Sonic hedgehog from the basal plate and the zona limitans intrathalamica exhibits differential activity on diencephalic molecular regionalization and nuclear structure

Vieira, Claudia; Martı́nez, Salvador

doi:10.1016/j.neuroscience.2006.08.032

Cited by 62 publications

(67 citation statements)

References 31 publications

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“…Interestingly, conditional deletion of Shh only in the diencephalic basal plate resulted in a similar fate switch within pTH-R (Jeong et al, 2011). These, along with other studies (Vieira and Martinez, 2006;Kiecker and Lumsden, 2004), collectively demonstrate that both ZLI and basal plate Shh sources are required for appropriate patterning of thalamic progenitor cells. In Ctnnb1; Shh double cko embryos (Olig3…”

Section: Research Article -Catenin Signaling Patterns the Thalamussupporting

confidence: 64%

β-Catenin signaling specifies progenitor cell identity in parallel with Shh signaling in the developing mammalian thalamus

et al. 2012

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SUMMARYNeural progenitor cells within the developing thalamus are spatially organized into distinct populations. Their correct specification is critical for generating appropriate neuronal subtypes in specific locations during development. Secreted signaling molecules, such as sonic hedgehog (Shh) and Wnts, are required for the initial formation of the thalamic primordium. Once thalamic identity is established and neurogenesis is initiated, Shh regulates the positional identity of thalamic progenitor cells. Although Wnt/-catenin signaling also has differential activity within the thalamus during this stage of development, its significance has not been directly addressed. In this study, we used conditional gene manipulations in mice and explored the roles of -catenin signaling in the regional identity of thalamic progenitor cells. We found -catenin is required during thalamic neurogenesis to maintain thalamic fate while suppressing prethalamic fate, demonstrating that regulation of regional fate continues to require extrinsic signals. These roles of -catenin appeared to be mediated at least partly by regulating two basic helix-loop-helix (bHLH) transcription factors, Neurog1 and Neurog2. -Catenin and Shh signaling function in parallel to specify two progenitor domains within the thalamus, where individual transcription factors expressed in each progenitor domain were regulated differently by the two signaling pathways. We conclude that -catenin has multiple functions during thalamic neurogenesis and that both Shh and -catenin pathways are important for specifying distinct types of thalamic progenitor cells, ensuring that the appropriate neuronal subtypes are generated in the correct locations.

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Section: Research Article -Catenin Signaling Patterns the Thalamussupporting

confidence: 64%

β-Catenin signaling specifies progenitor cell identity in parallel with Shh signaling in the developing mammalian thalamus

et al. 2012

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“…Because the prethalamus is not maintained, the ZLI and the boundary between thalamus and prethalamus will not form. Defects in ZLI formation or suppression of Shh expression in the ZLI promote caudalization of the mouse diencephalon (Hirata et al, 2006b) and defective thalamic and prethalamic induction in chicken (Kiecker and Lumsden, 2004;Vieira and Martinez, 2006) and zebrafish (Scholpp et al, 2006;Scholpp et al, 2007) embryos. Therefore, absence of the ZLI is probably at least partially responsible for the late-caudalization phenotype of the Six3-mutant brain.…”

Section: Rostral Diencephalic Development Depends On Six3 Repression mentioning

confidence: 99%

“…In chicken, the mutual repression of Six3 and Irx3 may control ZLI positioning (Kobayashi et al, 2002). Later, basal plate signals induce ZLI expansion through the alar plate, and signals from the dorsal diencephalon midline oppose its formation (Larsen et al, 2001;Zeltser, 2005;Vieira and Martinez, 2006). The ZLI expresses Shh (Echelard et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Six3inactivation causes progressive caudalization and aberrant patterning of the mammalian diencephalon

2008

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The homeobox gene Six3 represses Wnt1 transcription. It is also required in the anterior neural plate for the development of the mammalian rostral forebrain. We have now determined that at the 15-to 17-somite stage, the prospective diencephalon is the most-anterior structure in the Six3-null brain, and Wnt1 expression is anteriorly expanded. Consequently, the brain caudalizes, and at the 22-to 24-somite stage, the prospective thalamic territory is the most-anterior structure. At around E11.0, the pretectum replaces this structure. Analysis of Six3;Wnt1 double-null mice revealed that Six3-mediated repression of Wnt1 is necessary for the formation of the rostral diencephalon and that Six3 activity is required for the formation of the telencephalon. These results provide insight into the mechanisms that establish anteroposterior identity in the developing mammalian brain.

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“…6L-O). Regarding the restricted expression of Fgf19 in the diencephalic alar plate, in relation to the extended expression of Fgf15 in the mouse, a weaker phenotype can be predicted after Shh reduction in chicks and humans than in mice, as it was suggested by chick experiments (Vieira and Martinez, 2006), as well as by the absence of important thalamic anomalies in human holoprosencephaly caused by Shh mutations (Roessler et al, 1996, Schell-Apacik et al, 2003.…”

Section: Shh Qt6-expressing Cells Induce Ectopic Expression Of Fgf19mentioning

confidence: 99%

Expression of chick Fgf19 and mouse Fgf15 orthologs is regulated in the developing brain by Fgf8 and Shh

Gimeno

Martı́nez

2007

Developmental Dynamics

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Fibroblast growth factors (Fgfs) constitute a family of signaling molecules that play essential roles in development. We have studied the expression pattern of mouse Fgf15 in the developing brain. Fgf19 is another member of the FGF family that has been suggested as the chick and human ortholog of mouse and rat Fgf15. Here, we compare the expression pattern during neural development of chick Fgf19 with mouse Fgf15. Unlike Fgf15, Fgf19 presents an expression in the isthmic alar plate, diencephalic and mesencephalic parabasal plates, hindbrain basal plate, as well as in the zona limitans intrathalamica (zli). Moreover, we explored the regulation between Fgf19 and the signaling molecules of the isthmic and zli organizers: Fgf8 and Shh, respectively. Considering the possibility that Fgf19 plays a similar role in humans and chicks, this finding could explain the significant diencephalic phenotypic differences between humans and mice in models and diseases where the Shh pathway is affected. Developmental Dynamics 236:2285-2297, 2007.

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Sonic hedgehog from the basal plate and the zona limitans intrathalamica exhibits differential activity on diencephalic molecular regionalization and nuclear structure

Cited by 62 publications

References 31 publications

β-Catenin signaling specifies progenitor cell identity in parallel with Shh signaling in the developing mammalian thalamus

β-Catenin signaling specifies progenitor cell identity in parallel with Shh signaling in the developing mammalian thalamus

Six3inactivation causes progressive caudalization and aberrant patterning of the mammalian diencephalon

Expression of chick Fgf19 and mouse Fgf15 orthologs is regulated in the developing brain by Fgf8 and Shh

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