Fgf16 is essential for pectoral fin bud formation in zebrafish

Nomura, Ryohei; Kamei, Eriko; Hotta, Yuuhei; Konishi, Morichika; Miyake, Ayumi; Itoh, Nobuyuki

doi:10.1016/j.bbrc.2006.06.108

Cited by 51 publications

(77 citation statements)

References 28 publications

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“…As in mouse only Fgf4, Fgf8, Fgf9, and Fgf17 are known to be expressed in the AER (Niswander and Martin,'92;Heikinheimo et al,'94;Ohuchi et al,'94;Crossley and Martin,'95;Mahmood et al,'95), this suggests complex regulatory evolution and either the loss of function of Fgf16 in tetrapod limb development or the acquisition of fgf16 function in pectoral fin formation in ray-fin fish. Regardless of the exact evolutionary scenario, our results and those mentioned above (Reifers et al, '98;Draper et al, 2003;Fischer et al, 2003;Nomura et al, 2006) show that mechanisms of vertebrate limb development are less conserved than previously thought. More generally, these results call into question conclusions regarding the universality of gene function and developmental processes drawn from a few model organisms and point to the need to expand developmental studies beyond model clades and to interpret results in an evolutionary context.…”

Section: Divergence In Fgf Signaling During Appendage Formationcontrasting

confidence: 45%

“…Fgf24 acts upstream of Fgf10 and induces its expression in the LPM, but fgf24 expression in the AER occurs after the formation of the limb bud (Fischer et al, 2003). A more distantly related gene, fgf16, acts downstream of fgf10 to induce fgf4 and fgf8a expression in the AER of zebrafish (Nomura et al, 2006). Moreover, fgf24 in the mesenchyme (Fischer et al, 2003) and fgf16 in the AER (Nomura et al, 2006) induce sonic hedgehog (shh) expression in the mesenchyme underlying the AER.…”

Section: Divergence In Fgf Signaling During Appendage Formationmentioning

confidence: 99%

“…A more distantly related gene, fgf16, acts downstream of fgf10 to induce fgf4 and fgf8a expression in the AER of zebrafish (Nomura et al, 2006). Moreover, fgf24 in the mesenchyme (Fischer et al, 2003) and fgf16 in the AER (Nomura et al, 2006) induce sonic hedgehog (shh) expression in the mesenchyme underlying the AER. Nomura et al (2006) also showed that fgf16 and shh maintain and/or induce each other's expression.…”

Section: Divergence In Fgf Signaling During Appendage Formationmentioning

confidence: 99%

“…Moreover, fgf24 in the mesenchyme (Fischer et al, 2003) and fgf16 in the AER (Nomura et al, 2006) induce sonic hedgehog (shh) expression in the mesenchyme underlying the AER. Nomura et al (2006) also showed that fgf16 and shh maintain and/or induce each other's expression. This is different from the situation in tetrapods, because in mouse and chicken the interaction between the AER and the zone of polarizing activity , the inducer promoting antero-posterior differentiation of the limb, requires interaction between Fgf8 in the AER and shh in the mesenchyme (Laufer et al, '94;Niswander et al, '94;Sun et al, 2002).…”

Section: Divergence In Fgf Signaling During Appendage Formationmentioning

confidence: 99%

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Duplication and divergence of fgf8 functions in teleost development and evolution

Jovelin

Amores

et al. 2007

J Exp Zool Pt B

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Fibroblast growth factors play critical roles in many aspects of embryo patterning that are conserved across broad phylogenetic distances. To help understand the evolution of fibroblast growth factor functions, we identified members of the Fgf8/17/18-subfamily in the threespine stickleback Gasterosteus aculeatus, and investigated their evolutionary relationships and expression patterns. We found that fgf17b is the ortholog of tetrapod Fgf17, whereas the teleost genes called fgf8 and fgf17a are duplicates of the tetrapod gene Fgf8, and thus should be called fgf8a and fgf8b. Phylogenetic analysis supports the view that the Fgf8/17/18-subfamily expanded during the ray-fin fish genome duplication. In situ hybridization experiments showed that stickleback fgf8 duplicates exhibited common and unique expression patterns, indicating that tissue specialization followed the gene duplication event. Moreover, direct comparison of stickleback and zebrafish embryonic expression patterns of fgf8 co-orthologs suggested lineage-specific independent subfunction partitioning and the acquisition or the loss of ortholog functions. In tetrapods, Fgf8 plays an important role in the apical ectodermal ridge of the developing pectoral appendage. Surprisingly, differences in the expression of fgf8a in the apical ectodermal ridge of the pectoral fin bud in zebrafish and stickleback, coupled with the role of fgf16 and fgf24 in teleost pectoral appendage show that different Fgf genes may play similar roles in limb development in various vertebrates.

