Involvement of Androgen-Induced Growth Factor (FGF-8) Gene in Mouse Embryogenesis and Morphogenesis

Ohuchi, Hideyo; Yoshioka, Hidefumi; Tanaka, Akira; Kawakami, Yasuhiko; Nohno, Tsutomu; Noji, Sumihare

doi:10.1006/bbrc.1994.2542

Cited by 158 publications

(93 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…FGF8 may also induce sema3F expression in vivo because (1) Fgf8 expression at the MHB preceded sema3F and (2) SU5402, an FGF receptor tyrosine kinase inhibitor (Mohammadi et al, 1997), essentially abolished sema3F expression in the otx2-positive region in vitro. The findings that sema3F is expressed near Fgf8-expressing areas such as limb buds, kidneys, and brachial arches (Heikinheimo et al, 1994;Ohuchi et al, 1994;Crossley and Martin, 1995;Mahmood et al, 1995;Eckhardt and Meyerhans, 1998;Huber et al, 2005;Gammill et al, 2006) are consistent with our interpretation.…”

Section: Fgf8 Induces Sema3fsupporting

confidence: 89%

FGF8 Signaling Regulates Growth of Midbrain Dopaminergic Axons by Inducing Semaphorin 3F

Yamauchi¹,

Mizushima²,

Tamada³

et al. 2009

J. Neurosci.

View full text Add to dashboard Cite

Accumulating evidence indicates that signaling centers controlling the dorsoventral (DV) polarization of the neural tube, the roof plate and the floor plate, play crucial roles in axon guidance along the DV axis. However, the role of signaling centers regulating the rostrocaudal (RC) polarization of the neural tube in axon guidance along the RC axis remains unknown. Here, we show that a signaling center located at the midbrain-hindbrain boundary (MHB) regulates the rostrally directed growth of axons from midbrain dopaminergic neurons (mDANs). We found that beads soaked with fibroblast growth factor 8 (FGF8), a signaling molecule that mediates patterning activities of the MHB, repelled mDAN axons that extended through the diencephalon. This repulsion may be mediated by semaphorin 3F (sema3F) because (1) FGF8-soaked beads induced an increase in expression of sema3F, (2) sema3F expression in the midbrain was essentially abolished by the application of an FGF receptor tyrosine kinase inhibitor, and (3) mDAN axonal growth was also inhibited by sema3F. Furthermore, mDAN axons expressed a sema3F receptor, neuropilin-2 (nrp2), and the removal of nrp-2 by gene targeting caused caudal growth of mDAN axons. These results indicate that the MHB signaling center regulates the growth polarity of mDAN axons along the RC axis by inducing sema3F.

show abstract

Section: Fgf8 Induces Sema3fsupporting

confidence: 89%

FGF8 Signaling Regulates Growth of Midbrain Dopaminergic Axons by Inducing Semaphorin 3F

Yamauchi¹,

Mizushima²,

Tamada³

et al. 2009

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Because of the adaptation of the partially conserved developmental pathway, it has often been observed that the manipulation of some key upstream genes leads to drastic appendage phenotypes such as neogenesis of an "additional" limb by the overexpression of such factors as Fgf (Ohuchi et al, 1994;Cohn et al, 1995). In the case of limb formation, developmental cascades composed of several developmental genes, such as Wnt8, Fgf10, and Tbx(s) have been suggested to be early regulators before the onset of regulatory genes for outgrowth.…”

Section: Appendage Phenotype Elicited By Aberrant Growth Factor Gene mentioning

confidence: 99%

Molecular genetic cascades for external genitalia formation: An emerging organogenesis program

Yamada

Suzuki

Haraguchi

et al. 2006

Developmental Dynamics

111

109

View full text Add to dashboard Cite

“…To date, 23 Fgf ligands (Fgf1-23) have been described in tetrapods (reviewed by Ornitz and Itoh, 2001) and several of these ligands are known to be expressed in early mesodermal progenitors in mice, including Fgf3 (Wilkinson et al, 1988), Fgf4 (Niswander and Martin, 1992;Drucker and Goldfarb, 1993), Fgf5 (Haub and Goldfarb, 1991;Hébert et al, 1991) and Fgf8 (Heikinheimo et al, 1994;Ohuchi et al, 1994;Crossley and Martin, 1995). Mutational analyses in mice, however, suggest that not all of these ligands are required for the development of mesoderm.…”

Section: Introductionmentioning

confidence: 99%

Zebrafish fgf24functions withfgf8to promote posterior mesodermal development

2003

View full text Add to dashboard Cite

Fibroblast growth factor (Fgf) signaling plays an important role during development of posterior mesoderm in vertebrate embryos. Blocking Fgf signaling by expressing a dominant-negative Fgf receptor inhibits posterior mesoderm development. In mice, Fgf8 appears to be the principal ligand required for mesodermal development, as mouse Fgf8 mutants do not form mesoderm. In zebrafish, Fgf8 is encoded by the acerebellarlocus, and, similar to its mouse otholog, is expressed in early mesodermal precursors during gastrulation. However, zebrafish fgf8 mutants have only mild defects in posterior mesodermal development, suggesting that it is not the only Fgf ligand involved in the development of this tissue. We report here the identification of an fgf8-related gene in zebrafish, fgf24, that is co-expressed with fgf8 in mesodermal precursors during gastrulation. Using morpholino-based gene inactivation, we have analyzed the function of fgf24 during development. We found that inhibiting fgf24 function alone has no affect on the formation of posterior mesoderm. Conversely, inhibiting fgf24 function in embryos mutant for fgf8 blocks the formation of most posterior mesoderm. Thus, fgf8 and fgf24 are together required to promote posterior mesodermal development. We provide both phenotypic and genetic evidence that these Fgf signaling components interact with no tailand spadetail, two zebrafish T-box transcription factors that are required for the development of all posterior mesoderm. Last, we show that fgf24 is expressed in early fin bud mesenchyme and that inhibiting fgf24 function results in viable fish that lack pectoral fins.

show abstract

Involvement of Androgen-Induced Growth Factor (FGF-8) Gene in Mouse Embryogenesis and Morphogenesis

Cited by 158 publications

References 0 publications

FGF8 Signaling Regulates Growth of Midbrain Dopaminergic Axons by Inducing Semaphorin 3F

FGF8 Signaling Regulates Growth of Midbrain Dopaminergic Axons by Inducing Semaphorin 3F

Molecular genetic cascades for external genitalia formation: An emerging organogenesis program

Zebrafish fgf24functions withfgf8to promote posterior mesodermal development

Contact Info

Product

Resources

About