Expression of the Foxi2 and Foxi3 transcription factors during development of chicken sensory placodes and pharyngeal arches

Khatri, Safia B.; Groves, Andrew K.

doi:10.1016/j.gep.2012.10.001

Cited by 39 publications

(50 citation statements)

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“…We previously described Foxi3 as one of the earliest genes expressed in the PPR (Khatri and Groves, 2013; Ohyama and Groves, 2004). To determine the precise timing of its expression with respect to neural induction and PPR induction, we compared Foxi3 expression with the non-neural ectodermal genes Dlx5 and Gata3 (Pera and Kessel, 1999; Sheng and Stern, 1999), the pre-neural marker gene Sox3 (Collignon et al, 1996; Rex et al, 1997; Rogers et al, 2013; Uwanogho et al, 1995) and the PPR genes Six1 and Eya2 (Christophorou et al, 2009; Schlosser, 2007; Zou et al, 2004) between developmental stages HH2-HH7 in chick (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…A species-specific cDNA probe for the 3′ untranslated regions of chicken Foxi3 was obtained from the UMIST Chick EST Repository (chEST50h20; Khatri and Groves, 2013). Other cDNA probes were kindly provided as follows: Dlx5 (Michael Kessel), Gata3 (Doug Engel), Sox3 (Berta Alsina), Six1 (Guillermo Oliver), Six4 (Paola Bovolenta), Eya2 (Guillermo Oliver), Pax2 (Domingos Henrique), Pea3 (Annette Neubüser).…”

Section: Methodsmentioning

confidence: 99%

“…We have previously described Foxi3 expression in non-neural ectoderm and the PPR in both mouse and chick embryos (Khatri and Groves, 2013; Ohyama and Groves, 2004), suggesting it may play an analogous role in amniotes to that of foxi1 in zebrafish. We now show that Foxi3 can regulate both non-neural ectoderm genes such as Dlx5, and genes that define the pre-placodal region such as members of the Six and Eya gene families.…”

Section: Introductionmentioning

confidence: 99%

“…PPR marker genes are induced by FGF signals from underlying cranial paraxial mesoderm, and by BMP and Wnt antagonists from paraxial mesoderm and the neural plate (Ahrens and Schlosser, 2005; Brugmann et al, 2004; Grocott et al, 2012; Litsiou et al, 2005). A number of genes that are initially expressed broadly in non-neural ectoderm, such as members of the Dlx , Gata , and Foxi gene families later become restricted to the PPR prior to overt placode differentiation (Bhat et al, 2013; Grocott et al, 2012; Groves and Labonne, 2013; Khatri and Groves, 2013; Kwon et al, 2010; Litsiou et al, 2005; McLarren et al, 2003; Ohyama and Groves, 2004; Saint-Jeannet and Moody, 2014; Schlosser, 2006; Streit, 2007). …”

Section: Introductionmentioning

confidence: 99%

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Foxi3 is necessary for the induction of the chick otic placode in response to FGF signaling

Khatri

Edlund

Groves

2014

Developmental Biology

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Vertebrate cranial sensory organs are derived from region at the border of the anterior neural plate called the pre-placodal region (PPR). The otic placode, the anlagen of the inner ear, is induced from PPR ectoderm by FGF signaling. We have previously shown that competence of embryonic ectoderm to respond to FGF signaling during otic placode induction correlates with the expression of PPR genes, but the molecular basis of this competence is poorly understood. Here, we characterize the function of a transcription factor, Foxi3 that is expressed at very early stages in the non-neural ectoderm and later in the PPR of chick embryos. Ablation experiments showed that the underlying hypoblast is necessary for the initiation of Foxi3 expression. Mis-expression of Foxi3 was sufficient to induce markers of non-neural ectoderm such as Dlx5, and the PPR such as Six1 and Eya2. Electroporation of Dlx5, or Six1 together with Eya1 also induced Foxi3, suggesting direct or indirect positive regulation between non-neural ectoderm genes and PPR genes. Knockdown of Foxi3 in chick embryos prevented the induction of otic placode markers, and was able to prevent competent cranial ectoderm from expressing otic markers in response to FGF2. In contrast, Foxi3 expression alone was not sufficient to confer competence to respond to FGF on embryonic ectoderm. Our analysis of PPR and FGF-responsive genes after Foxi3 knockdown at gastrula stages suggests it is not necessary for the expression of PPR genes at these stages, nor for the transduction of FGF signals. The early expression but late requirement for Foxi3 in ear induction suggests it may have some of the properties associated with pioneer transcription factors.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Foxi3 is necessary for the induction of the chick otic placode in response to FGF signaling

