Fat Body Cells Are Motile and Actively Migrate to Wounds to Drive Repair and Prevent Infection.
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ABSTRACT:
SUBMITTER: Franz A
PROVIDER: S-EPMC6113741 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:modENCODE_submission_5522 This submission comes from a modENCODE project of David MacAlpine. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: Most terminally differentiated Drosophila tissues are either polyploid or polytene. Unlike normal chromosomes, where the entire chromosome must be replicated exactly once, polytene chromosomes are often differentially replicated with many regions underreplicated and some overreplicated. We will characterize five different polytene tissues using comparative genomic hybridization (CGH) to identify differentially replicated regions of each chromosome. These studies will also identify tissue specific amplicons, where the replication mediated amplification of specific loci is essential for up-regulation of mRNA levels encoding proteins critical for development. The differential replication of polytene chromosomes in Drosophila will provide a unique opportunity to understand how developmental cues and chromosomal domains influence replication initiation. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CGH. BIOLOGICAL SOURCE 1: Strain: Oregon-R Orr-Weaver(genotype : TBA outcross : TBA description : Wild-type Oregon-R population maintained by Terry Orr-Weaver. made_by : wt population ); Tissue: Fatbody; Developmental Stage: cleavage stage; Genotype: TBA; Sex: Unknown; BIOLOGICAL SOURCE 2: Strain: Oregon-R Orr-Weaver(genotype : TBA outcross : TBA description : Wild-type Oregon-R population maintained by Terry Orr-Weaver. made_by : wt population ); Tissue: Fatbody; Developmental Stage: cleavage stage; Genotype: TBA; Sex: Unknown; NUMBER OF REPLICATES: 1; EXPERIMENTAL FACTORS: Tissue Fatbody
2012-06-03 | E-GEOD-38440 | biostudies-arrayexpress
Project description:modENCODE_submission_5522 This submission comes from a modENCODE project of David MacAlpine. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: Most terminally differentiated Drosophila tissues are either polyploid or polytene. Unlike normal chromosomes, where the entire chromosome must be replicated exactly once, polytene chromosomes are often differentially replicated with many regions underreplicated and some overreplicated. We will characterize five different polytene tissues using comparative genomic hybridization (CGH) to identify differentially replicated regions of each chromosome. These studies will also identify tissue specific amplicons, where the replication mediated amplification of specific loci is essential for up-regulation of mRNA levels encoding proteins critical for development. The differential replication of polytene chromosomes in Drosophila will provide a unique opportunity to understand how developmental cues and chromosomal domains influence replication initiation. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf
2012-06-04 | GSE38440 | GEO
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Project description:Postnatal tissue quiescence is thought to be a default state in the absence of a proliferative stimulus such as injury. Although previous studies have demonstrated that certain embryonic developmental programs are reactivated aberrantly in adult organs to drive repair and regeneration, it is not well understood how quiescence is maintained in organs such as the lung, which displays a remarkably low level of cellular turnover. Here we demonstrate that quiescence in the adult lung is an actively maintained state and is regulated by hedgehog signalling. Epithelial-specific deletion of sonic hedgehog (Shh) during postnatal homeostasis in the murine lung results in a proliferative expansion of the adjacent lung mesenchyme. Hedgehog signalling is initially downregulated during the acute phase of epithelial injury as the mesenchyme proliferates in response, but returns to baseline during injury resolution as quiescence is restored. Activation of hedgehog during acute epithelial injury attenuates the proliferative expansion of the lung mesenchyme, whereas inactivation of hedgehog signalling prevents the restoration of quiescence during injury resolution. Finally, we show that hedgehog also regulates epithelial quiescence and regeneration in response to injury via a mesenchymal feedback mechanism. These results demonstrate that epithelial-mesenchymal interactions coordinated by hedgehog actively maintain postnatal tissue homeostasis, and deregulation of hedgehog during injury leads to aberrant repair and regeneration in the lung.
