Xenopus laevis POU91 protein, an Oct3/4 homologue, regulates competence transitions from mesoderm to neural cell fates

Snir, Mirit; Ofir, Rachel; Elias, Sarah; Frank, Dale

doi:10.1038/sj.emboj.7601238

Cited by 53 publications

(71 citation statements)

References 56 publications

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“…These results identify Oct3/4 as a factor contributing to the expression of the Cdx genes and actually activating one of the factors involved in its own repression. Several studies have shown that during gastrulation, the Xenopus Oct3/4 factors function in a manner consistent with the active maintenance of the pluripotent state like their mammalian homologues (Henig et al, 1998;Cao et al, 2006Cao et al, , 2007Morrison and Brickman, 2006;Snir et al, 2006). Thus, Cdx1 acting as a negative regulator of the Pou5f1 genes during gastrulation, would ultimately function to end the undifferentiated state and facilitate the transition into gastrulation.…”

Section: Discussionmentioning

confidence: 99%

“…A number of studies have described Pou5f1 morphant embryos with strong developmental defects. These embryos show defects or delays during gastrulation that in some instances have been attributed to abnormal differentiation of the germ layers (Cao et al, 2006;Snir et al, 2006). In the Pou5f1 morphants, expression of germ layer markers like Xbra and FGF8 is reduced (Morrison and Brickman, 2006).…”

Section: Cross-regulation Betweenmentioning

confidence: 99%

“…A possible role for Oct3/4 in promoting germ layer differentiation was observed in ES cells where increased Oct3/4 activity levels led to mesoderm and primitive endoderm differentiation (Niwa et al, 2000) supporting our observations on the promotion of germ layer marker expression. During early/mid gastrulation, the Oct3/4 genes repress the expression of germ line-specific markers (Cao et al, 2006(Cao et al, , 2007Morrison and Brickman, 2006;Snir et al, 2006). It has been suggested that a heterodimeric Oct3/4-Cdx complex has a gene repressive function (Niwa et al, 2005).…”

Section: Cross-regulation Betweenmentioning

confidence: 99%

“…A number of studies support the functional conservation between mouse Oct3/4 and the Xenopus Pou5f1 genes. The Xenopus Pou5f1 genes perform functions consistent with the maintenance of pluripotency, the regulation of gastrulation, the prevention of germ layer differentiation, and they can even maintain the pluripotency of mouse ES cells to different extents (Henig et al, 1998;Cao et al, 2006Cao et al, , 2007Morrison and Brickman, 2006;Snir et al, 2006). Also, the murine Oct3/4 protein can rescue the developmental malformations resulting from knock-down of the frog Pou5f1 gene activities (Cao et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

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Negative autoregulation of Oct3/4 through Cdx1 promotes the onset of gastrulation

et al. 2011

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Gastrulation marks the onset of germ layer formation from undifferentiated precursor cells maintained by a network including the Pou5f1 gene, Oct3/4. Negative regulation of the undifferentiated state is a prerequisite for germ layer formation and subsequent development. A novel cross-regulatory network was characterized including the Pou5f1 and Cdx1 genes as part of the signals controlling the onset of gastrulation. Of particular interest was the observation that, preceding gastrulation, the Xenopus Oct3/4 factors, Oct60, Oct25, and Oct91, positively regulate Cdx1 expression through FGF signaling, and during gastrulation the Oct3/4 factors become repressors of Cdx1. Cdx1 negatively regulates the Pou5f1 genes during gastrulation, thus contributing to the repression of the network maintaining the undifferentiated state and promoting the onset of gastrulation. These regulatory interactions suggest that Oct3/4 initiates its own negative autoregulation through Cdx1 up-regulation to begin the repression of pluripotency in preparation for the onset of gastrulation and germ layer differentiation. Developmental Dynamics 240:796-807,

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Section: Discussionmentioning

confidence: 99%

Section: Cross-regulation Betweenmentioning

confidence: 99%

Section: Cross-regulation Betweenmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Negative autoregulation of Oct3/4 through Cdx1 promotes the onset of gastrulation

et al. 2011

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“…This demonstrates that chch represses the movement of epiblast cells and allows them to remain in the prospective neural plate where they subsequently give rise to neural tissue (Sheng et al, 2003). Overexpression of chch in Xenopus embryos results in suppression of the mesodermal marker brachyury (Xbra) in embryos and animal cap assays (Sheng et al, 2003;Snir et al, 2006). FGF4 or FGF8 are sufficient to induce chch expression in the chick.…”

