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MACF1 promotes osteoblast differentiation by sequestering repressors in cytoplasm

ABSTRACT: MACF1 promotes osteoblast differentiation by sequestering repressors in cytoplasm

PROVIDER: PRJNA492304 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7883050_1.fastq.gz	Fastqsanger.gz
	SRR7883050_2.fastq.gz	Fastqsanger.gz
	SRR7883060_1.fastq.gz	Fastqsanger.gz
	SRR7883060_2.fastq.gz	Fastqsanger.gz
	SRR7883070_1.fastq.gz	Fastqsanger.gz

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MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [RNA-seq]

Project description:Osteoblast differentiation leading to bone formation requires a coordinated transcriptional program. We have recently demonstrated that microtubule actin crosslinking factor 1 (MACF1) promotes osteoblast differentiation, suggesting a key role in regulating early-phase osteoblast differentiation. Here, we showed that the early-phase osteoblast differentiation transcriptome dynamics was regulated by MACF1 and the transcription of TCF7/LEF1, key effectors of Wnt signaling that is important for osteoblast differentiation was suppressed by MACF1 knockdown. Co-IP and Protein mass spectrometry revealed that MACF1 interacted with a known and two previously unknown repressors of TCF7/LEF1, DKK1, CDK12 and MEAF6. ChIP-seq analysis of MACF1-associated promoters further revealed that MACF1 interacted with transcription factors TCF12 and E2F6, which also suppressed the transcription of TCF7/LEF1. Furthermore, all these four MACF-interacted proteins inhibited osteoblast differentiation. By studying the underlying mechanism, we found that cytoplasmic-nuclear localization of MACF1 was dependent on its level and the cytoplasmic-nuclear localization of TCF12 and E2F6 was regulated by MACF1 localization. In addition, MACF1 oppositely regulated the transcription activity of TCF12 and TCF7. Current study, for the first time to our knowledge, suggest that MACF1 acts as a sponge of osteoblast differentiation repressors to promote osteoblast differentiation, and indicate a novel mechanism for regulating the cellular location of transcription factors by a protein associated with microtubule and actin.

2021-02-17 | GSE120248 | GEO

MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [ChIP-seq]

2021-02-17 | GSE120251 | GEO

MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [ChIP-seq]

Project description:MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [ChIP-seq]

| PRJNA492306 | ENA

MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [RNA-seq]

Project description:MACF1 Promotes Osteoblast Differentiation by Sequestering Wnt Signaling Repressors in Cytoplasm [RNA-seq]

| PRJNA492300 | ENA

MACF1 promotes osteoblast differentiation by sequestering repressors in cytoplasm.

Project description:Osteoblast differentiation leading to bone formation requires a coordinated transcriptional program. Osteoblastic cells with low level of microtubule actin crosslinking factor 1 (MACF1) show reduced osteoblast differentiation ability, however, the comprehensive mechanism of MACF1's action remains unexplored. In the current study, we found that MACF1 knockdown suppressed osteoblast differentiation by altering the transcriptome dynamics. We further identified two MACF1-interacted proteins, cyclin-dependent kinase 12 (CDK12) and MYST/Esa1-associated factor 6 (MEAF6), and two MACF1-interacted transcription factors (TFs), transcription factor 12 (TCF12) and E2F transcription factor 6 (E2F6), which repress osteoblast differentiation by altering the expression of osteogenic TFs and genes. Moreover, we found that MACF1 regulated cytoplasmic-nuclear localization of itself, TCF12 and E2F6 in a concentration-dependent manner. MACF1 oppositely regulates the expression of TCF12 and transcription factor 7 (TCF7), two TFs that drive osteoblast differentiation to opposite directions. This study reveals that MACF1, a cytoskeletal protein, acts as a sponge for repressors of osteoblast differentiation to promote osteoblast differentiation and contributes to a novel mechanistic insight of osteoblast differentiation and transcription dynamics.

| S-EPMC8257666 | biostudies-literature

MACF1 promotes osteoblast differentiation by sequestering repressors in cytoplasm

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-17 | GSE120252 | GEO

miRNA for MACF1 regulates osteoblast differentiation

Project description:miRNA for MACF1 regulates osteoblast differentiation

| PRJNA837887 | ENA

METTL16 promotes translation and lung tumorigenesis by sequestering cytoplasmic eIF4E2

Project description:METTL16 was previously identified as an m6A methyltransferase. In this study, we validated the cytoplasmic location of METTL16 and explored its function in the cytoplasm. We found that METTL16 promoted translation by sequestering eIF4E2, a translation initiation repressor, from the 5' cap structure.

2022-03-07 | GSE197915 | GEO

miRNA for MACF1 regulates osteoblast differentiation

Project description:MC3T3-E1 cells were transfected with short hairpin RNA (shRNA) specifically targeting the murine MACF1 lentivirus vector or with scrambled shRNA, and the stably transfected cell lines were selected using puromycin. After 15 days of selection, all cells were collected for further study.

2022-10-27 | GSE202962 | GEO

Priming integrin alpha5 promotes human mesenchymal stromal cell osteoblast differentiation and osteogenesis

Project description:Human adult mesenchymal stromal cells (hMSC) have the potential to differentiate into chondrogenic, adipogenic or osteogenic lineages, providing a potential source for tissue regeneration. An important issue for efficient bone regeneration is to identify factors that can be targeted to promote the osteogenic potential of hMSCs. Using transcriptomic analysis, we found that integrin alpha5 (ITGA5) expression is upregulated during dexamethasone-induced hMSCs osteoblast differentiation. Gain-of-function studies showed that ITGA5 promotes the expression of osteoblast phenotypic markers as well as in vitro osteogenesis in hMSCs. Downregulation of endogenous ITGA5 using shRNA blunted osteoblast marker expression and osteogenic differentiation. Pharmacological and molecular analyses showed that the enhanced hMSCs osteoblast differentiation induced by ITGA5 was mediated by activation of FAK/ERK1/2-MAPKs and PI3K signaling pathways. Remarkably, activation of ITGA5 using a specific antibody that primes the integrin or a peptide that specifically activates ITGA5 was sufficient to enhance ERK1/2-MAPKs and PI3K signaling and to promote osteoblast differentiation and osteogenic capacity of hMSCs. We also demonstrate that hMSCs engineered to over-express ITGA5 exhibited a marked increase in their osteogenic potential in vivo. These findings not only reveal that ITGA5 is required for osteoblast differentiation of adult human MSCs but also provide a novel targeted strategy using ITGA5 agonists to promote the osteogenic capacity of hMSCs, which may be used for tissue regeneration in bone disorders where the recruitment or capacity of MSCs is compromised. Keywords: Time course of osteogenic differentiation processes

2009-09-10 | GSE18043 | GEO

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