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Project description:Histone H3 trimethylation at lysine 36 (H3K36me3) is an important histone mark involved in both transcription elongation and DNA mismatch repair (MMR). It is known that H3K36me3 recruits the mismatch-recognition protein MutS? to replicating chromatin via its physical interaction with MutS?'s PWWP domain, but the exact role of H3K36me3 in transcription is undefined. Using ChIP combined with whole-genome DNA sequencing analysis, we demonstrate here that H3K36me3, together with MutS?, is involved in protecting against mutation, preferentially in actively transcribed genomic regions. We found that H3K36me3 and MutS? are much more co-enriched in exons and actively transcribed regions than in introns and nontranscribed regions. The H3K36me3-MutS? co-enrichment correlated with a much lower mutation frequency in exons and actively transcribed regions than in introns and nontranscribed regions. Correspondingly, depleting H3K36me3 or disrupting the H3K36me3-MutS? interaction elevated the spontaneous mutation frequency in actively transcribed genes, but it had little influence on the mutation frequency in nontranscribed or transcriptionally inactive regions. Similarly, H2O2-induced mutations, which mainly cause base oxidations, preferentially occurred in actively transcribed genes in MMR-deficient cells. The data presented here suggest that H3K36me3-mediated MMR preferentially safeguards actively transcribed genes not only during replication by efficiently correcting mispairs in early replicating chromatin but also during transcription by directly or indirectly removing DNA lesions associated with a persistently open chromatin structure.
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Project description:Tissue interactions are critical for maintaining homeostasis; however, little is known about how remote tissue regulates regeneration. Previously, we established a genetic dual system that induces cell ablation in Drosophila larval imaginal discs and simultaneously manipulates genes in non-damaged tissues. Using humoral metabolome analysis and a genetic damage system, we found that the Tryptophan (Trp)-Kynurenine (Kyn) pathway in the fat body is required for disc repair. Genetic manipulation of Trp-Kyn metabolism in the fat body impaired disc regeneration without affecting wing development. In particular, the fat body-derived humoral kynurenic acid (KynA) was required for disc repair. The impairment of S-adenosylmethionine (SAM) synthesis from methionine (Met) in the fat body hampers the maintenance of KynA levels in hemolymph at the early stage of disc repair, suggesting a connection between Met-SAM and Trp-Kyn metabolisms. Our data indicate KynA from the fat body acts as a permissive metabolite for tissue repair and regeneration.
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Project description:Wound healing is a well-regulated but complex process that involves haemostasis, inflammation, proliferation and maturation. Recent reports suggest that microRNAs (miRs) play important roles in dermal wound healing. In fact, miR deregulation has been linked with impaired wound repair. miR-155 has been shown to be induced by inflammatory mediators and plays a central regulatory role in immune responses. We have investigated the potential role of miR-155 in wound healing. By creating punch wounds in the skin of mice, we found an increased expression of miR-155 in wound tissue when compared with healthy skin. Interestingly, analysis of wounds of mice lacking the expression of miR-155 (miR-155(-/-) ) revealed an increased wound closure when compared with wild-type animals. Also, the accelerated wound closing correlated with elevated numbers of macrophages in wounded tissue. Gene expression analysis of wounds tissue and macrophages isolated from miR-155(-/-) mice that were treated with interleukin-4 demonstrated an increased expression of miR-155 targets (BCL6, RhoA and SHIP1) as well as, the finding in inflammatory zone-1 (FIZZ1) gene, when compared with WT mice. Moreover, the up-regulated levels of FIZZ1 in the wound tissue of miR-155(-/-) mice correlated with an increased deposition of type-1 collagens, a phenomenon known to be beneficial in wound closure. Our data indicate that the absence of miR-155 has beneficial effects in the wound healing process.
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Project description:Transcription is controlled by the interactions of cis-acting DNA elements with diffusible trans-acting factors. Changes in cis or trans factors can drive expression divergence within and between species, and the relative prevalence of each can reveal the evolutionary path to variation. Previous work delineating the mode of expression divergence in animals has largely used whole body expression measurements in a single condition. Since cis-acting elements often drive expression in a subset of cell types or conditions, these measurements may not capture the complete contribution of cis-acting changes. Here, we quantify the mode of expression divergence in the Drosophila fat body, the primary immune organ, in several conditions. We performed allele-specific expression analysis using two geographically distinct lines of D. melanogaster and their F1 hybrids. We performed separate infections with Gram-negative S. marcescens or Gram-positive E. faecalis bacteria, which trigger the two primary signaling pathways in the Drosophila innate immune response. The mode of expression divergence strongly depends on the condition, with trans-acting effects dominating in response to Gram-positive infection and cis-acting effects dominating in Gram-negative and pre-infection conditions. Expression divergence in several receptor proteins may underlie the infection-specific trans effects. Before infection, when the fat body has a metabolic role, there are many compensatory effects, changes in cis and trans that counteract each other to maintain expression levels. This work demonstrates that within a single tissue, the mode of expression divergence varies between conditions and suggests that these differences reflect the diverse evolutionary histories of host-pathogen interactions.
2021-03-23 | GSE155033 | GEO