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Zfp352 over expression chip-seq result

ABSTRACT: Previous study has determined Dux regulates 2CLC trancriptome via binding and activating MERVL,but the mechanism about the change happned during the 2C-exit process are rarely determined.In this study,we try to illustrate how ZFP352 binds genome location to regulate its downstream trancriptome and 2C-exit process.And make some conclusion and hypothesis about ZFP352 co-binding and interact with other trancription factor:Dux,etc to regulate 2C-exit.

ORGANISM(S): Mus musculus

PROVIDER: GSE202158 | GEO | 2023/06/01

REPOSITORIES: GEO

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Time point RNA-seq of Dux over expression samples reveals different transcriptomes of Dux induction in mESC

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Transcriptome analysis in mouse ES cells deficient for Zfp352 or both Zfp352/Zfp353

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Zfp352 and Zfp352+Dux over expression chip-seq result

Project description:Zfp352 and Zfp352+Dux over expression chip-seq result

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Selective binding of retrotransposons by ZFP352 facilitates the timely dissolution of totipotency network

Project description:Acquisition of new stem cell fates relies on the dissolution of the prior regulatory network sustaining the existing cell fates. Currently, extensive insights have been revealed for the totipotency regulatory network around the zygotic genome activation (ZGA) period. However, how the dissolution of the totipotency network is triggered to ensure the timely embryonic development following ZGA is largely unknown. In this study, we identified the unexpected role of a highly expressed 2C embryo specific transcription factor, ZFP352, in facilitating the dissolution of the totipotency network. We found that ZFP352 has bifurcated binding and regulation towards two different retrotransposon sub-families. ZFP352 coordinates with DUX to bind and regulate the 2C specific MT2_Mm sub-family. On the other hand, without DUX, ZFP352 switched affinity to bind extensively onto SINE_B1/Alu sub-family. This leads to the activation of later developmental programs like ubiquitination pathways, to facilitate the dissolution of the 2C state. Correspondingly, depleting ZFP352 in mouse embryos impaired the 2C to morula transition process. Thus, through differential regulation of MT2_Mm and SINE_B1/Alu, ZFP352 can trigger spontaneous dissolution of the totipotency network. Our study highlights the importance of different retrotransposons sub-families in facilitating the timely and programmed cell fates transition during early embryogenesis.

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DUX-miR-344-ZMYM2-mediated activation of MERVL LTRs induces a totipotent 2C-like state [ATAC-seq]

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Zfp352 over expression ATAC-seq result

Project description:Our data delineated bifurcated binding and regulation of ZFP352 towards two distinct retrotransposons, MT2_Mm and SINE_B1/Alu,and whether ZFP352 can regulate mouse genome openness remains unknown,here we conduct ATAC-seq of Zfp352 over expression sample to detect ZFP352's role in regulating chromatin openness.

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DUX-miR-344-ZMYM2-mediated activation of MERVL LTRs induces a totipotent 2C-like state [LSD1 ChIP-seq]

Project description:Mouse embryonic stem cells (ESCs) sporadically express preimplantation two-cell-stage (2C) transcripts, including MERVL endogenous retrovirus and Zscan4 cluster genes. Such 2C-like cells (2CLCs) can contribute to both embryonic and extraembryonic tissues when reintroduced into early embryos. We examined global nucleosome occupancy and gene expression in 2CLCs and identified miR-344 as the noncoding molecule that positively controls 2CLC potency. We found that activation of endogenous MERVL or miR-344-2 alone is sufficient to induce 2CLCs with induction of 2C genes and an expanded potency. Mechanistically, miR-344 is activated by the 2C-state driver DUX and post-transcriptionally represses ZMYM2 and LSD1, which recruit the HDAC corepressor to MERVL LTR for transcriptional repression. Consistently, zygotic depletion of Zmym2 compromises the totipotency-to-pluripotency transition during early development. Our studies establish the novel DUXmiR-344--|Zmym2/LsdSD1 axis that controls MERVL for expanded stem cell potency.

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