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Transcriptional Reprogramming during Floral Fate Acquisition

ABSTRACT: Transcriptional Reprogramming during Floral Fate Acquisition

PROVIDER: PRJNA844340 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19505556_1.fastq.gz	Fastqsanger.gz
	SRR19505556_2.fastq.gz	Fastqsanger.gz
	SRR19505557_1.fastq.gz	Fastqsanger.gz
	SRR19505557_2.fastq.gz	Fastqsanger.gz
	SRR19505558_1.fastq.gz	Fastqsanger.gz

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Transcriptional Reprogramming during Floral Fate Acquisition II

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Transcriptional reprogramming during floral fate acquisition.

Project description:Coordinating growth and patterning is essential for eukaryote morphogenesis. In plants, auxin is a key regulator of morphogenesis implicated throughout development. Despite this central role, our understanding of how auxin coordinates cell fate and growth changes is still limited. Here, we addressed this question using a combination of genomic screens to delve into the transcriptional network induced by auxin at the earliest stage of flower development, prior to morphological changes. We identify a shoot-specific network suggesting that auxin initiates growth through an antagonistic regulation of growth-promoting and growth-repressive hormones, quasi-synchronously to floral fate specification. We further identify two DNA-binding One Zinc Finger (DOF) transcription factors acting in an auxin-dependent network that could interface growth and cell fate from the early stages of flower development onward.

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Transcriptional Reprogramming during Floral Fate Acquisition

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

2022-06-08 | GSE205299 | GEO

Transcriptional Reprogramming during Floral Fate Acquisition III

Project description:To gain insight into the auxin-dependent network during flower initiation, we used complementary RNAseq-based genomic analyses to obtain a global vision of the auxin-regulated gene network in the SAM before progressively converging on the identification of a high-confidence core network acting during the early phases of flower initiation.

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Transcriptional Reprogramming during Floral Fate Acquisition II

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Geminin represses mesendoderm cell fate acquisition in embryoid bodies

Project description:Geminin is a small nucleoprotein that neuralizes ectoderm in the Xenopus embryo. Geminin promotes neural fate acquisition of mouse embryonic stem cells: Geminin knockdown during neural fate acquisition decreased expression of neural precursor cell markers (Pax6, Sox1), while increasing expression of Pitx2, Lefty1 and Cited2, genes involved in formation of the mouse node. Here we differentiated mouse embryonic stem cells into embryoid bodies to study Geminin's ability to repress primitive streak mesendoderm fate acquisition. We used microarrays to define the sets of genes that are regulated by Geminin during cell fate acquisition in embryoid bodies, using Dox-inducible Geminin knockdown or overexpression mouse embryonic stem cell lines. ES cell lines for Geminin over-expression (GemOE) were treated without or with Dox from day 3 to day 5 of EB differentiation and were collected on days 4 or 5 for microarray analysis. Gem knockdown (KD) ES cell lines were treated without or with Dox from day 0 to day 4 of EB differentiation and were collected on day 4 for microarray analysis.

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Project description:Formation of the complex vertebrate nervous system begins when pluripotent cells of the early embryo are directed to acquire a neural fate. Although cell intrinsic controls play an important role in this process, the molecular nature of this regulation is not well defined. Here we assessed the role for Geminin, a nuclear protein expressed in embryonic cells, in neural fate acquisition from mouse embryonic stem (ES) cells. While Geminin knockdown does not affect the ability of ES cells to maintain or exit pluripotency, we found that it significantly impairs their ability to acquire a neural fate. Conversely, Geminin overexpression promotes neural gene expression, even in the presence of growth factor signaling that antagonizes neural transcriptional responses. These data demonstrate that Geminin’s activity contributes to mammalian neural cell fate acquisition. We investigated the mechanistic basis of this phenomenon and found that Geminin maintains a hyperacetylated and open chromatin conformation at neural genes. Interestingly, recombinant Geminin protein also rapidly alters chromatin acetylation and accessibility even when Geminin is combined with nuclear extract and chromatin in vitro. These findings define a novel activity for Geminin in regulation of chromatin structure. Together, these data support a role for Geminin as a cell intrinsic regulator of neural fate acquisition that promotes expression of neural genes by regulating chromatin accessibility and histone acetylation. Mouse embryonic stem cells were differentiated for two days in N2B27 medium, with or without Doxycycline-inducible shRNAmir knockdown of Geminin and compared by microarray. Three independent experiments were conducted, using two different mouse embryonic stem cell lines for Doxycycline-inducible knockdown of Geminin. The two ES lines express unique shRNAmir sequences targeting Geminin (shRNAmir #9 and #11) to control for off-target effects.

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