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ATAC-seq analyses with wild-type and PML KO mESCs

ABSTRACT: ATAC-seq analyses with wild-type and PML KO mESCs

PROVIDER: PRJNA559287 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9927150_1.fastq.gz	Fastqsanger.gz
	SRR9927150_2.fastq.gz	Fastqsanger.gz
	SRR9927147_1.fastq.gz	Fastqsanger.gz
	SRR9927147_2.fastq.gz	Fastqsanger.gz
	SRR9927148_1.fastq.gz	Fastqsanger.gz

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ATAC-seq analyses with wild-type and PML KO mESCs

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RNA-seq analyses of wild-type and PML KO mESCs

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ChIP-seq analysis of wild-type and PML KO mESCs

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Project description:TRIM33 is a chromatin reader required for mesendoderm differentiation upon activation of Nodal signaling. But, its role in mESCs is still elusive. Here, we found that TRIM33 co-localizes with promyelocytic leukemia nuclear bodies (PML NBs) specifically in mESCs to mediate Nodal signaling-directed transcription of Lefty1/2. We showed that TRIM33 puncta formation in mESCs depends on PML and specific assembly of PML NBs. Moreover, TRIM33 and PML co-regulate Lefty1/2 expression in mESCs. In addition, both PML and mESCs-specific PML NBs are required for TRIM33 recruitment at Lefty1/2 loci. Remarkably, PML NBs directly associate with the Lefty1/2 loci in mESCs. Finally, a TurboID proximity labeling experiment confirmed that TRIM33 is highly enriched in the mESCs-specific PML NBs. Thus, our study provides the mechanistic insight about TRIM33 condensate in regulating Nodal signaling-directed transcription in mESCs, it also reveals that PML NBs recruit distinct sets of client proteins in cell context dependent manner.

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