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confidence: 94%

Expression and regulation of the zinc finger transcription factor Churchill during zebrafish development

Londin

Mentzer

Gates

et al. 2007

Gene Expression Patterns

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During gastrulation dynamic cell movements establish the germ layers and shape the body axis of the vertebrate embryo. The zinc finger protein Churchill (chch) has been proposed to be a key regulator of these movements. We examined the expression pattern of chch in zebrafish and studied the regulation of chch by FGF signaling. We observed zygotic expression of chch during early cleavage stages. Two lines of evidence demonstrate that chch is zygotically expressed prior to the mid-blastula transition. First, blocking transcription during early cleavage stages represses chch expression. Second, endogenous levels of chch transcripts increase between 1-cell and 16-cell embryos. chch remains widely expressed during blastula and gastrula stages but scattered cells express higher levels of chch. By somitogenesis, chch is expressed in the ventral-most cells of the embryo adjacent to the yolk. In addition, transcripts are also observed in superficial cells on the surface of the yolk, in presumptive mucous cells and keratinocytes. By 30 hpf transcripts are observed in anterior neural tissue and ventral cells adjacent to the yolk. Over the next three days chch expression is indistinct until 4 dpf when we observe expression in the pharynx and gut. We show that activation of FGF signaling during gastrulation is sufficient to induce chch expression. In addition, we demonstrate that blocking FGF signaling between the 4-cell and shield stages represses chch expression. Results and DiscussionChurchill (chch) is a small, highly conserved zinc finger transcription factor identified in a differential screen to isolate genes induced by Hensen's node (Sheng et al., 2003). chch was proposed to function as a switch between the functions of FGF in neural and mesoderm induction (Sheng et al., 2003). Morpholino knockdown of chch in the chick epiblast results in inappropriate migration of cells through the primitive streak (Sheng et al., 2003). This demonstrates that chch represses the movement of epiblast cells and allows them to remain in the prospective neural plate where they subsequently give rise to neural tissue (Sheng et al., 2003). Overexpression of chch in Xenopus embryos results in suppression of the mesodermal marker brachyury (Xbra) in embryos and animal cap assays (Sheng et al., 2003;Snir et al., 2006). FGF4 or FGF8 are sufficient to induce chch expression in the chick. In Xenopus, chch expression is regulated by XLPOU91 which mediates FGF responsiveness (Snir et al., 2006 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (Sheng et al., 2003;Snir et al., 2006). Sip1 is a direct r...

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Churchill and Sip1a repress fibroblast growth factor signaling during zebrafish somitogenesis

Kok

Shepherd

Sirotkin

2010

Developmental Dynamics

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Cell-type specific regulation of a small number of growth factor signal transduction pathways generates diverse developmental outcomes. The zinc finger protein Churchill (ChCh) is a key effector of fibroblast growth factor (FGF) signaling during gastrulation. ChCh is largely thought to act by inducing expression of the multifunctional Sip1 (Smad Interacting Protein 1). We investigated the function of ChCh and Sip1a during zebrafish somitogenesis. Knockdown of ChCh or Sip1a results in misshapen somites that are short and narrow. As in wild-type embryos, cycling gene expression occurs in the developing somites in ChCh and Sip1a compromised embryos, but expression of her1 and her7 is maintained in formed somites. In addition, tail bud fgf8 expression is expanded anteriorly in these embryos. Finally, we found that blocking FGF8 restores somite morphology in ChCh and Sip1a compromised embryos. These results demonstrate a novel role for ChCh and Sip1a in repression of FGF activity. Developmental Dynamics 239:548-558,

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Xenopus laevis POU91 protein, an Oct3/4 homologue, regulates competence transitions from mesoderm to neural cell fates

Cited by 53 publications

References 56 publications

Negative autoregulation of Oct3/4 through Cdx1 promotes the onset of gastrulation

Negative autoregulation of Oct3/4 through Cdx1 promotes the onset of gastrulation

Expression and regulation of the zinc finger transcription factor Churchill during zebrafish development

Churchill and Sip1a repress fibroblast growth factor signaling during zebrafish somitogenesis

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