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The homeobox transcription factor DUXBL controls exit from the totipotent 2C state [RNA-seq]

ABSTRACT: The homeobox transcription factor DUXBL controls exit from the totipotent 2C state [RNA-seq]

PROVIDER: PRJNA868189 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21001964_1.fastq.gz	Fastqsanger.gz
	SRR21001964_2.fastq.gz	Fastqsanger.gz
	SRR21001965_1.fastq.gz	Fastqsanger.gz
	SRR21001965_2.fastq.gz	Fastqsanger.gz
	SRR21001966_1.fastq.gz	Fastqsanger.gz

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The homeobox transcription factor DUXBL controls exit from the totipotent 2C state [RNA-seq]

Project description:Upon exit from the totipotent 2-cell (2C) embryo stage, the 2C-associated transcriptional program needs to be efficiently silenced. However, the molecular mechanisms involved in this process remain mostly unknown. Here, we determined that the 2C-specific transcription factor DUX directly induced the expression of DUXBL to promote this silencing. CUT&RUN analysis revealed that DUXBL gained accessibility to DUX-bound regions in DUX-induced ESC while it was unable to bind those regions in uninduced cells. Importantly, DUX expression in Duxbl-knockout ESC caused increased induction of the 2C-transcriptional program, whereas DUXBL overexpression impaired 2C-associated transcription. Mechanistically, we determined that DUXBL interacted with TRIM24 and TRIM33, two members of the tripartite motif superfamily involved in gene silencing, and co-localized with them in nuclear condensates upon DUX expression. Importantly, DUXBL downregulation in mouse zygotes led to a penetrant 2C-stage arrest. Our data revealed an unexpected role for DUXBL in controlling the exit from totipotency.

2023-12-06 | GSE210891 | GEO

The homeobox transcription factor DUXBL controls exit from the totipotent 2C state [Cut&Run]

2023-12-06 | GSE210890 | GEO

The homeobox transcription factor DUXBL controls exit from the totipotent 2C state

Project description:The homeobox transcription factor DUXBL controls exit from the totipotent 2C state

| PRJNA868185 | ENA

The homeobox transcription factor DUXBL controls exit from totipotency

Project description:In mice, exit from the totipotent 2-cell (2C) embryo stage requires silencing of the 2C-associated transcriptional program. However, the molecular mechanisms involved in this process remain poorly understood. Here, we demonstrate that the 2C-specific transcription factor DUX mediates an essential negative feedback loop by inducing the expression of DUXBL to promote this silencing.We show that DUXBL gains accessibility to DUX-bound regions specifically upon DUX expression.Furthermore, we determine that DUXBL interacts with TRIM24 and TRIM33, members of the tripartite motif superfamily involved in gene silencing and co-localizes with them in nuclear foci upon DUX expression. Importantly, DUXBL overexpression impairs 2C-associated transcription, whereas Duxbl inactivation in ESC increases DUX-dependent induction of the 2C-transcriptional program. Consequently, DUXBL deficiency in embryos results in sustained expression of 2C-associated transcripts, leading to early developmental arrest.Our study identifies DUXBL as an essential regulator of totipotency exit enabling the first divergence of cell fates.

2023-12-07 | GSE234053 | GEO

The homeobox transcription factor DUXBL controls exit from the totipotent 2C state [Cut&Run]

Project description:The homeobox transcription factor DUXBL controls exit from the totipotent 2C state [Cut&Run]

| PRJNA868190 | ENA

The homeobox transcription factor DUXBL controls exit from totipotency

Project description:The homeobox transcription factor DUXBL controls exit from totipotency

| PRJNA979244 | ENA

The homeobox transcription factor DUXBL controls exit from the totipotent 2C state

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

2023-12-05 | GSE210892 | GEO

Lysosomal catabolic activity governs the exit of the murine totipotent 2-cell state by silencing early-embryonic retrotransposons [RNA-seq]

Project description:During the development in mouse early embryos, a subset of retrotransposons and genes are transiently expressed in the totipotent 2-cell embryos. These 2-cell-embryo-asscoiated (referred to as 2C) transcripts rapidly shut down their expression beyond the late 2-cell stage of embryos, and this timely shutdown governs the embryo to exit from the 2-cell stage. However, mechanisms regulating this wave of shutdown are not fully understood. In this study, we established a novel connection between lysosomal catabolic activity and 2C transcripts in regulating the exit of totipotent 2-cell state by using both in vitro 2-cell-like cells model and mouse embryos. Our results showed that the activation of lysosomal catabolism in mouse embryos governed the embryo to exit from the 2-cell state by suppressing the expression of 2C transcripts. Mechanistically, we found that lysosomal catabolic activity modulated 2C transcripts by inactivating transcriptional factors Tfe3/Tfeb and abolishing their transcriptional activation on 2C retrotransposons, MERVL/MT2-Mm. Collectively, our study elucidates the function of lysosomal activity in orchestrating transcriptomic landscape and early development in mouse embryos and reveals an unanticipated layer of transcriptional control on early-embryonic retrotransposons from lysosomal signaling.

2024-08-25 | GSE247082 | GEO

Lysosomal catabolic activity governs the exit of the murine totipotent 2-cell state by silencing early-embryonic retrotransposons [CUT&Tag]

2024-08-25 | GSE247081 | GEO

Duxbl-mediated suppression of ZGA drives totipotency to pluripotency transition in mice I

Project description:In mammalian embryos, Dux transcription factors (TF) drive a cleavage stage-specific transcriptional burst associated with zygotic genome activation (ZGA) during which hundreds of genes and endogenous retroviral (ERV) elements are transiently expressed. In mice, ZGA begins in late 1-cell (1C) embryos and is shut down within hours at the late 2-cell (2C) to 4-cell (4C) stage. While this transition is accompanied by the loss of totipotency, it is not clear whether shutdown of Dux-induced ZGA is required for this process and how ZGA is terminated. Here, we reveal an essential negative feedback axis by which the Dux family member Duxbl terminates Dux-induced ZGA from the mid 2C stage onward by direct suppression of genomic Dux target loci. Consequently, Duxbl inactivation results in sustained expression of Dux-induced ZGA leading to 4C arrest. Our study reveals the Dux/Duxbl axis that determines the timing of totipotency exit enabling the very first divergence of cell fates.

2023-12-07 | GSE213700 | GEO

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