Metaphocytes Are IL-22BP Producing Cells Regulated by ETS Transcription Factor Spic and Essential for Zebrafish Barrier Immunity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA951389 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24042928_1.fastq.gz | Fastqsanger.gz | |||
| SRR24042928_2.fastq.gz | Fastqsanger.gz | |||
| SRR24042929_1.fastq.gz | Fastqsanger.gz | |||
| SRR24042929_2.fastq.gz | Fastqsanger.gz | |||
| SRR24042930_1.fastq.gz | Fastqsanger.gz |
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Project description:This SuperSeries is composed of the SubSeries listed below.
2023-04-08 | GSE228748 | 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:Understanding mechanisms of epigenetic regulation in embryonic stem cells (ESCs) is of fundamental importance for stem cell and developmental biology. Here we identify Spic, a member of the ETS family of transcription factors, as a specific marker of ground state pluripotency. We show that Spic is rapidly induced in ESCs cultured with GSK3-, MEK-inhibitors and LIF (2iL), and in response to MEK/ERK inhibition. ChIP-seq analysis demonstrated that Spic binds to enhancer elements that are associated with pluripotency genes. Interaction proteomics and genomic profiling confirmed that SPIC interacts with NANOG and stabilizes its binding to chromatin in 2iL-ESCs. Additional gain of function and loss of function experiments revealed that Spic controls genes involved in one carbon (1C) metabolism, Bhmt, Bhmt2, and Dmgdh, and the flux of SAM-to-SAH in 2iL-ESCs. By maintaining low levels of SAM, Spic controls the level of H3K4me3 and H3R17me2 histone methylation in ground state ESCs. Our data highlight the role of uncharacterized axillary transcription factors that link cellular metabolism to epigenetic regulation in ground state pluripotency.
2025-05-06 | PXD039213 | Pride
Project description:RAG DSBs trigger ATM-dependent induction of SPIC, an ETS family transcriptional repressor with significant homology to PU.1. RAG DSB-mediated expression of SPIC results in displacement of PU.1 throughout the genome and induction of broad transcriptional changes in pre B cells. SPIC also binds and recruits a unique partner, BCLAF1 to gene regulatory elements that regulate expression of key B cell developmental genes.
2019-08-22 | GSE129124 | GEO
Project description:RAG DSBs trigger ATM-dependent induction of SPIC, an ETS family transcriptional repressor with significant homology to PU.1. RAG DSB-mediated expression of SPIC results in displacement of PU.1 throughout the genome and induction of broad transcriptional changes in pre B cells. SPIC also binds and recruits a unique partner, BCLAF1 to gene regulatory elements that regulate expression of key B cell developmental genes.
2019-08-22 | GSE129129 | GEO
Project description:Understanding mechanisms of epigenetic regulation in embryonic stem cells (ESCs) is of fundamental importance for stem cell and developmental biology. Here we identify Spic, a member of the ETS family of transcription factors, as a specific marker of ground state pluripotency. We show that Spic is rapidly induced in ESCs cultured with GSK3-, MEK-inhibitors and LIF (2iL), and in response to MEK/ERK inhibition. ChIP-seq analysis demonstrated that Spic binds to enhancer elements that are associated with pluripotency genes. Interaction proteomics and genomic profiling confirmed that SPIC interacts with NANOG and stabilizes its binding to chromatin in 2iL-ESCs. Additional gain of function and loss of function experiments revealed that Spic controls genes involved in one carbon (1C) metabolism, Bhmt, Bhmt2, and Dmgdh, and the flux of SAM-to-SAH in 2iL-ESCs. By maintaining low levels of SAM, Spic controls the level of H3K4me3 and H3R17me2 histone methylation in ground state ESCs. Our data highlight the role of uncharacterized axillary transcription factors that link cellular metabolism to epigenetic regulation in ground state pluripotency.
