Fgf-dependent otic induction requires competence provided by Foxi1 and Dlx3b

Hans, Stefan; Christison, Joe; Liu, Dong; Westerfield, Monte

doi:10.1186/1471-213x-7-5

Cited by 78 publications

(55 citation statements)

References 73 publications

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“…Mutation or knockdown of foxi1 either blocks or greatly reduces the induction of otic placode gene sin zebrafish (Nissen et al, 2003; Solomon et al, 2003; Hans et al, 2007). To test whether chick Foxi3 was necessary for otic placode induction, we electroporated a combination of translation- and splice-blocking Foxi3 morpholinos into the presumptive otic placode region of HH5-7 embryos and analyzed expression of early otic placode markers and otic placode formation (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…7B; n=6) We finally examined whether the FGF signaling pathway was activated in PPR ectoderm in the absence of Foxi3 . The Ets transcription factor family member Pea3 ( Etv4 ) is expressed in otic ectoderm in response to FGF inducing signals (Hans et al, 2007; Urness et al, 2010; Yang et al, 2013), and in presumptive trigeminal explants treated with FGF2 (Supplementary Fig. 2).…”

Section: Resultsmentioning

confidence: 99%

“…Co-expression of Six1 and Eya2 in non-neural ectoderm cannot confer competence to express Pax2 in response to FGF2 (Christophorou et al, 2009). Zebrafish foxi1 has been reported to confer competence for otic placode induction in response to FGF signaling (Hans et al, 2007; Hans and Westerfield, 2007), but this effect was only seen following treatment with retinoic acid, and was not seen reproducibly in untreated ectoderm alone (Hans et al, 2007; Hans and Westerfield, 2007). …”

Section: Discussionmentioning

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: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

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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“…To induce Fgf8a expression, we used embryos derived from heterozygous tg(hsp90l:fgf8a)(Hans et al, 2007) fish crossed to wildtype fish, resulting in 50% of the progeny carrying the transgene. All embryos, including those not carrying the transgene, were heat-shocked at 40°C for thirty minutes.…”

Section: Methodsmentioning

confidence: 99%

Zebrafish Tbx16 regulates intermediate mesoderm cell fate by attenuating Fgf activity

Warga¹,

Mueller²,

Ho³

et al. 2013

Developmental Biology

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Progenitors of the zebrafish pronephros, red blood and trunk endothelium all originate from the ventral mesoderm and often share lineage with one another, suggesting that their initial patterning is linked. Previous studies have shown that spadetail (spt) mutant embryos, defective in tbx16 gene function, fail to produce red blood cells, but retain the normal number of endothelial and pronephric cells. We report here that spt mutants are deficient in all the types of early blood, have fewer endothelial cells as well as far more pronephric cells compared to wildtype. In vivo cell tracing experiments reveal that blood and endothelium originate in spt mutants almost exclusively from the dorsal mesoderm whereas, pronephros and tail originate from both dorsal and ventral mesoderm. Together these findings suggest possible defects in posterior patterning. In accord with this, gene expression analysis show that mesodermal derivatives within the trunk and tail of spt mutants have acquired more posterior identity. Secreted signaling molecules belonging to the Fgf, Wnt and Bmp families have been implicated as patterning factors of the posterior mesoderm. Further investigation demonstrate that Fgf and Wnt signaling are elevated throughout the nonaxial region of the spt gastrula. By manipulating Fgf signaling we show that Fgfs both promote pronephric fate and repress blood and endothelial fate. We conclude that Tbx16 plays an important role in regulating the balance of intermediate mesoderm fates by attenuating Fgf activity.

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“…The wild-type line used was AB. The lines, acerebellar ti282a , a strong hypomorphic mutant allele of fgf8, ntl b195 , and the transgenic line tg(hsp:fgf8) have been described previously (4,20,21).…”

Section: Methodsmentioning

confidence: 99%

Smarcd3 Regulates the Timing of Zebrafish Myogenesis Onset

Ochi

Hans²,

Westerfield

2008

Journal of Biological Chemistry

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A cascade of signaling events triggers myogenesis in vertebrates. Although studies of zebrafish indicate that fibroblast growth factor (Fgf), Hedgehog (Hh), and the T-box transcription factors, No tail (Ntl) and T-box gene 16 (Tbx16), regulate myogenesis, the hierarchy of these factors has not been determined. Recently, another transcriptional cofactor, Smarcd3, a subunit of the SWI/SNF chromatin-remodeling complex, has been shown to be required for heart muscle formation in mouse. In zebrafish, fgf8 and ntl expression commences during blastula stages, whereas myogenesis, as indicated by myod expression, does not begin until much later during mid-gastrula stages. smarcd3b expression, on the other hand, becomes enriched in the marginal zone just prior to the beginning of myod expression. Overexpression of smarcd3 shifts the onset of myod and myf5 expression earlier, and myod and myf5 expression in adaxial cells, the earliest muscle precursors, requires Smarcd3, indicating that Smarcd3 is the limiting factor that regulates the onset of myogenesis. Smarcd3 physically interacts with Ntl, and Smarcd3 overexpression fails to rescue myod expression in ntl mutants, demonstrating that function of Smarcd3 depends on Ntl activity. We propose a model in which cooperative activity of Fgf, Ntl, and Smarcd3 is required for the onset of myogenesis, with Smarcd3b serving as the primary regulator of the timing of myogenesis onset.

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Fgf-dependent otic induction requires competence provided by Foxi1 and Dlx3b

Cited by 78 publications

References 73 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

Zebrafish Tbx16 regulates intermediate mesoderm cell fate by attenuating Fgf activity

Smarcd3 Regulates the Timing of Zebrafish Myogenesis Onset

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