Coordinate expression of Fgf8, Otx2, Bmp4, and Shh in the rostral prosencephalon during development of the telencephalic and optic vesicles

Crossley, Philip H.; Martı́nez, Salvador; Ohkubo, Yasushi; Rubenstein, John L.R.

doi:10.1016/s0306-4522(01)00411-0

Cited by 246 publications

(254 citation statements)

References 79 publications

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“…Interestingly, embryos subjected to cyclopamine treatment starting as late as stage 7 developed a cyclopic phenotype. This is in agreement with the continuous expression of Shh throughout the node at stage 4 and subsequently in the prechordal mesendoderm at stage 7, the crucial structure for ventral forebrain patterning (Crossley et al, 2001).…”

Section: Discussionsupporting

confidence: 87%

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NODAL and SHH dose-dependent double inhibition promotes an HPE-like phenotype in chick embryos

Mercier¹,

David²,

Ratié³

et al. 2013

Development

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Section: Discussionsupporting

confidence: 87%

“…markers of the developing forebrain (Crossley et al, 2001): they are targets of NODAL signaling during forebrain development and are specifically downregulated in animal models of HPE (Müller et al, 2000;Rohr et al, 2001).…”

Section: Implications and Future Directionsmentioning

confidence: 99%

NODAL and SHH dose-dependent double inhibition promotes an HPE-like phenotype in chick embryos

Mercier¹,

David²,

Ratié³

et al. 2013

Development

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“…8 in SI Appendix) at E10.5 (30 embryos of 50), E11.5 (eight of 18), and E13.5 (eight of 17). FGF8 is well established as a signaling molecule, and its expression pattern and function during CNS development in mice and chicks have been reported (23)(24)(25)(26)(27)(28). Because the expression of AS071 is restricted to the lateral diencephalon and hypothalamus, we compared the expression pattern of AS071 lacZ with that of Fgf8 by in situ hybridization at E10.5 and E11.5 ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Possible involvement of SINEs in mammalian-specific brain formation

Sasaki

Nishihara²,

Hirakawa³

et al. 2008

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

174

168

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Retroposons, such as short interspersed elements (SINEs) and long interspersed elements (LINEs), are the major constituents of higher vertebrate genomes. Although there are many examples of retroposons' acquiring function, none has been implicated in the morphological innovations specific to a certain taxonomic group. We previously characterized a SINE family, AmnSINE1, members of which constitute a part of conserved noncoding elements (CNEs) in mammalian genomes. We proposed that this family acquired genomic functionality or was exapted after retropositioning in a mammalian ancestor. Here we identified 53 new AmnSINE1 loci and refined 124 total loci, two of which were further analyzed. Using a mouse enhancer assay, we demonstrate that one SINE locus, AS071, 178 kbp from the gene FGF8 (fibroblast growth factor 8), is an enhancer that recapitulates FGF8 expression in two regions of the developing forebrain, namely the diencephalon and the hypothalamus. Our gain-of-function analysis revealed that FGF8 expression in the diencephalon controls patterning of thalamic nuclei, which act as a relay center of the neocortex, suggesting a role for FGF8 in mammalianspecific forebrain patterning. Furthermore, we demonstrated that the locus, AS021, 392 kbp from the gene SATB2, controls gene expression in the lateral telencephalon, which is thought to be a signaling center during development. These results suggest important roles for SINEs in the development of the mammalian neuronal network, a part of which was initiated with the exaptation of AmnSINE1 in a common mammalian ancestor.conserved noncoding element ͉ enhancer ͉ evolution ͉ mouse

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“…Expression of multiple Fgf genes, including Fgf8, is severely reduced in the Shh mutant; moreover, mouse lines engineered for defective Fgf signaling can develop a dorsal telencephalic midline (Garel et al, 2003;Gutin et al, 2006;Storm et al, 2006). Juxtaposed sources of Shh, Fgf8, and BMP/Wnt proteins regulate one another to pattern the telencephalon (Crossley et al, 2001;Ohkubo et al, 2002;Shimogori et al, 2004) but are not the only patterning cues. Given that dorsal epidermis induces roofplate in the spinal cord (Liem et al, 1995) and dorsal gene expression in the chick telencephalon (Gunhaga et al, 2003), dorsal telencephalic midline inductive signals seem likely to derive from adjacent mesenchyme and epidermis.…”

Section: Discussionmentioning

confidence: 99%

“…Similar defects occur in mice deficient in telencephalic , 2006); conversely, Fgf8 can induce an ectopic sulcus in the chick telencephalon that resembles the rostral sulcus (Crossley et al, 2001). Strongly suggesting that deficient Fgf signaling contributes to the Shh mutant phenotype, Fgf8 gene expression in the mutant telencephalon is weak and transient (Aoto et al, 2002;Ohkubo et al, 2002).…”

Section: Rostral Continuity Of the Hemispheres And Loss Of Fgf Signalingmentioning

confidence: 94%

Patterning the Dorsal Telencephalon: A Role for Sonic Hedgehog?

Rash¹,

Grove²

2007

J. Neurosci.

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Division of the telencephalic vesicle into hemispheres and specification of the cerebral cortex are key stages in forebrain development. We investigate the interplay in these processes of Sonic hedgehog (Shh), fibroblast growth factors (Fgfs), and the transcription factor Gli3, which in its repressor form (Gli3R) antagonizes Shh signaling and downregulates expression of several Fgf genes.Contrary to previous reports, Shh is not required for dorsal hemisphere separation. Mice lacking Shh develop a dorsal telencephalic midline, a cortical hem, and two cortical hemispheres. The hemispheres do not divide rostrally, probably because of reduced local Fgf gene expression, resulting from the loss of Shh inhibition of Gli3R. Removing one functional copy of Gli3 substantially rescues Fgf expression and rostral telencephalic morphology.In mice lacking Gli3 function, cortical development is arrested, and ventral gene expression invades the dorsal telencephalon. These defects are potentially explained by disinhibition of Shh activity. However, when both copies of Shh are removed from Gli3-null mice, dorsal telencephalic defects persist. One such defect is a large dorsal expansion of the expression of Fgf genes. Fgf15 expression, for example, expands from a discrete ventral domain throughout the dorsal telencephalon. We propose that Fgf signaling, known to ventralize the telencephalon in a Shh-independent manner, suppresses cortical fate in the absence of Gli3. Our findings point away from Shh involvement in dorsal telencephalic patterning and encourage additional exploration of Fgf signaling and Gli3 repression in corticogenesis.

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Coordinate expression of Fgf8, Otx2, Bmp4, and Shh in the rostral prosencephalon during development of the telencephalic and optic vesicles

Cited by 246 publications

References 79 publications

NODAL and SHH dose-dependent double inhibition promotes an HPE-like phenotype in chick embryos

NODAL and SHH dose-dependent double inhibition promotes an HPE-like phenotype in chick embryos

Possible involvement of SINEs in mammalian-specific brain formation

Patterning the Dorsal Telencephalon: A Role for Sonic Hedgehog?

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