Activation of Class I transcription factors by low level Sonic hedgehog signaling is mediated by Gli2-dependent and independent mechanisms

Pachikara, Abraham; Dolson, Diane K.; Martinu, Lenka; Riccomagno, Martin M.; Jeong, Yongsu; Epstein, Douglas J.

doi:10.1016/j.ydbio.2007.01.035

Cited by 5 publications

(5 citation statements)

References 44 publications

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“…During recent years a similar genetic cascade was corroborated in the hindbrain (Pachikara et al, 2007) and, more recently, in the midbrain (Agarwala et al, 2001;Agarwala and Ragsdale, 2002;Bayly et al, 2007) and forebrain (Bertrand and Dahmane, 2006;Rash and Grove, 2007). In the later case, there are more factors involved and an intricate genetic cascade is associated with the increase in structural and functional complexity of the forebrain.…”

Section: Introductionmentioning

confidence: 69%

Shh dependent and independent maintenance of basal midbrain

Pérez-Balaguer

Puelles

Wurst³

et al. 2009

Mechanisms of Development

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Sonic hedgehog (Shh) is well known as the molecule responsible for the induction and maintenance of ventral neural tube structures. Recent data have shown that ventral neuronal populations react differentially to the amount of this morphogen not only in the spinal cord, but also in more rostral parts of the brain, like the midbrain. A dorsal expansion in the Shh expression domain modifies the differentiation program in this territory. The lack of Shh produces alterations in the development of this area as well. Here, for the first time, we analyze in detail the development of the different mesencephalic basal nuclei in the absence of Shh. We report that the oculomotor complex is lost, the dopaminergic populations are strongly affected but the red nucleus is maintained. These results point out that not all the midbrain neuronal populations are dependent on Shh for their maintenance, as previously thought. Based on our results and recently published data, we suggest the existence of a specific genetic pathway for the specification of the mesencephalic red nucleus. Foxa2 could be the candidate gene that might control this genetic pathway.

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Section: Introductionmentioning

confidence: 69%

Shh dependent and independent maintenance of basal midbrain

Pérez-Balaguer

Puelles

Wurst³

et al. 2009

Mechanisms of Development

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“…2C) (Briscoe et al, 2000;Vallstedt et al, 2001;Pachikara et al, 2007). Primarily, crossrepressive interactions exist between two main classes of transcription factors, one of which is activated (or de-repressed) at low levels of Shh signalling and the other at high levels.…”

Section: Sonic Hedgehog In the Vertebrate Neural Tubementioning

confidence: 99%

Regulative feedback in pattern formation: towards a general relativistic theory of positional information

2008

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Positional specification by morphogen gradients is traditionally viewed as a two-step process. A gradient is formed and then interpreted, providing a spatial metric independent of the target tissue, similar to the concept of space in classical mechanics. However, the formation and interpretation of gradients are coupled, dynamic processes. We introduce a conceptual framework for positional specification in which cellular activity feeds back on positional information encoded by gradients, analogous to the feedback between mass-energy distribution and the geometry of space-time in Einstein's general theory of relativity. We discuss how such general relativistic positional information (GRPI) can guide systems-level approaches to pattern formation. IntroductionEver since Hans Driesch's famous experiments on sea urchin embryos, it has been evident that developmental processes are capable of global regulation (Driesch, 1892). A small part of an embryo, such as a single totipotent cell, can regenerate a whole intact embryo. Driesch was so baffled by his results that he rejected a materialist explanation for this phenomenon and turned to vitalism instead (Driesch, 1914). The problem of embryonic regulation essentially reduces to the problem of regulative positional specification: how do cells adopt a state that is appropriate to their relative position within a developing embryo?Classical embryology introduced the notion of a morphogenetic field to explain global regulatory capacities (reviewed by Gilbert et al., 1996). The morphogenetic field aims to capture the ability of the cells in a developing tissue to establish a pervasive influence that imparts information about the state of the whole tissue. Local interactions within the field then allow cells to access global information, and, in principle, to adopt states that lead to appropriate patterning of the tissue or embryo as a whole. However, owing to the lack of molecular evidence, the mechanistic basis of such fields has remained obscure.Lewis Wolpert sought to address the issue of the missing mechanistic basis of embryonic regulation and developmental fields in 1968, when he proposed his French flag model to illustrate the concept of positional information ( Fig. 1) (Wolpert, 1968). At the time, gene expression in development was largely considered to be a problem of temporal regulation based on the paradigm established by Jacob and Monod from their work on the lac operon of Escherichia coli (Jacob and Monod, 1961;Monod and Jacob, 1962). To shift focus back to the spatial aspects of pattern formation, Wolpert argued that cells must have some means of determining their relative position in a developing field (Wolpert, 1969). In contrast to the concept of the morphogenetic field, Wolpert suggested that this happens by a mechanism imposed on, instead of arising from within, the field. According to this view, embryonic fields are defined by their boundaries (Irvine and Rauskolb, 2001), and positional information provides a mechanism by which cells can measure their d...

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“…There is an Msx1 binding site in deletion block3 and Msx1 may act as a repressor in the dorsal neural tube in combination with other repressors that have binding sites in block1. Ventral neural tube patterning requires Sonic hedgehog (Shh) signaling and gradients of Shh signaling activates different Gli activator and repressor transcription factors (Pachikara et al, 2007). Ectopic expression of different levels of Shh affects cadherin-7 expression in neural tube (Stamataki et al, 2005; Luo et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

A combination of enhancer/silencer modules regulates spatially restricted expression of cadherin‐7 in neural epithelium

Prasad¹,

Paulson²

2011

Developmental Dynamics

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The spatially restricted expression of cadherin-7 to the intermediate domain of the neural epithelium and in migrating neural crest cells during early neural development is potentially regulated by multiple signaling inputs. To identify the regulatory modules involved in regulation of cadherin-7, evolutionary conserved non-coding sequences in the cadherin-7 locus were analyzed. This led to the identification of an evolutionary conserved region of 606 bp (ECR1) that together with the cadherin-7 promoter recapitulates endogenous cadherin-7 expression in intermediate neural tube, spinal motor neurons, interneurons, and dorsal root ganglia. Deletion analysis of ECR1 revealed a 19 bp block that is essential for ECR1 enhancer activity, while two separate blocks of 10 bp and 12 bp were found to be essential for ECR1 silencer activity in the dorsal and ventral neural epithelium respectively. Together these data provide an insight into tissue-specific regulatory regions that might be involved in regulation of cadherin-7 gene expression.

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Activation of Class I transcription factors by low level Sonic hedgehog signaling is mediated by Gli2-dependent and independent mechanisms

Cited by 5 publications

References 44 publications

Shh dependent and independent maintenance of basal midbrain

Shh dependent and independent maintenance of basal midbrain

Regulative feedback in pattern formation: towards a general relativistic theory of positional information

A combination of enhancer/silencer modules regulates spatially restricted expression of cadherin‐7 in neural epithelium

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