Calcium signals shape metabolic control of H3K27ac and H3K18la to regulate EGA
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ABSTRACT:
PROVIDER: PRJNA1260033 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Calcium dynamics drive metabolic regulation of epigenetic reprogramming at fertilization and alter EGA resulting in long term effects in offspring.
2025-05-20 | GSE296594 | GEO
Project description:We profiled the genome-wide distribution of H3K18la in samples originating from 6 different in vitro and in vivo mouse samples, representing 3 tissues: embryonic stem cells, macrophages and skeletal muscle as well as in human skeletal muscle and compared them to the profiles of other well-established histone modifications as well as gene expression patterns. Globally, we found that H3K18la profiles resemble H3K27ac profiles better than any other investigated hPTM, including H3K4me3, but that they do not copy them. For all samples, H3K18la marked active CGI promoters of highly expressed genes which were remarkably shared across the different mouse tissues and which contained many housekeeping genes. Promoter H3K18la levels correlated positively to both H3K27ac and H3K4me3 levels as well as to gene expression levels. In addition, we found that H3K18la is enriched at tissue-type specific, active enhancers, which are particularly tissue-type-specific, especially when compared to the H3K18la-marked promoter regions. Accordingly, enhancer H3K18la levels correlate positively to the expression of their nearest genes. Additionally, genes closest to enhancers with high H3K18la levels predominantly consist of tissue-type specific marker genes. Overall, we showed that H3K18la is not only a marker for active promoters, but that it also marks active enhancers, and this both in embryonic tissues and differentiated tissues, and both in mouse and in human.
2022-09-14 | GSE195859 | GEO
Project description:We profiled the genome-wide distribution of H3K18la in samples originating from 6 different in vitro and in vivo mouse samples, representing 3 tissues: embryonic stem cells, macrophages and skeletal muscle as well as in human skeletal muscle and compared them to the profiles of other well-established histone modifications as well as gene expression patterns. Globally, we found that H3K18la profiles resemble H3K27ac profiles better than any other investigated hPTM, including H3K4me3, but that they do not copy them. For all samples, H3K18la marked active CGI promoters of highly expressed genes which were remarkably shared across the different mouse tissues and which contained many housekeeping genes. Promoter H3K18la levels correlated positively to both H3K27ac and H3K4me3 levels as well as to gene expression levels. In addition, we found that H3K18la is enriched at tissue-type specific, active enhancers, which are particularly tissue-type-specific, especially when compared to the H3K18la-marked promoter regions. Accordingly, enhancer H3K18la levels correlate positively to the expression of their nearest genes. Additionally, genes closest to enhancers with high H3K18la levels predominantly consist of tissue-type specific marker genes. Overall, we showed that H3K18la is not only a marker for active promoters, but that it also marks active enhancers, and this both in embryonic tissues and differentiated tissues, and both in mouse and in human.
2022-09-14 | GSE195854 | GEO
Project description:We profiled the genome-wide distribution of H3K18la in samples originating from 6 different in vitro and in vivo mouse samples, representing 3 tissues: embryonic stem cells, macrophages and skeletal muscle as well as in human skeletal muscle and compared them to the profiles of other well-established histone modifications as well as gene expression patterns. Globally, we found that H3K18la profiles resemble H3K27ac profiles better than any other investigated hPTM, including H3K4me3, but that they do not copy them. For all samples, H3K18la marked active CGI promoters of highly expressed genes which were remarkably shared across the different mouse tissues and which contained many housekeeping genes. Promoter H3K18la levels correlated positively to both H3K27ac and H3K4me3 levels as well as to gene expression levels. In addition, we found that H3K18la is enriched at tissue-type specific, active enhancers, which are particularly tissue-type-specific, especially when compared to the H3K18la-marked promoter regions. Accordingly, enhancer H3K18la levels correlate positively to the expression of their nearest genes. Additionally, genes closest to enhancers with high H3K18la levels predominantly consist of tissue-type specific marker genes. Overall, we showed that H3K18la is not only a marker for active promoters, but that it also marks active enhancers, and this both in embryonic tissues and differentiated tissues, and both in mouse and in human.
2022-09-14 | GSE195856 | GEO
Project description:L-lactate was reported as a precursor that can label and stimulate histone lysine-N-L-lactylation (Kla), which represents a new epigenetic mark affecting gene expression directly via histone PTMs under conditions of high glycolysis, such as the Warburg effect. To investigate the genome-wide targeting of H3K18la, we performed ChIP-seq in H1299 cells using anti-H3K18la antibody. 50.6% of the H3K18la binding sites displayed enrichment close to -1kb promoter of genes. More importantly, our ChIP-seq data showed that H3K18la is enriched in many genes that related with replication processes, highlighted the importance of histone Kla involved in DNA replication.
