Survey of fibroblast growth factor expression during chick organogenesis

Karabağlı, Hakan; Karabagli, Pinar; Ladher, Raj K.; Schoenwolf, Gary C.

doi:10.1002/ar.10129

Cited by 34 publications

(26 citation statements)

References 31 publications

(31 reference statements)

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“…Several Fgf molecules are produced by the somites (Karabagli et al, 2002). We find in fact that Fgf4 and Fgf6 ventrolateral somitic expression is greatly diminished in Six1 -/-Six4 -/-E10.5 embryos.…”

Section: Six1 and Six4 Control Fgf Production In The Myotomesmentioning

confidence: 58%

Six1 and Six4 homeoproteins are required for Pax3 and Mrf expression during myogenesis in the mouse embryo

et al. 2005

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In mammals, Six5, Six4 and Six1 genes are co-expressed during mouse myogenesis. Six4 and Six5 single knockout (KO)mice have no developmental defects, while Six1 KO mice die at birth and show multiple organ developmental defects. We have generated Six1Six4 double KO mice and show an aggravation of the phenotype previously reported for the single Six1 KO. Six1Six4 double KO mice are characterized by severe craniofacial and rib defects, and general muscle hypoplasia. At the limb bud level, Six1 and Six4homeogenes control early steps of myogenic cell delamination and migration from the somite through the control of Pax3 gene expression. Impaired in their migratory pathway, cells of the somitic ventrolateral dermomyotome are rerouted, lose their identity and die by apoptosis. At the interlimb level, epaxial Met expression is abolished, while it is preserved in Pax3-deficient embryos. Within the myotome, absence of Six1and Six4 impairs the expression of the myogenic regulatory factors myogenin and Myod1, and Mrf4 expression becomes undetectable. Myf5 expression is correctly initiated but becomes restricted to the caudal region of each somite. Early syndetomal expression of scleraxis is reduced in the Six1Six4 embryo, while the myotomal expression of Fgfr4 and Fgf8 but not Fgf4 and Fgf6 is maintained. These results highlight the different roles played by Six proteins during skeletal myogenesis.

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Section: Six1 and Six4 Control Fgf Production In The Myotomesmentioning

confidence: 58%

Six1 and Six4 homeoproteins are required for Pax3 and Mrf expression during myogenesis in the mouse embryo

et al. 2005

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“…FGF8, 9, 18 are expressed in the epithelium lining the nasal slit in the stage-24 frontonasal mass (McGonnell et al, 1998;Karabagli et al, 2002;Havens et al, 2006;Szabo-Rogers et al, 2008) whereas FGF2 is expressed more generally throughout the epithelium and mesenchyme . We have shown that certain regions of the frontonasal mass are dependent on FGF signaling for normal outgrowth and lip fusion (Szabo-Rogers et al, 2008) and that FGFs can replace epithelium and promote outgrowth of the frontonasal mass skeleton .…”

Section: Fgfs Are Required For the Induction Of Tbx22 In The Frontonamentioning

confidence: 99%

The function and regulation of TBX22 in avian frontonasal morphogenesis

Higashihori¹,

Buchtová²,

Richman³

2010

Developmental Dynamics

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The frontonasal mass gives rise to the facial midline and fuses with the maxillary prominence to form the upper lip. Here we focus on the regulation and function of TBX22, a repressor dynamically expressed in the frontonasal mass. Both FGF and Noggin (a BMP antagonist) strongly induce gTBX22, however, each has opposite effects on morphogenesis -Noggin inhibits whereas FGF stimulates growth. To determine whether TBX22 mediates these effects, we used retroviruses to locally increase expression levels. RCAS::hTBX22 decreased proliferation, reduced expression of MSX2 and DLX5 and caused cleft lip. Decreased levels of endogenous gTBX22 were also observed but were not the primary cause of the phenotype as determined in rescue experiments. Our data suggest that genetic or environmental insults such as those affecting the BMP pathway could lead to a gain-of-function of TBX22 and predispose an individual to cleft lip. Developmental Dynamics 239:458-473,

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“…As shown for BMP2 in developing AV valve precursor cells (Lincoln et al, 2006a), the present studies show that BMP4 is sufficient to activate Smad 1/5/8 signaling. Less is known about the roles of FGF signaling during heart valve development, but several FGF ligands, including FGF4 and downstream signaling molecules, are expressed in the heart during cushion formation (Karabagli et al, 2002;Sugi et al, 2003;Liberatore and Yutzey, 2004;Lincoln et al, 2006a). These expression patterns support the importance of FGF signaling in regulating gene expression of tendon-associated genes during cell lineage diversification, consistent with the FGF and dpERK activation of scleraxis in the developing somites (Sugi et al, 2003;Brent and Tabin, 2004;Smith et al, 2005).…”

Section: Discussionmentioning

confidence: 67%