Pou5f1 Transcription Factor Controls Zygotic Gene Activation In Vertebrates

Leichsenring, Manuel; Maes, Julia; Mössner, Rebecca; Driever, Wolfgang; Onichtchouk, Daria

doi:10.1126/science.1242527

Cited by 233 publications

(250 citation statements)

References 54 publications

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“…It has been shown recently that, in addition to their well defined role as canonical pluripotency factors, Pou5f1, Sox2, and Nanog function in a manner similar to ZLD to drive global activation of the zygotic genome during the initial stages of zebrafish embryonic development (39,40). These data indicate a connection between zygotic genome activation and the establishment of the pluripotent state.…”

Section: Truncated Splice Isoforms Of Zld May Regulate Gene Expressiomentioning

confidence: 62%

Transcriptional Activation Is a Conserved Feature of the Early Embryonic Factor Zelda That Requires a Cluster of Four Zinc Fingers for DNA Binding and a Low-complexity Activation Domain

Hamm

Bondra

Harrison

2015

Journal of Biological Chemistry

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Background: Zelda initiates widespread transcription of the zygotic genome during embryogenesis. Results: Zelda binds DNA using C-terminal zinc fingers and activates transcription through a low-complexity domain. Conclusion: Transcriptional activation by Zelda is conserved in insects and uses domains we have identified to bind cisregulatory regions and drive gene expression. Significance: We provide the first insights into the functional domains of the essential activator Zelda.

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Section: Truncated Splice Isoforms Of Zld May Regulate Gene Expressiomentioning

confidence: 62%

Transcriptional Activation Is a Conserved Feature of the Early Embryonic Factor Zelda That Requires a Cluster of Four Zinc Fingers for DNA Binding and a Low-complexity Activation Domain

Hamm

Bondra

Harrison

2015

Journal of Biological Chemistry

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“…In the two-cell-stage embryo, the role of Oct4 and other potency factors is not established. Oct4 may be needed for zygotic genome activation in zebrafish [107,108], and the authors suggest that conservation of binding sites suggests similar roles in mammals. Oct4 and Cdx2 are necessary at the blastocyst stage to allocate ESC and TSC lineages, respectively [109], and knockouts for either of these are lethal at the blastocyst stage [51,110].…”

Section: Discussionmentioning

confidence: 99%

Commonly used fertility drugs, a diet supplement, and stress force AMPK-dependent block of stemness and development in cultured mammalian embryos

Bolnick

Abdulhasan

Kilburn

et al. 2016

J Assist Reprod Genet

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Purpose The purpose of the present study is to test whether metformin, aspirin, or diet supplement (DS) BioResponse-3, 3′-Diindolylmethane (BR-DIM) can induce AMP-activated protein kinase (AMPK)-dependent potency loss in cultured embryos and whether metformin (Met) + Aspirin (Asa) or BR-DIM causes an AMPK-dependent decrease in embryonic development. Methods The methods used were as follows: culture post-thaw mouse zygotes to the two-cell embryo stage and test effects after 1-h AMPK agonists' (e.g., Met, Asa, BR-DIM, control hyperosmotic stress) exposure on AMPK-dependent loss of Oct4 and/or Rex1 nuclear potency factors, confirm AMPK dependence by reversing potency loss in two-cell-stage embryos with AMPK inhibitor compound C (CC), test whether Met + Asa (i.e., co-added) or DS BR-DIM decreases development of two-cell to blastocyst stage in an AMPK-dependent (CCsensitive) manner, and evaluate the level of Rex1 and Oct4 nuclear fluorescence in two-cell-stage embryos and rate of two-cell-stage embryo development to blastocysts. Result(s) Met, Asa, BR-DIM, or hyperosmotic sorbitol stress induces rapid~50-85 % Rex1 and/or Oct4 protein loss in twocell embryos. This loss is~60-90 % reversible by co-culture with AMPK inhibitor CC. Embryo development from twocell to blastocyst stage is decreased in culture with either Met + Asa or BR-DIM, and this is either >90 or~60 % reversible with CC, respectively. Conclusion These experimental designs here showed that Met-, Asa-, BR-DIM-, or sorbitol stress-induced rapid potency loss in two-cell embryos is AMPK dependent as suggested by inhibition of Rex1 and/or Oct4 protein loss with an AMPK inhibitor. The DS BR-DIM or fertility drugs (e.g., Met + Asa)Capsule Drugs metformin and aspirin and diet supplement BR-DIM cause AMPK-dependent potency loss and decrease embryonic development from two-cell to blastocyst stage. Reprod Genet (2016) 33:1027-1039 DOI 10.1007 that are used to enhance maternal metabolism to support fertility can also chronically slow embryo growth and block development in an AMPK-dependent manner.

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“…However, it is still not clear whether these transcription factors actively recruit the SMAD complexes, or whether they act as pioneer factors to create a favorable chromatin environment that allows SMAD complexes to bind (Lee et al 2013;Leichsenring et al 2013).…”

Section: Smad-interacting Transcription Factorsmentioning

confidence: 99%

Transcriptional Control by the SMADs

Hill

2016

Cold Spring Harb Perspect Biol

289

256

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The transforming growth factor-b (TGF-b) family of ligands elicit their biological effects by initiating new programs of gene expression. The best understood signal transducers for these ligands are the SMADs, which essentially act as transcription factors that are activated in the cytoplasm and then accumulate in the nucleus in response to ligand induction where they bind to enhancer/promoter sequences in the regulatory regions of target genes to either activate or repress transcription. This review focuses on the mechanisms whereby the SMADs achieve this and the functional implications. The SMAD complexes have weak affinity for DNA and limited specificity and, thus, they cooperate with other site-specific transcription factors that act either to actively recruit the SMAD complexes or to stabilize their DNA binding. In some situations, these cooperating transcription factors function to integrate the signals from TGF-b family ligands with environmental cues or with information about cell lineage. Activated SMAD complexes regulate transcription via remodeling of the chromatin template. Consistent with this, they recruit a variety of coactivators and corepressors to the chromatin, which either directly or indirectly modify histones and/or modulate chromatin structure.

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Pou5f1 Transcription Factor Controls Zygotic Gene Activation In Vertebrates

Cited by 233 publications

References 54 publications

Transcriptional Activation Is a Conserved Feature of the Early Embryonic Factor Zelda That Requires a Cluster of Four Zinc Fingers for DNA Binding and a Low-complexity Activation Domain

Transcriptional Activation Is a Conserved Feature of the Early Embryonic Factor Zelda That Requires a Cluster of Four Zinc Fingers for DNA Binding and a Low-complexity Activation Domain

Commonly used fertility drugs, a diet supplement, and stress force AMPK-dependent block of stemness and development in cultured mammalian embryos

Transcriptional Control by the SMADs

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