2023-07-30 | GSE207814 | GEO
Project description:In this study, we found that H3K18la level is elevated in adipose stem and progenitor cells of facial infiltrating lipomatosis (FIL-ASPCs). To further explore the potential functional significance of H3K18la in FIL, we performed genome-wide cleavage under targets and tagmentation (CUT&Tag) analysis to identify candidate genes regulated by H3K18la in FIL-ASPCs and CON-ASPCs. Following CUT&Tag, H3K18la-associated DNAs were amplified using non-biased conditions, labeled, and sequenced with Illumina NovaSeq 150PE.
2025-08-25 | GSE296002 | GEO
Project description:In malaria parasites, cGMP signalling is mediated by a single cGMP-dependent protein kinase (PKG). One of the major functions of PKG is to control calcium signals essential for the parasite to exit red blood cells or for the transmission of the gametocyte stages to the mosquito. However, how PKG controls these signals in the absence of known second messenger-dependent calcium channels or scaffolding proteins remains a mystery. Here we use pull-down approaches to identify a PKG partner protein in both Plasmodium falciparum schizonts and P. berghei gametocytes. This partner, named ICM1, is a polytopic membrane protein with homologies to transporters and calcium channels, raising the possibility of a direct functional link between PKG and calcium homeostasis. Phosphoproteomic analyses in both Plasmodium species highlight a densely phosphorylated region of ICM1 with multiple phosphorylation events dependent on PKG activity. Conditional disruption of the P. falciparum ICM1 gene results in reduced cGMP-dependent calcium mobilisation associated with defective egress and invasion. Stage-specific depletion of ICM1 in P. berghei gametocytes blocks gametogenesis due to the inability of mutant parasites to mobilise intracellular calcium upon PKG activation. These results provide us with new insights into the atypical calcium homeostasis in malaria parasites
2021-01-25 | PXD020189 | Pride
Project description:In malaria parasites, cGMP signalling is mediated by a single cGMP-dependent protein kinase (PKG) . One of the major functions of PKG is to control calcium signals essential for the parasite to exit red blood cells or for the transmission of the gametocyte stages to the mosquito . However, how PKG controls these signals in the absence of known second messenger-dependent calcium channels or scaffolding proteins remains a mystery. Here we use pull-down approaches to identify a PKG partner protein in both Plasmodium falciparum schizonts and P. berghei gametocytes. This partner, named ICM1, is a polytopic membrane protein with homologies to transporters and calcium channels, raising the possibility of a direct functional link between PKG and calcium homeostasis. Phosphoproteomic analyses in both Plasmodium species highlight a densely phosphorylated region of ICM1 with multiple phosphorylation events dependent on PKG activity. Conditional disruption of the P. falciparum ICM1 gene results in reduced cGMP-dependent calcium mobilisation associated with defective egress and invasion. Stage-specific depletion of ICM1 in P. berghei gametocytes blocks gametogenesis due to the inability of mutant parasites to mobilise intracellular calcium upon PKG activation. These results provide us with new insights into the atypical calcium homeostasis in malaria parasites.
2021-01-25 | PXD020210 | Pride
Project description:H3K18la marks active tissue-specific enhancers
| PRJNA802354 | ENA
Project description:In malaria parasites, all cGMP-dependent signalling is mediated through a single cGMP-dependent protein kinase (PKG). A major function of PKG is to control calcium signals essential for the parasite to exit red blood cells or for transmission to the mosquito vector. However, how PKG controls these signals in the absence of known second messenger-dependent calcium channels or scaffolding proteins remains a mystery. Here we identify a tightly-associated PKG partner protein in both Plasmodium falciparum asexual blood stages and P. berghei gametocytes. Named ICM1, the partner is a polytopic membrane protein with homology to transporters and calcium channels, raising the possibility of a direct functional link between PKG and calcium homeostasis. Phosphoproteomic analyses in both Plasmodium species highlight a densely phosphorylated region of ICM1 with multiple phosphorylation events dependent upon PKG activity. Stage-specific depletion of ICM1 in P. berghei blocks gametogenesis due to the inability of mutant parasites to mobilise intracellular calcium upon PKG activation, whilst conditional disruption of P. falciparum ICM1 results in reduced cGMP-dependent calcium mobilisation associated with defective egress and invasion. Our findings provide new insights into the atypical calcium homeostasis in malaria parasites essential for pathology and disease transmission.
2021-02-10 | PXD020381 | Pride