen at -80M-BM-0C six hours post-injection at one and four weeks of age for use in the microarray study. Lines were chosen to represent the range of changes in age-specific clearance ability: four of the lines chosen exhibited the most dramatic decline in clearance ability with age, four of the lines exhibited the least amount of change in clearance, and the remaining four lines exhibited the most dramatic improvement in clearance ability with age (Please note that the clearance ability of each line was not considered in the microarray data analysis). In this case all of the expression data came from pooling the RNA extracted from individuals from each line (8-15 individuals) at each age from each treatment (sham injected vs. infected).

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Jenny Drnevich

PROVIDER: E-GEOD-37708 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Age-specific variation in immune response in Drosophila melanogaster has a genetic basis.

Project description:Immunosenescence, the age-related decline in immune system function, is a general hallmark of aging. While much is known about the cellular and physiological changes that accompany immunosenescence, we know very little about the genetic influences on this phenomenon. We used microarrays to determine genome-wide expression profiles in twelve inbred D. melanogaster lines that varied in their ability to to clear an E. coli infection at one and four weeks of age.

2012-05-03 | GSE37708 | GEO

Transcriptional profiling of young and old mouse macrophages interacting with nanoparticles [scRNA-seq]

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Transcriptional profiling of young and old mouse macrophages interacting with nanoparticles [Bulk RNA-seq]

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Syringaresinol delays immunosenescence in aged mice: rejuvenating the immune system and reconstituting the gut microbiota

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2017-02-08 | GSE75825 | GEO

Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia

Project description:Aging of immune organs, termed as immunosenescence, is suspected to promote systemic inflammation and age-associated disease. The cause of immunosenescence and how it promotes disease, however, has remained unexplored. We report that the Drosophila fat body, a major immune organ, undergoes immunosenescence and mounts strong systemic inflammation that leads to de-regulation of immune deficiency (IMD) signaling in the midgut of old animals. Inflamed old fat bodies secrete circulating peptidoglycan recognition proteins that repress IMD activity in the midgut, thereby promoting gut hyperplasia. Further, fat body immunosenecence is caused by ageassociated lamin-B reduction specifically in fat body cells, which then contributes to heterochromatin loss and de-repression of genes involved in immune responses. As lamin-associated heterochromatin domains are enriched for genes involved in immune response in both Drosophila and mammalian cells, our findings may provide insights into the cause and consequence of immunosenescence during aging.

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Age-associated loss of lamin-B leads to systemic inflammation and gut hyperplasia

2014-10-23 | E-GEOD-62580 | biostudies-arrayexpress

AginAging: a portrait from gene expression profile in blood cells: a portrait from gene expression profile in blood cells.

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2016-08-19 | GSE67220 | GEO

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2015-05-18 | E-GEOD-54152 | biostudies-arrayexpress

Systematic Transcriptome Analysis of Zebrafish Model of Diamond-Blackfan Anemia from RPS24 Deficiency (miRNA-Seq)

Project description:In this study, we found RPS24 is required for both the primitive hematopoiesis and definitive hematopoiesis process partly mediated by P53 pathway. With the RNA-seq and miRNA-seq technique, several deregulated genes and miRNAs were found to be related with hematopoiesis, vascular development and apoptosis process in RPS24-deficient zebrafish. Meanwhile, a comprehensive regulatory network was firstly constructed to indentify the mechanisms of key miRNAs and gene pathways in this Model of Diamond-Blackfan Anemia. Interestingly, we found that the central nodes genes in the network were almost all targeted by significantly deregulated miRNAs, with partial verification from previous studies, revealing that our network-based approach is promising for the identification of new and important miRNAs in DBA. The present study provided comprehensive potential pathogenic genes and miRNAs data that are associated with RPS24-deficient zebrafish embryos as a model of DBA, which should provide a valuable resource for understanding the complex molecular pathogenesis of mutant RPS24-mediated human diseases. Determine the differences of miRNome between RPS24-deficient and MO control zebrafish embryos for understanding the complex molecular pathogenesis of mutant RPS24-mediated human diseases

2015-05-18 | E-GEOD-54259 | biostudies-arrayexpress

Transcriptome analysis of the Zebrafish model of Diamond-Blackfan Anemia from RPS19 deficiency via p53-dependent and -independent pathways

Project description:To determine the effect on the whole transcriptome of RPS19 morpholino and to identify the function of p53 in RPS19-deficient embryos, we analyzed the genome-wide transcript profiles of control morpholino (control), RPS19 morpholino knockdown (RPS19 MO), and RPS19 and p53 morpholino knockdown simultaneously (RPS19+p53 MO) using the Illumina Hi-seq 2000 Genome Analyzer platform with paired-end 100 base-pair tags to a depth of 35-60 million reads. We found that genes enriched in the functions of hematological systems and nervous system development and that skeletal and muscular disorders had significant differential expression in RPS19 MO embryos compared with controls. Co-inhibition of p53 partially alleviates the abnormalities for RPS19-deficient embryos. However, the hematopoietic genes, which were down-regulated significantly in RPS19 MO embryos, were not completely recovered by the co-inhibition of p53. Furthermore, we identified the genome-wide p53-dependent and -independent genes and pathways. These results indicate that not only p53 family members but also several other factors have important impacts on RPS19-deficient embryos. The detection of potential pathogenic genes and pathways provides us a new paradigm for research on DBA, which is a systematic and complex hereditary disease. Compare mRNA transcriptomes of three different souces of zebrafish embryos

2013-10-09 | E-GEOD-45699 | biostudies-arrayexpress

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