The homeodomain protein Vax1 is required for axon guidance and major tract formation in the developing forebrain

Bertuzzi, Stefano; Hindges, Robert; Mui, Stina; O’Leary, Dennis D.M.; Lemke, Greg

doi:10.1101/gad.13.23.3092

Cited by 137 publications

(179 citation statements)

References 53 publications

(44 reference statements)

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“…Detailed expression studies and functional analyses support a direct or indirect role for some of these patterning genes in the formation or the refinement of axon trajectories Mastick et al, 1997;Ba-Charvet et al, 1998;Bertuzzi et al, 1999;Hallonet et al, 1999;Hjorth and Key, 2001). The cues controlling the location and size of the first differentiation clusters have been comparatively less well studied.…”

Section: Introductionmentioning

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

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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.

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Section: Introductionmentioning

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

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“…The induction of these two genes negatively controls the expression of Pax6 in the optic cup (Macdonald et al 1995;Hallonet et al 1999). Later, Shh secreted from RGCs maintains Pax2 in the optic stalk and disc via Vax1 expression, which is necessary for their specification as glial cells (Bertuzzi et al 1999;Dakubo et al 2003). The optic nerve undergoes gliogenesis similar to general CNS gliogenesis.…”

Section: The Optic Nerve and Ganglion Cell Axon Pathfindingmentioning

confidence: 99%

Molecular regulation of visual system development: more than meets the eye

Harada¹,

Harada²,

Parada³

2007

Genes Dev.

122

103

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Vertebrate eye development has been an excellent model system to investigate basic concepts of developmental biology ranging from mechanisms of tissue induction to the complex patterning and bidimensional orientation of the highly specialized retina. Recent advances have shed light on the interplay between numerous transcriptional networks and growth factors that are involved in the specific stages of retinogenesis, optic nerve formation, and topographic mapping. In this review, we summarize this recent progress on the molecular mechanisms underlying the development of the eye, visual system, and embryonic tumors that arise in the optic system.For humans, the visual system is a principal conduit for acquiring external sensory information. Thus, "quality of vision" is intimately tied with "quality of life." Despite extensive clinical and laboratory investigation, many diseases that impair vision, ranging from congenital abnormalities to sporadic forms of retinal degeneration, lack effective treatments. One hope is that improved understanding of development of the visual system, from the eye to the visual cortex, will provide insight into methods for attenuating or reversing these disorders. Development of the neural retina and visual system, especially the mechanism of axon remodeling during synaptogenesis, is complex. Studies have shown that numerous genes are involved in the differentiation and formation of the retina acting at specific stages of the development of visual system. In this review, we will summarize recent progress on the molecular mechanisms underlying the development of the eye and visual system. Anatomy of eye developmentThe basic components of the complex optic system are derived from four embryonic sources: forebrain neuroectoderm, intercalating mesoderm, surface ectoderm, and neural crest (Fig. 1). The neuroectoderm differentiates into the retina, iris, and optic nerve; the surface ectoderm gives rise to lens and corneal epithelium; the mesoderm differentiates into the extraocular muscles and the fibrous and vascular coats of the eye; and neural crest cells become the corneal stroma sclera and corneal endothelium. The vertebrate eye originates from bilateral telencephalic optic grooves. In humans, optic vesicles emerge at the end of the fourth week of development and soon thereafter contact the surface ectoderm to induce lens formation. When the lens placode invaginates to form the lens vesicle, the distal part of optic vesicle begins to invaginate to form the optic cup. As the optic vesicles grow, the proximal ends expand and their connections with the forebrain constrict to form optic stalks. Through the retinal fissure, a groove at the inferior aspect of the optic vesicle, the hyaloid artery, enters the eye and nourishes the optic cup and lens vesicle. The retinal fissure normally closes at ∼7 wk of development, and proximal parts of the hyaloid vessels persist to form the central artery and vein of the retina, a branch of the ophthalmic artery. Defects in closure of the fissure result in...

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“…In contrast, proximal exon 5 of KIAA1803 is present in both control genomic DNA and derivative 9 containing hybrids and is not found in the derivative 2 line, indicating that the KIAA1803 breakpoint is located between exons 5 and 7 of this gene. (d) PCR products from cDNA isolated from both normal (lanes 1,3,5,7,9,11) and patient (2,4,6,8,10,12) lymphoblasts for the indicated primer pairs. While the expected wild-type fragments were amplified for the endogenous genes in both normal and patient cDNA, the fusion transcripts are only detected in patient samples.…”

Section: Mapping the Breakpointsmentioning

confidence: 99%

Reciprocal fusion transcripts of two novel Zn-finger genes in a female with absence of the corpus callosum, ocular colobomas and a balanced translocation between chromosomes 2p24 and 9q32

et al. 2003

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We have identified a female patient with a complex phenotype that includes complete agenesis of the corpus callosum, bilateral periventricular nodular heterotopia, and bilateral chorioretinal and iris colobomas. Karyotype analysis revealed an apparently balanced, reciprocal, de novo chromosome translocation t(2;9)(p24;q32). Physical mapping of the translocation breakpoint by fluorescence in situ hybridization and PCR analysis led to the identification of two novel, ubiquitously expressed, Zn-fingerencoding transcripts that are disrupted in this patient. Unexpectedly, the rearrangement produced in-frame reciprocal fusion transcripts, making genotype -phenotype correlation difficult.

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The homeodomain protein Vax1 is required for axon guidance and major tract formation in the developing forebrain

Cited by 137 publications

References 53 publications

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

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

Molecular regulation of visual system development: more than meets the eye

Reciprocal fusion transcripts of two novel Zn-finger genes in a female with absence of the corpus callosum, ocular colobomas and a balanced translocation between chromosomes 2p24 and 9q32

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