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Section: Divergence In Fgf Signaling During Appendage Formationcontrasting

confidence: 45%

Section: Divergence In Fgf Signaling During Appendage Formationmentioning

confidence: 99%

Section: Divergence In Fgf Signaling During Appendage Formationmentioning

confidence: 99%

Section: Divergence In Fgf Signaling During Appendage Formationmentioning

confidence: 99%

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Duplication and divergence of fgf8 functions in teleost development and evolution

Jovelin

Amores

et al. 2007

J Exp Zool Pt B

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“…Analysis of FGF9-deficient mice has identified FGF9 as a reciprocal epithelial-to-mesenchymal signal required for morphogenesis of the lung, cecum, small intestine, and inner ear (14,49,65,71). In addition, studies in zebra fish show that FGF16 and FGF20 are apical ectodermal ridge factors that are required for pectoral fin bud outgrowth and, in general, for cell proliferation and differentiation of the mesenchyme (41,66).…”

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confidence: 99%

Homodimerization Controls the Fibroblast Growth Factor 9 Subfamily's Receptor Binding and Heparan Sulfate-Dependent Diffusion in the Extracellular Matrix

Kalinina

Byron

Makarenkova

et al. 2009

Molecular and Cellular Biology

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Uncontrolled fibroblast growth factor (FGF) signaling can lead to human diseases, necessitating multiple layers of self-regulatory control mechanisms to keep its activity in check. Herein, we demonstrate that FGF9 and FGF20 ligands undergo a reversible homodimerization, occluding their key receptor binding sites. To test the role of dimerization in ligand autoinhibition, we introduced structure-based mutations into the dimer interfaces of FGF9 and FGF20. The mutations weakened the ability of the ligands to dimerize, effectively increasing the concentrations of monomeric ligands capable of binding and activating their cognate FGF receptor in vitro and in living cells. Interestingly, the monomeric ligands exhibit reduced heparin binding, resulting in their increased radii of heparan sulfate-dependent diffusion and biologic action, as evidenced by the wider dilation area of ex vivo lung cultures in response to implanted mutant FGF9-loaded beads. Hence, our data demonstrate that homodimerization autoregulates FGF9 and FGF20's receptor binding and concentration gradients in the extracellular matrix. Our study is the first to implicate ligand dimerization as an autoregulatory mechanism for growth factor bioactivity and sets the stage for engineering modified FGF9 subfamily ligands, with desired activity for use in both basic and translational research.Fibroblast growth factor (FGF) signaling plays pleiotropic roles throughout the life spans of mammalian organisms, ranging from germ cell maturation, mesoderm induction, body plan formation, and organogenesis during embryonic development to serum phosphate homeostasis and glucose, bile acid, lipid, and cholesterol metabolism in the adult (3,23,27,28,57,60,62). The diversity of FGF signaling is underscored by virtue of the fact that aberrant FGF signaling leads to a wide array of human diseases, including skeletal and olfactory/reproductive syndromes, phosphate wasting disorders, and cancer (16,60,67). Recent data also implicate dysregulated FGF signaling in the etiology of neurodegenerative disorders, such as major depressive disorder and Parkinson's disease (10,63,64).Based on pairwise sequence homology and phylogeny, the 18 bona fide mammalian FGFs (FGF1 to FGF10 and FGF16 to FGF23) are divided into six subfamilies (45). Five FGF subfamilies have high-to-moderate affinity for pericellular heparan sulfate (HS) glycosaminoglycans and thus diffuse locally within tissues to act in a paracrine fashion, whereas the poor affinity of the FGF19 subfamily for HS enables this subfamily to act in an endocrine manner (28, 38). All FGFs share a core homology region of about 120 amino acids, which fold into 12 antiparallel ␤ strands (␤1 to ␤12) that are arranged into three sets of four-stranded ␤ sheets (␤-trefoil fold) (39). The globular FGF core domain is flanked by highly divergent N-and C-terminal extensions, which are the principal regions responsible for the different biology of FGFs. FGFs exert their diverse actions by binding and activating FGF receptors (FGFRs) in an HS-depe...

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Fgf16^IRESCre mice: A tool to inactivate genes expressed in inner ear cristae and spiral prominence epithelium

Hatch

Urness

Mansour

2009

Developmental Dynamics

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Fibroblast growth factors play important roles in inner ear development. Previous studies showed that mouse Fgf16 is expressed asymmetrically during the otic cup and vesicle stages of development, suggesting roles in regulating or responding to anteroposterior axial cues. Here, we studied otic Fgf16 expression throughout embryonic development and found transcripts in the developing cristae and in a few cells in the lateral wall of the cochlear duct. To determine the otic function of Fgf16 and to follow the fate of Fgf16-expressing cells, we generated an Fgf16 IRESCre allele. We show that Fgf16 does not have a unique role in inner ear development and that the Fgf16 lineage is found throughout the three cristae, in portions of the semicircular canal ducts, and in the cochlear spiral prominence epithelial cells. This strain will be useful for gene ablations in these tissues. Developmental Dynamics 238:358 -366, 2009.

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Fgf16 is essential for pectoral fin bud formation in zebrafish

Cited by 51 publications

References 28 publications

Duplication and divergence of fgf8 functions in teleost development and evolution

Duplication and divergence of fgf8 functions in teleost development and evolution

Homodimerization Controls the Fibroblast Growth Factor 9 Subfamily's Receptor Binding and Heparan Sulfate-Dependent Diffusion in the Extracellular Matrix

Fgf16^IRESCre mice: A tool to inactivate genes expressed in inner ear cristae and spiral prominence epithelium

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Fgf16 is essential for pectoral fin bud formation in zebrafish

Cited by 51 publications

References 28 publications

Duplication and divergence of fgf8 functions in teleost development and evolution

Duplication and divergence of fgf8 functions in teleost development and evolution

Homodimerization Controls the Fibroblast Growth Factor 9 Subfamily's Receptor Binding and Heparan Sulfate-Dependent Diffusion in the Extracellular Matrix

Fgf16IRESCre mice: A tool to inactivate genes expressed in inner ear cristae and spiral prominence epithelium

Contact Info

Product

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Fgf16^IRESCre mice: A tool to inactivate genes expressed in inner ear cristae and spiral prominence epithelium