Formation of posterior cranial placode derivatives requires the Iroquois transcription factor irx4a

Feijóo, Carmen G.; Saldias, Marioli P.; Paz, Javiera F. De la; Gómez-Skármeta, José Luis; Allende, Miguel L.

doi:10.1016/j.mcn.2008.11.003

Cited by 15 publications

(11 citation statements)

References 63 publications

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“…So, it is possible that Irx genes may be involved in cell death control. Supporting this hypothesis, in other systems the deletion of Irx genes results in cell death, for instance, Irx1a , Irx4a or Irxl1 morphants show extensive cell death in the rostral region of the zebrafish embryo [27], in the CNS [28] and in the developing head and trunk along the neural tube [29], respectively. Moreover, antisense knockdown of pulmonary Irx1 , Irx2 , Irx3 , and Irx5 together increases apoptosis in the mesenchymal compartment of rat lung explants [30].…”

Section: Discussionmentioning

confidence: 85%

Irx1 and Irx2 Are Coordinately Expressed and Regulated by Retinoic Acid, TGFβ and FGF Signaling during Chick Hindlimb Development

et al. 2013

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The Iroquois homeobox (Irx) genes play a crucial role in the regionalization and patterning of tissues and organs during metazoan development. The Irx1 and Irx2 gene expression pattern during hindlimb development has been investigated in different species, but its regulation during hindlimb morphogenesis has not been explored yet. The aim of this study was to evaluate the gene expression pattern of Irx1 and Irx2 as well as their regulation by important regulators of hindlimb development such as retinoic acid (RA), transforming growth factor β (TGFβ) and fibroblast growth factor (FGF) signaling during chick hindlimb development. Irx1 and Irx2 were coordinately expressed in the interdigital tissue, digital primordia, joints and in the boundary between cartilage and non-cartilage tissue. Down-regulation of Irx1 and Irx2 expression at the interdigital tissue coincided with the onset of cell death. RA was found to down-regulate their expression by a bone morphogenetic protein-independent mechanism before any evidence of cell death. Furthermore, TGFβ protein regulated Irx1 and Irx2 in a stage-dependent manner at the interdigital tissue, it inhibited their expression when it was administered to the interdigital tissue at developing stages before their normal down-regulation. TGFβ administered to the interdigital tissue at developing stages after normal down-regulation of Irx1 and Irx2 evidenced that expression of these genes marked the boundary between cartilage tissue and non-cartilage tissue. It was also found that at early stages of hindlimb development FGF signaling inhibited the expression of Irx2. In conclusion, the present study demonstrates that Irx1 and Irx2 are coordinately expressed and regulated during chick embryo hindlimb development as occurs in other species of vertebrates supporting the notion that the genomic architecture of Irx clusters is conserved in vertebrates.

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Section: Discussionmentioning

confidence: 85%

Irx1 and Irx2 Are Coordinately Expressed and Regulated by Retinoic Acid, TGFβ and FGF Signaling during Chick Hindlimb Development

et al. 2013

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“…Iro/Irx genes are also involved in the initiation of expression of the neural determination/differentiation bHLH factors. Later, they play important roles in patterning the CNS (Rodriguez‐Sequel et al, 2009; Stedman et al, 2009) and appear to regulate the number of cranial placode progenitors (Feijoo et al, 2009).…”

Section: How Might Nfs Genes Regulate Neural Stem Cells?mentioning

confidence: 99%

Neural induction and factors that stabilize a neural fate

Rogers

Moody

Casey

2009

Birth Defects Research Pt C

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The neural ectoderm of vertebrates forms when the BMP signaling pathway is suppressed. Herein we review the molecules that directly antagonize extracellular BMP and the signaling pathways that further contribute to reduce BMP activity in the neural ectoderm. Downstream of neural induction, a large number of “neural fate stabilizing” (NFS) transcription factors are expressed in the presumptive neural ectoderm, developing neural tube, and ultimately in neural stem cells. Herein we review what is known about their activities during normal development to maintain a neural fate and regulate neural differentiation. Further elucidation of how the NFS genes interact to regulate neural specification and differentiation should ultimately prove useful for regulating the expansion and differentiation of neural stem and progenitor cells.

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“…Within the Pax2-labelled proximal pharyngeal ectoderm, the epibranchial placodes could be identified as thickened epithelial cells, whereas the surrounding interplacodal pharyngeal ectoderm thinned out and adopted a surface epithelial morphology (Müller and O'Rahilly, 1988;Tripathi et al, 2009;Washausen et al, 2005). We further examined the epibranchial placodal area using Sox2, a placodal marker gene; Irx5, which is expressed in PPA (Feijoo et al, 2009;Glavic et al, 2004); and acetylated tubulin, which marks motile cilia on ciliated cells. We found that the epibranchial placodal cells expressing Sox2 were marked with acetylated tubulin (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…We next addressed the question of how the pool of Pax2 + PPA progenitors may segregate into three discrete epibranchial placodes as well as interplacodal pharyngeal ectodermal cells. We first investigated the spatiotemporal patterning of the epibranchial placodes from E8.5 to E9.5 using a series of placodal and pharyngeal markers including Eya1 and Six1 ( placodal progenitor markers); Neurog2 (the earliest pre-neural marker in epibranchial placode; Fode et al, 1998); Sox2 (essential for epibranchial neural competence; Gou et al, 2018;Tripathi et al, 2009); Irx5 (expressed in PPA; Feijoo et al, 2009;Glavic et al, 2004); vestigial-like2 (Vgll2) (expressed in the pharyngeal region; Chen et al, 2017;Johnson et al, 2011); Fgf3; and the FGF downstream target Etv5 (essential for pharyngeal morphogenesis) (Urness et al, 2011).…”

Section: Stepwise Regionalization Of Epibranchial Placode and Proximamentioning

confidence: 99%

Notch signalling regulates epibranchial placode patterning and segregation

et al. 2020

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Epibranchial placodes are the geniculate, petrosal and nodose placodes that generate parts of cranial nerves VII, IX and X, respectively. How the three spatially separated placodes are derived from the common posterior placodal area is poorly understood. Here, we reveal that the broad posterior placode area is first patterned into a Vgll2 + /Irx5 + rostral domain and a Sox2 + /Fgf3 + / Etv5 + caudal domain relative to the first pharyngeal cleft. This initial rostral and caudal patterning is then sequentially repeated along each pharyngeal cleft for each epibranchial placode. The caudal domains give rise to the neuronal and non-neuronal cells in the placode, whereas the rostral domains are previously unrecognized structures, serving as spacers between the final placodes. Notch signalling regulates the balance between the rostral and caudal domains: high levels of Notch signalling expand the caudal domain at the expense of the rostral domain, whereas loss of Notch signalling produces the converse phenotype. Collectively, these data unravel a new patterning principle for the early phases of epibranchial placode development and a role for Notch signalling in orchestrating epibranchial placode segregation and differentiation.

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Formation of posterior cranial placode derivatives requires the Iroquois transcription factor irx4a

Cited by 15 publications

References 63 publications

Irx1 and Irx2 Are Coordinately Expressed and Regulated by Retinoic Acid, TGFβ and FGF Signaling during Chick Hindlimb Development

Irx1 and Irx2 Are Coordinately Expressed and Regulated by Retinoic Acid, TGFβ and FGF Signaling during Chick Hindlimb Development

Neural induction and factors that stabilize a neural fate

Notch signalling regulates epibranchial placode patterning and segregation

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