Similar Datasets
Project description:We analyzed Origin Recognition Complex Subunit 2 (ORC2) ChIP-seq from hand-dissected fat body tissue from 68hr (after egg laying, AEL), 92hr AEL, and late-third wandering Drosophila melanogaster larvae. Fat body was dissected from wild-type (OrR) males and testes were removed. We examined ORC2 binding genome-wide with particular focus on the underreplicated regions in the fat body.
2018-07-25 | GSE90916 | GEO
Project description:mRNA-seq and ORC2 ChIP-seq in Drosophila larval fat body
| PRJNA356316 | ENA
Project description:We performed mRNA-seq from hand-dissected fat body tissue from 68hr (after egg laying, AEL) and 92hr AEL Drosophila melanogaster larvae. Fat body was dissected from wild-type (OrR) males and testes were removed. We examined gene expression genome-wide with particular focus on genes in the underreplicated regions in the fat body.
2018-07-25 | GSE90915 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-04-04 | GSE218762 | GEO
Project description:In Drosophila, the humoral response characterised by the synthesis of antimicrobial peptides (AMPs) in the fat body (the equivalent of the mammalian liver) and the cellular response mediated by haemocytes (blood cells) engaged in phagocytosis represent two major reactions that counter pathogens. Although considerable analysis has permitted the elucidation of mechanisms pertaining to the two responses individually, the mechanism of their coordination has been unclear. To characterise the signals with which infection might be communicated between blood cells and fat body, we ablated circulating haemocytes and defined the parameters of AMP gene activation in larvae. We found that targeted ablation of blood cells influenced the levels of AMP gene expression in the fat body following both septic injury and oral infection. Expression of the AMP gene drosomycin (a Toll target) was blocked when expression of the Toll ligand Spätzle was knocked down in haemocytes. These results show that in larvae, integration of the two responses in a systemic reaction depend on the production of a cytokine (spz), a process that strongly parallels the mammalian immune response.
| S-EPMC2787462 | biostudies-literature
Project description:In Drosophila, the fat body undergoes a massive burst of autophagy at the end of larval development in preparation for the pupal transition. To identify genes involved in this process, we carried out a microarray analysis. We found that mRNA levels of the homologs of Atg8, the coat protein of early autophagic structures, and lysosomal hydrolases were upregulated, consistent with previous results. Genes encoding mitochondrial proteins and many chaperones were downregulated, including the inhibitor of eIF2alpha kinases and the peptidyl-prolyl cis-trans isomerase FK506-binding protein of 39 kDa (FKBP39). Genetic manipulation of FKBP39 expression had a significant effect on autophagy, potentially through modulation of the transcription factor Foxo. Accordingly, we found that Foxo mutants cannot properly undergo autophagy in response to starvation, and that overexpression of Foxo induces autophagy.
| S-EPMC2084463 | biostudies-literature
Project description:Protein homeostasis (proteostasis) is crucial for the maintenance of cellular homeostasis. Impairment of proteostasis activates proteotoxic and unfolded protein response pathways to resolve cellular stress or induce apoptosis in damaged cells. However, the responses of individual tissues to proteotoxic stress and evoking cell death program have not been extensively explored in vivo. Here, we show that a reduction in Nascent polypeptide-associated complex protein alpha subunit (Nacα) specifically and progressively induces cell death in Drosophila fat body cells. Nacα mutants disrupt both ER integrity and the proteasomal degradation system, resulting in caspase activation through JNK and p53. Although forced activation of the JNK and p53 pathways was insufficient to induce cell death in the fat body, the reduction of Nacα sensitized fat body cells to intrinsic and environmental stresses. Reducing overall protein synthesis by mTor inhibition or Minute mutants alleviated the cell death phenotype in Nacα mutant fat body cells. Our work revealed that Nacα is crucial for protecting the fat body from cell death by maintaining cellular proteostasis, thus demonstrating the coexistence of a unique vulnerability and cell death resistance in the fat body.
| S-EPMC10474126 | biostudies-literature
Project description:The midgut and fat body of insects control key physiological processes, including growth, digestion, metabolism, and stress response. Single-nucleus RNA sequencing (snRNA-seq) is a promising way to reveal organ complexity at the cellular level, yet data for lepidopteran insects are lacking. We utilized snRNA-seq to assess cellular diversity in the midgut and fat body of Spodoptera frugiperda. Our study identified 20 distinct clusters in the midgut, including enterocytes, enteroendocrine, stem-like cells, and muscle cells, and 27 clusters in the fat body, including adipocytes, hemocytes, and epithelial cells. This dataset, containing all identified cell types in midgut and fat body, is valuable for characterizing the cellular composition of these organs and uncovering new cell-specific biomarkers. This cellular atlas enhances our understanding of cellular heterogeneity of fat and midgut, serving as a basis for future functional and comparative analyses. As the first snRNA-seq study on the midgut and fat body of S. frugiperda, it will also support future research, contribute to lepidopteran studies, and aid in developing targeted pest control strategies.
| S-EPMC11822134 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2016-04-06 | E-GEOD-77342 | biostudies-arrayexpress
Project description:Gene expression variation is pervasive across all levels of organismal organization, including development. Few studies, however, have examined variation in developmental transcriptional dynamics among populations, or how it contributes to phenotypic divergence. Indeed, the evolution of gene expression dynamics when both the evolutionary and temporal timescale are comparatively short remains relatively uncharacterized. Here, we examined coding and non-coding gene expression in the fat body of an ancestral African and a derived European Drosophila melanogaster population across three developmental stages spanning ten hours of larval development. Between populations, expression divergence was largely stage-specific. We detected higher expression variation during the late wandering stage, which may be a general feature of this stage. During this stage, we also detected higher and more extensive lncRNA expression in Europe, suggesting that lncRNA expression may be more important in derived populations. Interestingly, the temporal breadth of protein-coding and lncRNA expression became more restricted in the derived population. Taken together with the signatures of potential local adaptation that we detected at the sequence level in 9-25% of candidate genes (those showing evidence of expression divergence between populations), this finding suggests that gene expression becomes more developmental stage-specific during adaptation to new environments. We further used RNAi to identify several candidate genes that likely contribute to known phenotypic divergence between these populations. Our results shed light on the evolution and dynamics of expression variation over short developmental and evolutionary timescales, and how this variation contributes to population and phenotypic divergence.
| S-EPMC10166500 | biostudies-literature