2023-09-06 | GSE222053 | GEO
Project description:Understanding mechanisms of epigenetic regulation in embryonic stem cells (ESCs) is of fundamental importance for stem cell and developmental biology. Here we identify Spic, a member of the ETS family of transcription factors, as a specific marker of ground state pluripotency. We show that Spic is rapidly induced in ESCs cultured with GSK3-, MEK-inhibitors and LIF (2iL), and in response to MEK/ERK inhibition. ChIP-seq analysis demonstrated that Spic binds to enhancer elements that are associated with pluripotency genes. Interaction proteomics and genomic profiling confirmed that SPIC interacts with NANOG and stabilizes its binding to chromatin in 2iL-ESCs. Additional gain of function and loss of function experiments revealed that Spic controls genes involved in one carbon (1C) metabolism, Bhmt, Bhmt2, and Dmgdh, and the flux of SAM-to-SAH in 2iL-ESCs. By maintaining low levels of SAM, Spic controls the level of H3K4me3 and H3R17me2 histone methylation in ground state ESCs. Our data highlight the role of uncharacterized axillary transcription factors that link cellular metabolism to epigenetic regulation in ground state pluripotency.
2023-09-06 | GSE222057 | GEO
Project description:Splenic red pulp macrophages (RPM) degrade senescent erythrocytes and recycle heme-associated iron. The transcription factor Spic is selectively expressed by RPM and is required for their development, but the physiologic stimulus inducing Spic is unknown. Here, we report that Spic also regulated the development of F4/80+VCAM+ bone marrow macrophages (BMM) and that Spic expression in BMM and RPM development was induced by heme, a metabolite of erythrocyte degradation. Pathologic hemolysis induced loss of RPM and BMM due to excess heme but induced Spic in monocytes to generate new RPM and BMM. Spic expression in monocytes was constitutively inhibited by the transcriptional repressor Bach1. Heme induced proteasome-dependent BACH1 degradation and rapid Spic derepression. Further, cysteine-proline dipeptide motifs in BACH1 that mediate heme-dependent degradation were necessary for Spic induction by heme. These findings are the first example of metabolite-driven differentiation of a tissue-resident macrophage subset and provide new insight into iron homeostasis. Bone marrow derived macrophages were generated in vitro by culturing WT and Bach1 knock out bone marrow in the presence of GM-CSF and their global gene expression pattern were compared in the presence or absence of heme at the various indicated time points after treatment. GMP and MPP populations were sorted from fetal liver chimeras and pooled by donor genotype. RNA was isolated using an RNAqueous-Micro Kit (Ambion) and submitted for amplification, labeling and hybridization. Expression values were analyzed after RMA quantile normalization using ArrayStar software (DNASTAR).
2014-03-14 | E-GEOD-53796 | biostudies-arrayexpress
Project description:Splenic red pulp macrophages (RPM) degrade senescent erythrocytes and recycle heme-associated iron. The transcription factor Spic is selectively expressed by RPM and is required for their development, but the physiologic stimulus inducing Spic is unknown. Here, we report that Spic also regulated the development of F4/80+VCAM+ bone marrow macrophages (BMM) and that Spic expression in BMM and RPM development was induced by heme, a metabolite of erythrocyte degradation. Pathologic hemolysis induced loss of RPM and BMM due to excess heme but induced Spic in monocytes to generate new RPM and BMM. Spic expression in monocytes was constitutively inhibited by the transcriptional repressor Bach1. Heme induced proteasome-dependent BACH1 degradation and rapid Spic derepression. Further, cysteine-proline dipeptide motifs in BACH1 that mediate heme-dependent degradation were necessary for Spic induction by heme. These findings are the first example of metabolite-driven differentiation of a tissue-resident macrophage subset and provide new insight into iron homeostasis. Bone marrow derived macrophages were generated in vitro by culturing WT and Bach1 knock out bone marrow in the presence of GM-CSF and their global gene expression pattern were compared in the presence or absence of heme at the various indicated time points after treatment.
2014-03-14 | GSE53796 | 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