TMBIM6 deficiency leads to bone loss by accelerating osteoclastogenesis
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE231889 | GEO | 2023/07/10
REPOSITORIES: GEO
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Project description:Clarification of the mechanisms underlying osteoclast differentiation enable us to understand the physiology of bone metabolism as well as the pathophysiology of bone diseases, such as osteoporosis. Recently, it has been reported that epigenetics can determine the cell fate and regulate cell type specific gene expression. However, little is known about epigenetics during osteoclastogenesis. To reveal a part of epigenetics, especially focused on chromatin dynamics, during early osteoclastogenesis and identify novel transcription factors involved in osteoclastogenesis, we investigated genome-wide analysis of open chromatin during receptor activator of nuclear factor-M-NM-:B ligand (RANKL)-induced osteoclastogenesis using DNase I hypersensitive sites sequencing (DNase-seq). DNase-seq was performed using the extracted nuclei obtained from RAW264 cells treated with or without RANKL for 24 hours, followed by several bioinformatic analyses. DNase I hypersensitive sites (DHSs) during RANKL-induced osteoclastogenesis were dynamically changed and accumulated in promoter regions, although the distributions of DHSs among cis-regulatory DNA regions were identical regardless of RANKL stimulation. Motif discoveries from DHSs successfully identified well-known osteoclastogenic transcription factors such as Jun, CREB1, FOS, ATF2 and ATF4, but also novel transcription factors for osteoclastogenesis such as Zscan10, Atf1 Nrf1 and Srebf2. siRNA knockdown of these identified novel transcription factors impaired osteoclastogenesis. Taken together, DNase-seq can be a useful tool for comprehension of epigenetics, especially chromatin dynamics during osteoclastogenesis and for identification of novel transcription factors involved in osteoclastogenesis. This study may reveal underlying mechanisms that determine cell-type specific differentiation of bone cells and may lead to investigate novel therapeutic targets for osteoporosis. Examination of genome-wide DNase Hypersensitive Sites in differentiated and undifferentiated RAW264 cells.
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Project description:Purpose: The goals of this study are to describe the DNA methylation profile during RANKL induced osteoclastogenesis. Methods: Primary bone marrow cells were isolated and treated with M-CSF (30ng/mL) to generate bone marrow macrophages (BMMs). BMMs were then used to generate preosteoclast (pOC) stimulated by M-CSF (30ng/mL) together with RANKL (100ng/mL) for 24 h and mature osteoclast (mOC) stimulated by M-CSF (30ng/mL) together with RANKL (100ng/mL) for 72 h or more. DNA methylation profiles of BMM, pOC and mOC were generated by deep sequencing, using Illumina NovaSeq 6000. Results: After acquiring of clean reads, we used Hisat2 for spliced mapping. We mapped about 40 million sequence reads per sample of the WGBS results. Saturation rate analysis was then performed evaluating the gene coverage rate along with read depth increase. The transcripts mapping to difference functional region of the genome was then analyzed. Circos software was used to map the consistency of samples with mouse genome on a chromosomal level. The quantification of transcript intensity was analyzed using RPKM (Reads Per Kb per Million reads). Conclusions: Our study represents the first high-throughput WGBS sequencing data of DNA methylation during osteoclastogenesis.
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