Characterization of avian frizzled genes in cranial placode development

Stark, M. J.; Biggs, Jeremy; Schoenwolf, Gary C.; Rao, Mahendra S.

doi:10.1016/s0925-4773(00)00263-x

Cited by 62 publications

(52 citation statements)

References 17 publications

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“…Frizzled receptors, which have at least 10 orthologs in mammals, were detected in the lens. Frizzled 1, 2 and 7 are expressed in the chick lens placode (Stark et al, 2000). Also, Frizzled 1, 2, 3, 4, 6 and 7 are expressed in the embryonic and postnatal lens (Stump et al, 2003;Liu et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…The Wnt receptors Frizzled 1, Frizzled 2 and Frizzled 7 were detected in the lens placode during lens induction (Stark et al, 2000). Transcripts encoding Wnt3, Wnt5a, Wnt5b, Wnt7a, Wnt7b, Wnt8a, Wnt8b and Wnt13, and Frizzled receptors were identified in the postnatal lens epithelium and transitional zone at the lens equator (Jasoni et al, 1999;Stump et al, 2003;Liu et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Wnt signaling enhances FGF2-triggered lens fiber cell differentiation

Lyu

Joo

2004

Development

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Wnt signaling is implicated in many developmental processes, including cell fate changes. Several members of the Wnt family, as well as other molecules involved in Wnt signaling, including Frizzled receptors, LDL-related protein co-receptors, members of the Dishevelled and Dickkopf families, are known to be expressed in the lens during embryonic or postembryonic development. However, the function of Wnt signaling in lens fiber differentiation remains unknown. Here, we show that GSK-3β kinase is inactivated and that β-catenin accumulates during the early stages of lens fiber cell differentiation. In an explant culture system, Wnt conditioned medium (CM) induced the accumulation of β-crystallin, a marker of fiber cell differentiation, without changing cell shape. In contrast, epithelial cells stimulated with Wnt after priming with FGF elongated, accumulated β-crystallin, aquaporin-0, p57kip2, and altered their expression of cadherins. Treatment with lithium, which stabilizes β-catenin, induced the accumulation of β-crystallin, but explants treated with lithium after FGF priming did not elongate as they did after Wnt application. These results show that Wnts promote the morphological aspects of fiber cell differentiation in a process that requires FGF signaling, but is independent of β-catenin. Wnt signaling may play an important role in lens epithelial-tofiber differentiation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Wnt signaling enhances FGF2-triggered lens fiber cell differentiation

Lyu

Joo

2004

Development

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“…Embryos stained for analysis of gene or protein expression were cryoprotected in sucrose and sectioned at 14 µm using a Leica cryostat as described (Stark et al, 2000).…”

Section: Cryosectioningmentioning

confidence: 99%

Fgf3andFgf10are required for mouse otic placode induction

2003

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The inner ear, which contains the sensory organs specialised for audition and balance, develops from an ectodermal placode adjacent to the developing hindbrain. Tissue grafting and recombination experiments suggest that placodal development is directed by signals arising from the underlying mesoderm and adjacent neurectoderm. In mice, Fgf3 is expressed in the neurectoderm prior to and concomitant with placode induction and otic vesicle formation,but its absence affects only the later stages of otic vesicle morphogenesis. We show here that mouse Fgf10 is expressed in the mesenchyme underlying the prospective otic placode. Embryos lacking both Fgf3and Fgf10 fail to form otic vesicles and have aberrant patterns of otic marker gene expression, suggesting that FGF signals are required for otic placode induction and that these signals emanate from both the hindbrain and mesenchyme. These signals are likely to act directly on the ectoderm, as double mutant embryos showed normal patterns of gene expression in the hindbrain. Cell proliferation and survival were not markedly affected in double mutant embryos, suggesting that the major role of FGF signals in otic induction is to establish normal patterns of gene expression in the prospective placode. Finally, examination of embryos carrying three out of the four mutant Fgf alleles revealed intermediate phenotypes, suggesting a quantitative requirement for FGF signalling in otic vesicle formation.

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“…Hybridization probes were generated from plasmids containing: Pax2 (Dressler et al, 1990), Dlx5 (Depew et al, 1999), Gbx2 (Wassarman et al, 1997), Hmx3 (Nkx5.1) (Merlo et al, 2002), Lfng (Morsli et al, 1998), Fgf10 (Xu et al, 1998), Wnt1 and Wnt3a (Parr et al, 1993), Wnt2b (Grove et al, 1998), Bmp4 (Jones et al, 1991), Otx2 (Simeone et al, 1993) Mafb (Cordes and Barsh, 1994) and Gata3 (George et al, 1994). Stained embryos were cryoprotected in sucrose and cryosectioned as described (Stark et al, 2000). Two to six embryos of each genotype were analyzed with each probe.…”

Section: Paint-filling and Rna In Situ Hybridizationmentioning

confidence: 99%

Fgf3is required for dorsal patterning and morphogenesis of the inner ear epithelium

et al. 2007

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The inner ear, which contains sensory organs specialized for hearing and balance, develops from an ectodermal placode that invaginates lateral to hindbrain rhombomeres (r) 5-6 to form the otic vesicle. Under the influence of signals from intra-and extraotic sources, the vesicle is molecularly patterned and undergoes morphogenesis and cell-type differentiation to acquire its distinct functional compartments. We show in mouse that Fgf3, which is expressed in the hindbrain from otic induction through endolymphatic duct outgrowth, and in the prospective neurosensory domain of the otic epithelium as morphogenesis initiates, is required for both auditory and vestibular function. We provide new morphologic data on otic dysmorphogenesis in Fgf3 mutants, which show a range of malformations similar to those of Mafb (Kreisler), Hoxa1 and Gbx2 mutants, the most common phenotype being failure of endolymphatic duct and common crus formation, accompanied by epithelial dilatation and reduced cochlear coiling. The malformations have close parallels with those seen in hearing-impaired patients. The morphologic data, together with an analysis of changes in the molecular patterning of Fgf3 mutant otic vesicles, and comparisons with other mutations affecting otic morphogenesis, allow placement of Fgf3 between hindbrain-expressed Hoxa1 and Mafb, and otic vesicle-expressed Gbx2, in the genetic cascade initiated by WNT signaling that leads to dorsal otic patterning and endolymphatic duct formation. Finally, we show that Fgf3 prevents ventral expansion of r5-6 neurectodermal Wnt3a, serving to focus inductive WNT signals on the dorsal otic vesicle and highlighting a new example of cross-talk between the two signaling systems.

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Characterization of avian frizzled genes in cranial placode development

Cited by 62 publications

References 17 publications

Wnt signaling enhances FGF2-triggered lens fiber cell differentiation

Wnt signaling enhances FGF2-triggered lens fiber cell differentiation

Fgf3andFgf10are required for mouse otic placode induction

Fgf3is required for dorsal patterning and morphogenesis of the inner ear epithelium

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