Zebrafish<i>foxi1</i>mediates otic placode formation and jaw development

Solomon, Keely S.; Kudoh, Tetsuhiro; Dawid, Igor B.; Fritz, Andreas

doi:10.1242/dev.00308

Cited by 159 publications

(235 citation statements)

References 74 publications

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“…However, their expression domains are larger than that of sox3 at the one-somite stage, and they likely also represent the presumptive common cranial sensory placode that generates the nasal, lens, and otic placodes (Streit, 2004). It has also been shown that, in zebrafish, foxi1, a gene that encodes a member of the forkhead transcription factor family, is expressed in the epibranchial placode region and that it is required for neurogenesis in the epibranchial placode (Lee et al, 2003;Nissen et al, 2003;Solomon et al, 2003). However, foxi1 expression is initially restricted to the entire non-neural ectoderm region at the early gastrula stage, whereas it is expressed in other embryonic regions, such as in neural crest cells and endodermal pouches after the 10-somite stage (Nissen et al, 2003).…”

Section: Zebrafish Sox3 Is Specifically Expressed In the Developing Ementioning

confidence: 99%

Initial specification of the epibranchial placode in zebrafish embryos depends on the fibroblast growth factor signal

Nikaido

Doi

Shimizu³

et al. 2006

Developmental Dynamics

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In vertebrates, cranial sensory ganglia are mainly derived from ectodermal placodes, which are focal thickenings at characteristic positions in the embryonic head. Here, we provide the first description of the early development of the epibranchial placode in zebrafish embryos using sox3 as a molecular marker. By the one-somite stage, we saw a pair of single sox3-expressing domains appear lateral to the future hindbrain. The sox3 domain, which is referred to here as the early lateral placode, is segregated during the early phase of segmentation to form a pax2a-positive medial area and a pax2a-negative lateral area. The medial area subsequently developed to form the otic placode, while the lateral area was further segregated along the anteroposterior axis, giving rise to four sox3-positive subdomains by 26 hr postfertilization. Given their spatial relationship with the expression of the markers for the epibranchial ganglion, as well as their positions and temporal changes, we propose that these four domains correspond to the facial, glossopharyngeal, vagal, and posterior lateral line placodes in an anterior-to-posterior order. The expression of sox3 in the early lateral placode was absent in mutants lacking functional fgf8, while implantation of fibroblast growth factor (FGF) beads restored the sox3 expression. Using SU5402, which inhibits the FGF signal, we were able to demonstrate that formation of both the early lateral domains and later epibranchial placodes depends on the FGF signal operating at the beginning of somitogenesis. Together, these data provide evidence for the essential role of FGF signals in the development of the epibranchial placodes. Developmental Dynamics 236:564 -571, 2007.

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Section: Zebrafish Sox3 Is Specifically Expressed In the Developing Ementioning

confidence: 99%

Initial specification of the epibranchial placode in zebrafish embryos depends on the fibroblast growth factor signal

Nikaido

Doi

Shimizu³

et al. 2006

Developmental Dynamics

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“…Combined loss of function for dlx3b/4b leads to a reduction or absence of otic placodes and a loss of pax2a expression in otic precursor tissue, although pax8 expression initiates normally (Solomon and Fritz, 2002;Liu et al, 2003). Zebrafish foxi1, a Forkhead domain-containing transcription factor (Weigel and Jackle, 1990), is also expressed within otic precursor tissue and appears to function even earlier than dlx3b/4b (Solomon et al, 2003a). Embryos homozygous for a mutations in foxi1, including hearsay (hsy; Solomon et al, 2003a), foxi one (Nissen et al, 2003), and no soul (Lee et al, 2003), display reduced otic placodes/vesicles and completely lack pax8 expression in the otic primordia.…”

Section: Introductionmentioning

confidence: 99%

“…Zebrafish foxi1, a Forkhead domain-containing transcription factor (Weigel and Jackle, 1990), is also expressed within otic precursor tissue and appears to function even earlier than dlx3b/4b (Solomon et al, 2003a). Embryos homozygous for a mutations in foxi1, including hearsay (hsy; Solomon et al, 2003a), foxi one (Nissen et al, 2003), and no soul (Lee et al, 2003), display reduced otic placodes/vesicles and completely lack pax8 expression in the otic primordia. Moreover, overexpression of foxi1 can induce ectopic pax8 expression within the same tissue (Solomon et al, 2003a).…”

