Detection of isoform‐specific fibroblast growth factor receptors by whole‐mount in situ hybridization in early chick embryos

Nishita, Junko; Ohta, Sho; Bleyl, Steven B.; Schoenwolf, Gary C.

doi:10.1002/dvdy.22616

Cited by 10 publications

(11 citation statements)

References 31 publications

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“…The boundary expression of FGFRs 1–3 has been demonstrated (Nishita et al, 2011; Walshe and Mason, 2000; Weisinger et al, 2010) and is also shown here, together with the expression of FGFR4, which is demonstrated at hindbrain boundaries for the first time. While FGFRs 1 , 3 , 4 (Fig.…”

Section: Resultssupporting

confidence: 75%

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Expression of hindbrain boundary markers is regulated by FGF3

Weisinger¹,

Kohl²,

Kayam³

et al. 2011

Biology Open

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SummaryCompartment boundaries act as organizing centers that segregate adjacent areas into domains of gene expression and regulation, and control their distinct fates via the secretion of signalling factors. During hindbrain development, a specialized cell-population forms boundaries between rhombomeres. These boundary cells demonstrate unique morphological properties and express multiple genes that differs them from intra-rhombomeric cells. Yet, little is known regarding the mechanisms that controls the expression or function of these boundary markers.Multiple components of the FGF signaling system, including ligands, receptors, downstream effectors as well as proteoglycans are shown to localize to boundary cells in the chick hindbrain. These patterns raise the possibility that FGF signaling plays a role in regulating boundary properties. We provide evidence to the role of FGF signaling, particularly the boundary-derived FGF3, in regulating the expression of multiple markers at hindbrain boundaries. These findings enable further characterization of the unique boundary-cell population, and expose a new function for FGFs as regulators of boundary-gene expression in the chick hindbrain.

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Section: Resultssupporting

confidence: 75%

“…This suggests that some receptors are more prominent than others at different parts of the boundaries. Unravelling which of the FGFRs (and their precise spliced isoforms; Nishita et al, 2011) are indeed active at hindbrain boundaries will be necessary.…”

Section: Discussionmentioning

confidence: 99%

Expression of hindbrain boundary markers is regulated by FGF3

Weisinger¹,

Kohl²,

Kayam³

et al. 2011

Biology Open

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“…The most likely explanation for this species difference is that some of the receptors binding FGF2 are only weakly expressed in the chick telencephalon at the age when we inject exogenous FGF2 (33,34). We also note that the rodent studies focused exclusively on neocortical development, leaving some uncertainty about whether FGF2 affects mammalian midbrain development.…”

Section: Resultsmentioning

confidence: 97%

“…This differential effect is unlikely to be caused by a difference in FGF2 levels, as the embryonic tectum produces very little endogenous FGF2 (32) and the injected FGF2 appears to diffuse homogeneously through the cerebral ventricles. However, the differential FGF2 effect could be related to spatial differences in FGF2 receptor distribution (33,34) or to the normal rostroventral to caudodorsomedial gradient of neurogenesis observed within the avian tectum (35). Alternatively, the effects of FGF2 on tectal morphology may depend on interactions between the developing tectal surface and overlying nonneural tissues.…”

Section: Resultsmentioning

confidence: 99%

Expansion, folding, and abnormal lamination of the chick optic tectum after intraventricular injections of FGF2

McGowan

Alaama

Freise

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Comparative research has shown that evolutionary increases in brain region volumes often involve delays in neurogenesis. However, little is known about the influence of such changes on subsequent development. To get at this question, we injected FGF2-which delays cell cycle exit in mammalian neocortex-into the cerebral ventricles of chicks at embryonic day (ED) 4. This manipulation alters the development of the optic tectum dramatically. By ED7, the tectum of FGF2-treated birds is abnormally thin and has a reduced postmitotic layer, consistent with a delay in neurogenesis. FGF2 treatment also increases tectal volume and ventricular surface area, disturbs tectal lamination, and creates small discontinuities in the pia mater overlying the tectum. On ED12, the tectum is still larger in FGF2-treated embryos than in controls. However, lateral portions of the FGF2-treated tectum now exhibit volcano-like laminar disturbances that coincide with holes in the pia, and the caudomedial tectum exhibits prominent folds. To explain these observations, we propose that the tangential expansion of the ventricular surface in FGF2-treated tecta outpaces the expansion of the pial surface, creating abnormal mechanical stresses. Two alternative means of alleviating these stresses are tectal foliation and the formation of pial holes. The latter probably alter signaling gradients required for normal cell migration and may generate abnormal patterns of cerebrospinal fluid flow; both abnormalities would generate disturbances in tectal lamination. Overall, our findings suggest that evolutionary expansion of sheet-like, laminated brain regions requires a concomitant expansion of the pia mater.brain evolution | evolutionary developmental biology | proliferation | meninges | cortical folding E volutionary increases in brain region volumes are common (1).For example, the neocortex is disproportionately enlarged in primates relative to other mammals, and the telencephalon is disproportionately enlarged in parrots and songbirds relative to other birds (1-4). Recent work in evolutionary developmental neurobiology has shown that these evolutionary increases in brain region volumes are often caused by delays in cell cycle exit of neuronal precursors (5, 6). Among birds, for example, parrots and songbirds exhibit delayed telencephalic neurogenesis relative to chicken-like birds (7-9). Among mammals, cell cycle exit in the neocortex is similarly delayed in primates, which have a disproportionately enlarged neocortex (5, 10-12).Unfortunately, the downstream effects of delayed cell cycle exit on subsequent developmental processes and adult morphology remain poorly understood. One way to fill this gap in our knowledge is to experimentally recreate the key species differences in the laboratory by means of carefully selected developmental manipulations. A good example of this phenocopy approach was the creation of transgenic mice with a constitutively active form of β-catenin that prolongs proliferation, increases neocortical volume, and generates cortica...

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“…Although the receptor affinities for FGF molecules have been reported for the mouse, they have not been reported in the chick and it is, therefore, not clear if the affinities are comparable. A recent detailed chick FGF receptor expression study provides some insight into potentially important regions of ligand-receptor interaction (Nishita et al, 2011). For example, FGF5 and FGF6 act mainly through FGFR1c and 2c, whereas FGF7 acts through FGFR2b.…”

Section: Resultsmentioning

confidence: 99%

Cloning and expression analysis of Fgf5, 6 and 7 during early chick development

Kumar

Chapman

2012

Gene Expression Patterns

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FGFs1 with similar sequences can play different roles depending on the model organisms examined. Determining these roles requires knowledge of spatio-temporal Fgf gene expression patterns. In this study, we report the cloning of chick Fgf5, 6 and 7, and examine their gene expression patterns by whole mount in situ hybridization. We show that Fgf5's spatio-temporally restricted expression pattern indicates a potentially novel role during inner ear development. Fgf6 and Fgf7, although belonging to different subfamilies with diverged sequences, are expressed in similar patterns within the mesoderm. Alignment of protein sequences and phylogenetic analysis demonstrate that FGF5 and FGF6 are highly conserved between chick, human, mouse and zebrafish. FGF7 is similarly conserved except for the zebrafish, which has considerably diverged.

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Detection of isoform‐specific fibroblast growth factor receptors by whole‐mount in situ hybridization in early chick embryos

Cited by 10 publications

References 31 publications

Expression of hindbrain boundary markers is regulated by FGF3

Expression of hindbrain boundary markers is regulated by FGF3

Expansion, folding, and abnormal lamination of the chick optic tectum after intraventricular injections of FGF2

Cloning and expression analysis of Fgf5, 6 and 7 during early chick development

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