Zebrafish juvenile mpeg+ macrophages
Ontology highlight
ABSTRACT:
ORGANISM(S): Danio rerio
PROVIDER: GSE149787 | GEO | 2020/05/05
REPOSITORIES: GEO
Similar Datasets
Project description:We used zebrafish lacking functional csf1r to unravel how and when csf1r is necessary for the development of early tissue macrophages from embryonic macrophages. Transcriptomic analysis of mpeg+ macrophages revealed that csf1r deficient macrophages show a macrophage transcriptome, but reduced expression of cell cycle and RNA/DNA metabolism related genes. Transcriptional changes over time were similar between wildtype controls als csf1r deficient embryonic macrophages.
2020-05-05 | GSE149786 | GEO
Project description:Zebrafish juvenile mpeg+ macrophages
| PRJNA630163 | ENA
Project description:We compared hematopoietic and non-hematopoietic mpeg1.1+ cells from the skin of wild-type fish with non-hematopoietic cells from the skin of zebrafish lacking functional csf1r. We reval that non-hematopoietic mpeg1.1 cells from wild-type and csf1rDM fish show no major differences and likely represent metaphocytes, a newly characterized ectoderm-derived cell population in the skin. Both non-hematopoietic mpeg1.1+ cell populations from wild-type and csf1r mutatns show a major downregulations in canonical macrophages signature genes as compared to hematopoietic mpeg1.1 cells from wild-type fish.
2020-05-05 | GSE149788 | GEO
Project description:In an HPV-induced hyperplastic epithelium mouse model, hyperproliferative Keratinocytes (KCs) showed reduced Interleukin 34 (IL34) expression and chromatin accessibility, associating disturbing cell-cell interaction and immune response genes. Correspondingly, Langerhans cells (LCs) exhibited altered chromatin accessibility, including increased accessibility of IL34's receptor - the colony-stimulating factor 1 receptor (Csf1r) and reduced accessibility in antigen uptake and presentation genes.
2024-10-30 | GSE268544 | GEO
Project description:Juvenile Fluorescence Raw sequence reads
| PRJNA436185 | ENA
Project description:Background. Juvenile hormone (JH) has been demonstrated to control adult lifespan in a number of non-model insects where surgical removal of the corpora allata eliminates the hormone’s source. In contrast, little is known about how juvenile hormone affects adult Drosophila melanogaster. Previous work suggests that insulin signaling may modulate Drosophila aging in part through its impact on juvenile hormone titer, but no data yet addresses whether reduction of juvenile hormone is sufficient to control Drosophila life span. Here we adapt a recent genetic approach to knock out the corpora allata in adult Drosophila melanogaster and characterize adult life history phenotypes produced by reduction of juvenile hormone. With this system we test potential explanations for how juvenile hormone modulates aging. Conclusions. Reduced juvenile hormone alone is sufficient to extend lifespan of Drosophila melanogaster. Reduced juvenile hormone limits reproduction by inhibiting the production of yolked eggs, and this may arise because juvenile hormone is required for the post-eclosion development of vitellogenin-producing adult fat body. Our data do not support a mechanism for juvenile hormone control of longevity simply based on reducing the physiological costs of reproductive. Nor does the longevity benefit appear to function through mechanisms by which dietary restriction extends longevity. We identify transcripts that change in response to juvenile hormone independent of reproductive state and suggest these represent somatically expressed genes that could modulate how juvenile hormone controls persistence and longevity.
2013-07-26 | GSE48145 | GEO
Project description:Metaphocytes are tissue-resident myeloid-like cells of non-hematopoietic origin in zebrafish barrier tissues. How metaphocytes acquire myeloid cell properties from non-hematopoietic precursors during the development remains unknown. Here we show that metaphocytes are in situ generated from local progenitors guided by the ETS transcription factor Spic. Tg(spic:EGFP) transgenic fish were found to label both metaphocytes and their progenitor cells. While spic is dispensable for the formation of the metaphocyte progenitors, it is required for the progenitors to differentiate into immature metaphocytes. To decipher the molecular basis underlying the developmental arrest of metaphocytes in spic mutants, we sorted the metaphocyte progenitor cells from the epidermis and gill of the mutants and siblings and performed bulk RNA-seq analysis. The data suggests that Spic orchestrates the development of metaphocytes by promoting the expression of myeloid-associated genes, either directly or indirectly through downstream transcription factors.
2023-04-08 | GSE228732 | GEO
Project description:Metaphocytes are tissue-resident myeloid-like cells of non-hematopoietic origin in zebrafish barrier tissues. How metaphocytes acquire myeloid cell properties from non-hematopoietic precursors during the development remains unknown. Here we show that metaphocytes are in situ generated from local progenitors guided by the ETS transcription factor Spic. Tg(spic:EGFP) transgenic fish were found to label both metaphocytes and their progenitor cells. To reveal the genetic programs underlying the development of metaphocytes, we performed single-cell RNA sequencing analysis of spic:GFP+ cells in the epidermis of adult Tg(spic:EGFP) fish. The result further supports that mature metaphocytes are generated from spic+ progenitors via an intermediate immature state and gradually obtain their myeloid characteristics during this process.
2023-04-08 | GSE228737 | GEO
Project description:CSF1R is a receptor involved in differentiation and survival of macrophages. We designed this study to explore the consequences of CSF1R targeting on human macrophage transcriptome. We also seek to explore the influence of oxygen environnment on the consequences of CSF1R blocakde . Our data provide an extensive characterization of the various pathways connected to CSF1/CSF1R pathway in human macrophages.
2024-04-18 | GSE263919 | GEO
Project description:Background. Juvenile hormone (JH) has been demonstrated to control adult lifespan in a number of non-model insects where surgical removal of the corpora allata eliminates the source of hormone. In contrast, little is known about how juvenile hormone affects adult Drosophila melanogaster. Previous work suggests that insulin signaling may modulate Drosophila aging in part through its impact on juvenile hormone titer, but no data yet addresses whether reduction of juvenile hormone is sufficient to control Drosophila life span. Here we adapt a recent genetic approach to knock out the corpora allata in adult Drosophila melanogaster and characterize adult life history phenotypes produced by reduction of juvenile hormone. With this system we test potential explanations for how juvenile hormone modulates aging. Conclusions. Reduced juvenile hormone alone is sufficient to extend lifespan of Drosophila melanogaster. Reduced juvenile hormone limits reproduction by inhibiting the production of yolked eggs, and this may arise because juvenile hormone is required for the post-eclosion development of vitellogenin-producing adult fat body. Our data do not support a mechanism for juvenile hormone control of longevity simply based on reducing the physiological costs of reproductive. Nor does the longevity benefit appear to function through mechanisms by which dietary restriction extends longevity. We identify transcripts that change in response to juvenile hormone independent of reproductive state and suggest these represent somatically expressed genes that could modulate how juvenile hormone controls persistence and longevity. Four genotypes were analyzed. They are CA knockout (CAKO), wildtype (wDah/w1118 ), CAKO with OvoD1 mutation and control (wDah/w1118) with OvoD1 mutation. Three biological replicates for each genotype.
2013-07-26 | E-GEOD-48145 | biostudies-arrayexpress