The Nodal Pathway Acts Upstream of Hedgehog Signaling to Specify Ventral Telencephalic Identity

Röhr, Klaus; Barth, Katrin; Varga, Zoltán; Wilson, Stephen W.

doi:10.1016/s0896-6273(01)00210-0

Cited by 158 publications

(175 citation statements)

References 71 publications

Supporting

Mentioning

170

Contrasting

Order By: Relevance

“…Wnt8b downregulates Foxb1 in the MAM of zebrafish (Kim et al, 2002), controls mammillary neurogenesis (Lee et al, 2006), and could be a local organizer (Erter et al, 2001;Houart et al, 2002). The interplay Shh/Wnt in Foxb1 control is presumably downstream the Nodal pathway (Strähle et al, 1996;Erter et al, 2001;Rohr et al, 2001;Houart et al, 2002;Mathieu et al, 2002) (Fig. 8T ).…”

Section: Neural Shh In the Pth And Emtmentioning

confidence: 95%

Role of NeuroepithelialSonic hedgehogin Hypothalamic Patterning

et al. 2009

View full text Add to dashboard Cite

The hypothalamus is a region of the diencephalon with particularly complex patterning. Sonic hedgehog (Shh), encoding a protein with key developmental roles, shows a peculiar and dynamic diencephalic expression pattern. Here, we use transgenic strategies and in vitro experiments to test the hypothesis that Shh expressed in the diencephalic neuroepithelium (neural Shh) coordinates tissue growth and patterning in the hypothalamus. Our results show that neural Shh coordinates anteroposterior and dorsoventral patterning in the hypothalamus and in the diencephalon-telencephalon junction. Neural Shh also coordinates mediolateral hypothalamic patterning, since it is necessary for the lateral hypothalamus to attain proper size and is required for the specification of hypocretin/orexin cells. Finally, neural Shh is necessary to maintain expression of differentiation markers including survival factor Foxb1.

show abstract

Section: Neural Shh In the Pth And Emtmentioning

confidence: 95%

Role of NeuroepithelialSonic hedgehogin Hypothalamic Patterning

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Several signaling factors originate from the PCP. Among those, Nodal signals have received most attention and are involved in forebrain induction and patterning in zebrafish (Rohr et al, 2001;Mathieu et al, 2002, and references therein). We thus tested whether deficient Nodal signaling from the impaired PCP in bon could influence the number of fore/mid six3-positive cells.…”

Section: Pcp Factor Controlling the Number Of Fore/mid Six3-positive mentioning

confidence: 99%

Selective control of neuronal cluster size at the forebrain/midbrain boundary by signaling from the prechordal plate

Tallafuß

Adolf

Bally‐Cuif

2003

Developmental Dynamics

View full text Add to dashboard Cite

Within the vertebrate embryonic neural plate, the first neuronal clusters often differentiate at the border of patterning identities. Whether the information inherent in the intersection of patterning identities alone controls all aspects of neuronal cluster development (location, identity, and size) is unknown. Here, we focus on the cluster of the medial longitudinal fascicle (nMLF) and posterior commissure (nPC), located at the forebrain/midbrain (fore/mid) boundary, to address this issue. We first identify expression of the transcription factor Six3 as a common and distinct molecular signature of nMLF and nPC neurons in zebrafish, and we use this marker to monitor mechanisms controlling the location and number of nMLF/nPC neurons. We demonstrate that six3 expression is induced at the fore/mid boundary in pax2.1/no-isthmus and smoothened/slow muscle omitted mutants, where identities adjacent to the six3 cluster are altered; however, in these mutants, the subpopulation of six3-positive cells located within the mispatterned territory is reduced. These results show that induction of the six3 cluster is triggered by the information derived from the intersection in patterning identities alone, whereas correct cluster size depends, in a modular manner, on the identities themselves. The size of the six3 cluster is also controlled independently of neural tube patterning: we demonstrate that the prechordal plate (PCP) is impaired in mixer/bonnie and clyde mutants and that this phenotype secondarily results in an increased production of six3-positive cells at the fore/mid boundary, without correlatively affecting patterning in this area. Thus, a signaling process originating from the PCP distinguishes between neural patterning and the control of six3 cluster size at the fore/mid junction in vivo. Together, our results suggest that a combination of patterning-related and -unrelated mechanisms specifically controls the size of individual early neuronal clusters within the anterior neural plate. Developmental Dynamics 227:524 -535, 2003.

show abstract

“…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%

“…SHH and NODAL signals interact and Hedgehog signaling acts downstream from NODAL activity to pattern the ventral telencephalon (Müller et al, 2000;Rohr et al, 2001). Indeed, expression of Shh is severely reduced in mutants for the NODAL pathway, particularly in anterior regions (Strähle et al, 1997;Hagos and Dougan, 2007).…”

mentioning

confidence: 99%

“…The mechanism by which NODAL signaling regulates SHH activity during gastrulation has yet to be determined. However, several studies have indicated that the NODAL pathway regulates ventral forebrain patterning through SHH-independent mechanisms (Rohr et al, 2001;Monuki, 2007). SHH might have to reach a threshold concentration to ensure proper forebrain development (Young et al, 2010).…”

mentioning

confidence: 99%

See 1 more Smart Citation