2010
DOI: 10.1242/dev.054288
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Abstract: SUMMARYThe deployment of morphogen gradients is a core strategy to establish cell diversity in developing tissues, but little is known about how small differences in the concentration of extracellular signals are translated into robust patterning output in responding cells. We have examined the activity of homeodomain proteins, which are presumed to operate downstream of graded Shh signaling in neural patterning, and describe a feedback circuit between the Shh pathway and homeodomain transcription factors that… Show more

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Cited by 74 publications
(102 citation statements)
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“…2F). These results are consistent with the notion that Nkx2.2 exerts its patterning action in part by negative-feedback regulation of Hedgehog pathway components (Lek et al, 2010).…”
Section: Resultssupporting
confidence: 92%
See 1 more Smart Citation
“…2F). These results are consistent with the notion that Nkx2.2 exerts its patterning action in part by negative-feedback regulation of Hedgehog pathway components (Lek et al, 2010).…”
Section: Resultssupporting
confidence: 92%
“…Our data highlight a previously unappreciated breadth of direct fate exclusion, modulation of ongoing upstream Shh signaling input through multiple signaling nodes (Lek et al, 2010) and Sox2 input into available enhancers, with a resulting cell type-specific output directing a specific neural progenitor type (Oosterveen et al, 2012;Peterson et al, 2012).…”
Section: Introductionmentioning
confidence: 79%
“…Our present results showing upregulation of Nkx2.2 in Olig2 progenitors at the stage of the MN-to-OPC fate switch in the mouse strongly argue in favor of a timely regulated elevation of Shh activity also conserved in mice. Indeed, Nkx2.2 expression depends on a high level of Shh activity, and this transcription factor has also been reported to intrinsically strengthen Shh response in neural progenitors Lei et al, 2006;Dessaud et al, 2007;Lek et al, 2010). Our data showing genetic interaction between sulf1 and shh in the mouse, as well as downregulation of Shh-responsive genes in Olig2 progenitors after inactivation of Sulf1, establish a critical role for the enzyme in controlling Shh activity in the developing ventral spinal cord.…”
Section: Discussionsupporting
confidence: 58%
“…Therefore, as observed in chicken, dorsal extension of Nkx2.2 expression in mouse embryos also depends on Sulf1 activity. Moreover, because Nkx2.2 is recognized as a direct target of Shh (Lei et al, 2006;Vokes et al, 2007;Lek et al, 2010), these results bring additional support to Sulf1 acting by positively regulating Shh signaling activity.…”
Section: Sulf1 Is a Positive Regulator Of Shh Signaling In Olig2 Progmentioning
confidence: 77%
“…Recent fate-mapping studies based on the Cre-loxP strategy indicated that the Nkx2-2 and Olig2 cell lineages may share a common origin (Wu et al, 2006;Dessaud et al, 2007Dessaud et al, , 2010Holz et al, 2010;Chen et al, 2011;Wang et al, 2011), a result that is supported by the analysis of the temporal expression profile of several transcription factors (Jeong and McMahon, 2005;Lek et al, 2010). It is therefore important to understand how the Olig2/Nkx2-2 double-positive (Olig2 + /Nkx2-2 + ) cells diversify into Olig2 + pMN progenitors and Nkx2-2 + p3 progenitors.…”
Section: Introductionmentioning
confidence: 99%