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ZMAT1 promotes osteoclast formation and bone loss through TRIM46 mediated YAP1 degradation. [CUT&Tag]

ABSTRACT: ZMAT1 promotes osteoclast formation and bone loss through TRIM46 mediated YAP1 degradation. [CUT&Tag]

PROVIDER: PRJNA1147164 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30208023_1.fastq.gz	Fastqsanger.gz
	SRR30208023_2.fastq.gz	Fastqsanger.gz
	SRR30208024_1.fastq.gz	Fastqsanger.gz
	SRR30208024_2.fastq.gz	Fastqsanger.gz

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ZMAT1 promotes osteoclast formation and bone loss through TRIM46 mediated YAP1 degradation. [CUT&Tag]

Project description:Osteoclasts and osteoblasts play a critical role in bone remodeling, and their dysregulation leads to pathological bone loss. However, precise regulation of their differentiation remains not fully elucidated. This study investigates the role of transcriptional regulator Zinc Finger Matrin-Type 1 (Zmat1) in both osteoclastogenesis and osteoblastogenesis. Zmat1 deficiency resulted in decreased osteoclast activity, and reduced bone resorption. Mechanististically, ZMAT1 was significantly upregulated during osteoclast differentiation and acted as a transcriptional repressor of the E3 ubiquitin ligase TRIM46, which then regulates YAP1 degradation via K48-linked ubiquitination. Furthermore, Zmat1 deficiency also enhanced osteoblast activity and bone formation. These findings highlight a novel ZMAT1/TRIM46/YAP1 axis, providing new insights into the transcriptional regulation of both osteoclast and osteoblast differentiation, and present potential therapeutic targets for osteoporosis.

2024-08-15 | GSE274533 | GEO

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ZMAT1 promotes osteoclast formation and bone loss through TRIM46 mediated YAP1 degradation.

Project description:ZMAT1 promotes osteoclast formation and bone loss through TRIM46 mediated YAP1 degradation.

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ZMAT1 promotes osteoclast formation and bone loss through TRIM46 mediated YAP1 degradation II

Project description:ZMAT1 promotes osteoclast formation and bone loss through TRIM46 mediated YAP1 degradation II

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scNanoSeq-CUT&Tag: a long-read single-cell CUT&Tag sequencing method for efficient chromatin modification profiling within individual cells

Project description:We developed scNanoSeq-CUT&Tag, a streamlined method by adapting a modified CUT&Tag protocol to Oxford Nanopore sequencing platform for efficient chromatin modification profiling at single-cell resolution. We firstly tested the performance of scNanoSeq-CUT&Tag on six human cell lines: K562, 293T, GM12878, HG002, H9, HFF1 and adult mouse blood cells, it showed that scNanoSeq-CUT&Tag can accurately distinguish different cell types in vitro and in vivo. Moreover, scNanoSeq-CUT&Tag enables to effectively map the allele-specific epigenomic modifications in the human genome andallows to analyze co-occupancy of histone modifications. Taking advantage of long-read sequencing,scNanoSeq-CUT&Tag can sensitively detect epigenomic state of repetitive elements. In addition, by applying scNanoSeq-CUT&Tag to testicular cells of adult mouse B6D2F1, we demonstrated that scNanoSeq-CUT&Tag maps dynamic epigenetic state changes during mouse spermatogenesis. Finally, we exploited the epigenetic changes of human leukemia cell line K562 during DNA demethylation, it showed that NanoSeq-CUT&Tag can capture H3K27ac signals changes along DNA demethylation. Overall, we prove that scNanoSeq-CUT&Tag is a valuable tool for efficiently probing chromatin state changes within individual cells.

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