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Molecular mechanisms of tiling and self-avoidance in neural development.

Cameron S, Rao Y - Mol Brain (2010)

Bottom Line: Dscams and Turtle (Tutl), two Ig superfamily proteins, have been shown to mediate contact-dependent homotypic interactions in tiling and self-avoidance.By contrast, the Activin pathway regulates axonal tiling in a contact-independent manner.These cell surface signals may directly or indirectly regulate the activity of the Tricornered kinase pathway and/or other intracellular signaling pathways to prevent the overlap between same-type neuronal arbors in the sensory or synaptic input field.

View Article: PubMed Central - HTML - PubMed

Affiliation: McGill Centre for Research in Neuroscience, McGill University Health Centre, 1650 Cedar Avenue, Montreal, Quebec H3G 1A4, Canada.

ABSTRACT
Recent studies have begun to unravel the molecular basis of tiling and self-avoidance, two important cellular mechanisms that shape neuronal circuitry during development in both invertebrates and vertebrates. Dscams and Turtle (Tutl), two Ig superfamily proteins, have been shown to mediate contact-dependent homotypic interactions in tiling and self-avoidance. By contrast, the Activin pathway regulates axonal tiling in a contact-independent manner. These cell surface signals may directly or indirectly regulate the activity of the Tricornered kinase pathway and/or other intracellular signaling pathways to prevent the overlap between same-type neuronal arbors in the sensory or synaptic input field.

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Co-operation between the Activin pathway and Tutl in the tiling of Drosophila R7 photoreceptor axons. Activin functions as an autocrine signal to activate its receptor Babo on R7 terminals, which in turn induces the phosphorylation of Smad2. The phosphorylated Smad2 is then transported by Importin α3 into the nucleus to regulate the expression of some unknown target genes, which directly control R7 terminal growth. This Activin-mediated intrinsic growth control functions together with Tutl-mediated homotypic interaction to regulate R7 tiling. Circles, Ig domains; Rectangles, fibronectin type-III repeats.
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Figure 4: Co-operation between the Activin pathway and Tutl in the tiling of Drosophila R7 photoreceptor axons. Activin functions as an autocrine signal to activate its receptor Babo on R7 terminals, which in turn induces the phosphorylation of Smad2. The phosphorylated Smad2 is then transported by Importin α3 into the nucleus to regulate the expression of some unknown target genes, which directly control R7 terminal growth. This Activin-mediated intrinsic growth control functions together with Tutl-mediated homotypic interaction to regulate R7 tiling. Circles, Ig domains; Rectangles, fibronectin type-III repeats.

Mentions: While it is well established that contact-dependent homotypic repulsion plays a key role in axonal/dendritic tiling, several studies indicate that tiling also involves a contact-independent mechanism [6,19]. For instance, it was shown that in Brn3b-/- and Math5-/- mice, although retinal ganglion neurons do not contact each other throughout development due to the great reduction in the number of ganglion neurons, they nevertheless displayed a regular mosaic pattern and normal dendritic morphology [19]. Similarly, Ashley and Katz reported that in the Drosophila visual system, R7 photoreceptor axons were still restricted to their own columns even when their neighboring R7 neurons were removed by genetic manipulation [6]. These studies indicate the existence of an intrinsic mechanism restricting the growth of neuronal arbors in the absence of neighboring same-type neurons. However, it appears clear that when same-type neighbors are present, this intrinsic growth control has to function together with a contact-dependent tiling mechanism to overcome the high affinity between same-type neurites due to the presence of homophilic cell adhesion molecules (e.g. NCAM in vertebrate retinal neurons and N-cadherin in Drosophila R7 photoreceptors). While the nature of the intrinsic mechanism in the vertebrate visual system remains unknown, a recent study by Lee and colleagues provides convincing evidence that in the Drosophila visual system, the Activin signaling pathway contributes to the contact-independent tiling mechanism [49] (Fig. 4).