Section: Introductionmentioning

confidence: 99%

“…Embryos homozygous for a mutations in foxi1, including hearsay (hsy; Solomon et al, 2003a), foxi one (Nissen et al, 2003), and no soul (Lee et al, 2003), display reduced otic placodes/vesicles and completely lack pax8 expression in the otic primordia. Moreover, overexpression of foxi1 can induce ectopic pax8 expression within the same tissue (Solomon et al, 2003a). Therefore, foxi1 may represent one of the earliestacting genes regulating otic placode formation.…”

Section: Introductionmentioning

confidence: 99%

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Genetic interactions underlying otic placode induction and formation

Solomon

Kwak

Fritz

2004

Developmental Dynamics

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The formation of the otic placode is a complex process requiring multiple inductive signals. In zebrafish, fgf3 and fgf8, dlx3b and dlx4b, and foxi1 have been identified as the earliest-acting genes in this process. fgf3 and fgf8 are required as inductive signals, whereas dlx3b, dlx4b, and foxi1 appear to act directly within otic primordia. We have investigated potential interactions among these genes. Depletion of either dlx3b and dlx4b or foxi1 leads to a delay of pax2a expression in the otic primordia and reduction of the otic vesicle. Depletion of both foxi1 and dlx3b results in a complete ablation of otic placode formation. A strong synergistic interaction is also observed among foxi1, fgf3, and fgf8, and a weaker interaction among dlx3b, fgf3, and fgf8. Misexpression of foxi1 can induce expression of pax8, an early marker for the otic primordia, in embryos treated with an inhibitor of fibroblast growth factor (FGF) signaling. Conversely, morpholino knockdown of foxi1 blocks ectopic pax8 expression and otic vesicle formation induced by misexpression of fgf3 and/or fgf8. The observed genetic interactions suggest a model in which foxi1 and dlx3b/dlx4b act in independent pathways together with distinct phases of FGF signaling to promote otic placode induction and development. Developmental Dynamics 230:419 -433, 2004.

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“…Acerebellar (ace) zebrafish mutants, which inactivate the fgf8 gene, typically have a small otocyst, abnormal semicircular canals, and only one otolith (Leger and Brand, 2002). The foxi1 mutant hearsay often forms a single otic vesicle with one otolith (Solomon et al, 2003). Foxi1 is upstream of several transcription factors required for normal otic morphogenesis and regulates the expression of the anion transporter pendrin which is important in endolymph ionic regulation (discussed below) ( Table 1).…”

Section: Form a Normal Otocystmentioning

confidence: 99%

Mixing model systems: Using zebrafish and mouse inner ear mutants and other organ systems to unravel the mystery of otoconial development

Hughes

Thalmann

et al. 2006

Brain Research

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Human vestibular dysfunction is an increasing clinical problem. Degeneration or displacement of otoconia is a significant etiology of age-related balance disorders and Benign Positional Vertigo (BPV). In addition, commonly used antibiotics, such as aminoglycoside antibiotics, can lead to disruption of otoconial structure and function. Despite such clinical significance, relatively little information has been compiled about the development and maintenance of otoconia in humans. Recent studies in model organisms and other mammalian organ systems have revealed some of the proteins and processes required for the normal biomineralization of otoconia and otoliths in the inner ear of vertebrates. Orchestration of extracellular biomineralization requires bringing together ionic and proteinaceous components in time and space. Coordination of these events requires the normal formation of the otocyst and sensory maculae, specific secretion and localization of extracellular matrix proteins, as well as tight regulation of the endolymph ionic environment. Disruption of any of these processes can lead to the formation of abnormally shaped, or ectopic, otoconia, or otoconial agenesis. We propose that normal generation of otoconia requires a complex temporal and spatial control of developmental and biochemical events. In this review, we suggest a new hypothetical model for normal otoconial and otolith formation based on matrix vesicle mineralization in bone which we believe to be supported by information from existing mutants, morphants, and biochemical studies.

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Zebrafishfoxi1mediates otic placode formation and jaw development

Cited by 159 publications

References 74 publications

Initial specification of the epibranchial placode in zebrafish embryos depends on the fibroblast growth factor signal

Initial specification of the epibranchial placode in zebrafish embryos depends on the fibroblast growth factor signal

Genetic interactions underlying otic placode induction and formation

Mixing model systems: Using zebrafish and mouse inner ear mutants and other organ systems to unravel the mystery of otoconial development

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