Khatri

Edlund

Groves

2014

Developmental Biology

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“…Whole mount in situ hybridization was performed as recently described (Khatri and Groves, 2013). After in situ hybridization, stained embryos were equilibrated in 15% sucrose in PBS and embedded in 7.5% gelatin with 15% sucrose in PBS for sectioning.…”

Section: Methodsmentioning

confidence: 99%

Foxi transcription factors promote pharyngeal arch development by regulating formation of FGF signaling centers

Edlund

Ohyama

Kantarci

et al. 2014

Developmental Biology

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The bones of the vertebrate face develop from transient embryonic branchial arches that are populated by cranial neural crest cells. We have characterized a mouse mutant for the Forkhead family transcription factor Foxi3, which is expressed in branchial ectoderm and endoderm. Foxi3 mutant mice are not viable and display severe branchial arch-derived facial skeleton defects, including absence of all but the most distal tip of the mandible and complete absence of the inner, middle and external ear structures. Although cranial neural crest cells of Foxi3 mutants are able to migrate, populate the branchial arches and display some elements of correct proximo distal patterning, they succumb to apoptosis from embryonic day 9.75 onwards. We show this cell death correlates with a delay in expression of Fgf8 in branchial arch ectoderm and a failure of neural crest cells in the arches to express FGF responsive genes. Zebrafish foxi1 is also expressed in branchial arch ectoderm and endoderm, and morpholino knockdown of foxi1 also causes apoptosis of neural crest in the branchial arches. We show that heat shock induction of fgf3 in zebrafish arch tissue can rescue cell death in foxi1 morphants. Our results suggest that Foxi3 may play a role in the establishment of signaling centers in the branchial arches that are required for neural crest survival, patterning and the subsequent development of branchial arch derivatives.

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Development of Neurogenic Placodes in Vertebrates

Buzzi

Hintze

Streit

2019

Encyclopedia of Life Sciences

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The cranial sensory nervous system comprises a diverse set of organs: the eye, ear and nose and the sensory ganglia that transmit touch, pain, temperature and gustatory information to the brain. Despite the structural and functional diversity of the adult organs, during development, they arise from a common pool of sensory progenitor cells. These progenitors are specified early during embryonic development in the nonneural ectoderm next to the future brain. Subsequently, they diversify to form sensory placodes, special patches of thickened epithelium adjacent to the developing neural tube. Each placode acquires its unique identity under the influence of signals from surrounding tissues and later generates specialised cell types that characterise each organ. Key Concepts Evolution of elaborate sensory systems in the head allowed vertebrate evolution. Sensory placodes are transient structures that form in the head ectoderm outside of the central nervous system and contribute to the sense organs and cranial sensory ganglia. All sensory placodes arise from a pool of multipotent progenitors that have initially the potential to give rise to all placode derivatives, but their potential becomes restricted as the embryo develops. Placode progenitors develop in close association with central nervous system precursors and neural crest cells in a territory termed the ‘neural plate border’. Placode progenitors are induced gradually in the ectoderm surrounding the anterior neural plate by signals from the underlying mesoderm. These signals differ along the rostro‐caudal axis with FGFs, BMP and Wnt antagonists inducing posterior progenitors, while anterior progenitors also require Shh and neuropeptides. Localised sources of different signals induce olfactory, trigeminal, otic and epibranchial placodes from sensory progenitor cells. Signals induce the expression of transcription factors in broad ectodermal domains, and mutual repression between them sharpen boundaries between neural, neural crest and placodal and between precursors for different placodes.

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Expression of the Foxi2 and Foxi3 transcription factors during development of chicken sensory placodes and pharyngeal arches

Cited by 39 publications

References 21 publications

Foxi3 is necessary for the induction of the chick otic placode in response to FGF signaling

Foxi3 is necessary for the induction of the chick otic placode in response to FGF signaling

Foxi transcription factors promote pharyngeal arch development by regulating formation of FGF signaling centers

Development of Neurogenic Placodes in Vertebrates

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