Molecular mechanisms of tiling and self-avoidance in neural development.

Cameron S, Rao Y - Mol Brain (2010)

Co-operation between the Activin pathway and Tutl in the tiling of Drosophila R7 photoreceptor axons. Activin functions as an autocrine signal to activate its receptor Babo on R7 terminals, which in turn induces the phosphorylation of Smad2. The phosphorylated Smad2 is then transported by Importin α3 into the nucleus to regulate the expression of some unknown target genes, which directly control R7 terminal growth. This Activin-mediated intrinsic growth control functions together with Tutl-mediated homotypic interaction to regulate R7 tiling. Circles, Ig domains; Rectangles, fibronectin type-III repeats.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2959082&req=5

Figure 4: Co-operation between the Activin pathway and Tutl in the tiling of Drosophila R7 photoreceptor axons. Activin functions as an autocrine signal to activate its receptor Babo on R7 terminals, which in turn induces the phosphorylation of Smad2. The phosphorylated Smad2 is then transported by Importin α3 into the nucleus to regulate the expression of some unknown target genes, which directly control R7 terminal growth. This Activin-mediated intrinsic growth control functions together with Tutl-mediated homotypic interaction to regulate R7 tiling. Circles, Ig domains; Rectangles, fibronectin type-III repeats.
Mentions: While it is well established that contact-dependent homotypic repulsion plays a key role in axonal/dendritic tiling, several studies indicate that tiling also involves a contact-independent mechanism [6,19]. For instance, it was shown that in Brn3b-/- and Math5-/- mice, although retinal ganglion neurons do not contact each other throughout development due to the great reduction in the number of ganglion neurons, they nevertheless displayed a regular mosaic pattern and normal dendritic morphology [19]. Similarly, Ashley and Katz reported that in the Drosophila visual system, R7 photoreceptor axons were still restricted to their own columns even when their neighboring R7 neurons were removed by genetic manipulation [6]. These studies indicate the existence of an intrinsic mechanism restricting the growth of neuronal arbors in the absence of neighboring same-type neurons. However, it appears clear that when same-type neighbors are present, this intrinsic growth control has to function together with a contact-dependent tiling mechanism to overcome the high affinity between same-type neurites due to the presence of homophilic cell adhesion molecules (e.g. NCAM in vertebrate retinal neurons and N-cadherin in Drosophila R7 photoreceptors). While the nature of the intrinsic mechanism in the vertebrate visual system remains unknown, a recent study by Lee and colleagues provides convincing evidence that in the Drosophila visual system, the Activin signaling pathway contributes to the contact-independent tiling mechanism [49] (Fig. 4).

Bottom Line: Dscams and Turtle (Tutl), two Ig superfamily proteins, have been shown to mediate contact-dependent homotypic interactions in tiling and self-avoidance.By contrast, the Activin pathway regulates axonal tiling in a contact-independent manner.These cell surface signals may directly or indirectly regulate the activity of the Tricornered kinase pathway and/or other intracellular signaling pathways to prevent the overlap between same-type neuronal arbors in the sensory or synaptic input field.

View Article: PubMed Central - HTML - PubMed

Affiliation: McGill Centre for Research in Neuroscience, McGill University Health Centre, 1650 Cedar Avenue, Montreal, Quebec H3G 1A4, Canada.

ABSTRACT
Recent studies have begun to unravel the molecular basis of tiling and self-avoidance, two important cellular mechanisms that shape neuronal circuitry during development in both invertebrates and vertebrates. Dscams and Turtle (Tutl), two Ig superfamily proteins, have been shown to mediate contact-dependent homotypic interactions in tiling and self-avoidance. By contrast, the Activin pathway regulates axonal tiling in a contact-independent manner. These cell surface signals may directly or indirectly regulate the activity of the Tricornered kinase pathway and/or other intracellular signaling pathways to prevent the overlap between same-type neuronal arbors in the sensory or synaptic input field.

Show MeSH