Atypical Transcriptional Activation by TCF via a Zic Transcription Factor in C. elegans Neuronal Precursors

Murgan, Sabrina; Kari, Willi; Rothbächer, Ute; Iché-Torres, Magali; Mélénec, Pauline; Hobert, Oliver; Bertrand, Vincent

doi:10.1016/j.devcel.2015.04.018

Cited by 44 publications

(66 citation statements)

References 29 publications

(54 reference statements)

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“…S4E) (Hudson et al, 2016). The mechanism of nβ-catenin-mediated transcriptional repression described in the present and previous (Oda- Ishii et al, 2016) studies is different from other mechanisms described in Caenorhabditis elegans and Drosophila melanogaster (Bertrand, 2016;Blauwkamp et al, 2008;Murgan et al, 2015). Thus, nuclear β-catenin-dependent transcriptional repression appears to be mediated by diverse mechanisms.…”

Section: Discussioncontrasting

confidence: 46%

Antagonism between β-catenin and Gata.a sequentially segregates the germ layers of ascidian embryos

et al. 2016

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Many animal embryos use nuclear β-catenin (nβ-catenin) during the segregation of endomesoderm (or endoderm) from ectoderm. This mechanism is thus likely to be evolutionarily ancient. In the ascidian embryo, nβ-catenin reiteratively drives binary fate decisions between ectoderm and endomesoderm at the 16-cell stage, and then between endoderm and margin (mesoderm and caudal neural) at the 32-cell stage. At the 16-cell stage, nβ-catenin activates endomesoderm genes in the vegetal hemisphere. At the same time, nβ-catenin suppresses the DNA-binding activity of a maternal transcription factor, Gata.a, through a physical interaction, and Gata.a thereby activates its target genes only in the ectodermal lineage. In the present study, we found that this antagonism between nβ-catenin and Gata.a also operates during the binary fate switch at the 32-cell stage. Namely, in marginal cells where nβ-catenin is absent, Gata.a directly activates its target, Zic-r.b (ZicL), to specify the marginal cell lineages. Thus, the antagonistic action between nβ-catenin and Gata.a is involved in two consecutive stages of germ layer segregation in ascidian embryos.

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Section: Discussioncontrasting

confidence: 46%

Antagonism between β-catenin and Gata.a sequentially segregates the germ layers of ascidian embryos

et al. 2016

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“…In other contexts, zic2 has been shown to directly modulate Nodal signaling and canonical Wnt signaling (Fujimi et al, 2012; Houtmeyers et al, 2016; Murgan et al, 2015; Pourebrahim et al, 2011) and may function in this capacity in the developing zebrafish. Exciting recent data identify Zic2 as a key co-factor for chromatin remodeling in embryonic stem cells (Luo et al, 2015), and may function in this capacity in the developing embryos.…”

Section: Discussionmentioning

confidence: 99%

Zebrafish zic2 controls formation of periocular neural crest and choroid fissure morphogenesis

Sedykh

Yoon

Roberson

et al. 2017

Developmental Biology

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The vertebrate retina develops in close proximity to the forebrain and neural crest-derived cartilages of the face and jaw. Coloboma, a congenital eye malformation, is associated with aberrant forebrain development (holoprosencephaly) and with craniofacial defects (frontonasal dysplasia) in humans, suggesting a critical role for cross-lineage interactions during retinal morphogenesis. ZIC2, a zinc-finger transcription factor, is linked to human holoprosencephaly. We have previously used morpholino assays to show zebrafish zic2 functions in the developing forebrain, retina and craniofacial cartilage. We now report that zebrafish with genetic lesions in zebrafish zic2 orthologs, zic2a and zic2b, develop with retinal coloboma and craniofacial anomalies. We demonstrate a requirement for zic2 in restricting pax2a expression and show evidence that zic2 function limits Hh signaling. RNA-seq transcriptome analysis identified an early requirement for zic2 in periocular neural crest as an activator of alx1, a transcription factor with essential roles in craniofacial and ocular morphogenesis in human and zebrafish. Collectively, these data establish zic2 mutant zebrafish as a powerful new genetic model for in-depth dissection of cell interactions and genetic controls during craniofacial complex development.

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“…In the anterior nucleus, there is a low SYS‐1 to POP‐1 ratio, POP‐1 is mostly free of SYS‐1 and acts as a transcriptional repressor . Figure (b) illustrates the reiterative use of this pathway in an embryonic neuronal lineage leading to a diversification of neuronal cell fates …”

Section: Reiterative β‐Catenin Asymmetries Driving Cell Fate Specificmentioning

confidence: 99%

“…However, how END‐1 or CEH‐10 represses anterior daughter markers is unknown. Recently, a more direct mechanism of regulation for anterior target genes has been described . In an anterior daughter (the SMDD/AIY neuroblast), expression of the ttx‐3 gene is activated via a binding site for a Zic transcription factor, REF‐2 (Figure (b)).…”

Section: Integration Of β‐Catenin Asymmetries Into Gene Regulatory Nementioning

confidence: 99%

β‐catenin‐driven binary cell fate decisions in animal development

Bertrand

2016

WIREs Developmental Biology

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The Wnt/β‐catenin pathway plays key roles during animal development. In several species, β‐catenin is used in a reiterative manner to regulate cell fate diversification between daughter cells following division. This binary cell fate specification mechanism has been observed in animals that belong to very diverse phyla: the nematode Caenorhabditis elegans, the annelid Platynereis, and the ascidian Ciona. It may also play a role in the regulation of several stem cell lineages in vertebrates. While the molecular mechanism behind this binary cell fate switch is not fully understood, it appears that both secreted Wnt ligands and asymmetric cortical factors contribute to the generation of the difference in nuclear β‐catenin levels between daughter cells. β‐Catenin then cooperates with lineage specific transcription factors to induce the expression of novel sets of transcription factors at each round of divisions, thereby diversifying cell fate. WIREs Dev Biol 2016, 5:377–388. doi: 10.1002/wdev.228For further resources related to this article, please visit the WIREs website.

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Atypical Transcriptional Activation by TCF via a Zic Transcription Factor in C. elegans Neuronal Precursors

Cited by 44 publications

References 29 publications

Antagonism between β-catenin and Gata.a sequentially segregates the germ layers of ascidian embryos

Antagonism between β-catenin and Gata.a sequentially segregates the germ layers of ascidian embryos

Zebrafish zic2 controls formation of periocular neural crest and choroid fissure morphogenesis

β‐catenin‐driven binary cell fate decisions in animal development

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