Expression of two zebrafish homologues of the murine Six3 gene demarcates the initial eye primordia

Seo, Hee-Chan; Drivenes, Øyvind; Ellingsen, Ståle; Fjose, Anders

doi:10.1016/s0925-4773(98)00028-8

Cited by 142 publications

(117 citation statements)

References 45 publications

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“…During neurulation, expression of the transcription factors Six3a and Pax6 in the anterior neural plate specify the ocular tissues (Loosli et al, 1998(Loosli et al, , 1999(Loosli et al, , 2003Nornes et al, 1998;Seo et al, 1998;Wargelius et al, 2003). Through subsequent morphogenetic movements and inductive interactions, the zebrafish eyes develop from bilateral paddle-shaped masses of cells that evaginate from the forebrain (Schmitt and Dowling, 1994).…”

Section: Eye Developmentmentioning

confidence: 99%

Zebrafish: A model system for the study of eye genetics

Fadool

Dowling

2008

Progress in Retinal and Eye Research

193

172

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Over the last decade, the use of the zebrafish as a genetic model has moved beyond the proof-ofconcept for the analysis of vertebrate embryonic development to demonstrated utility as a mainstream model organism for the understanding of human disease. The initial identification of a variety of zebrafish mutations affecting the eye and retina, and the subsequent cloning of mutated genes have revealed cellular, molecular and physiological processes fundamental to visual system development. With the increasing development of genetic manipulations, sophisticated techniques for phenotypic characterization, behavioral approaches and screening strategies, the identification of novel genes or novel gene functions will have important implications for our understanding of human eye diseases, pathogenesis, and treatment.

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Section: Eye Developmentmentioning

confidence: 99%

Zebrafish: A model system for the study of eye genetics

Fadool

Dowling

2008

Progress in Retinal and Eye Research

193

172

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“…The following probes and antibodies were used: bon/mixer (Kikuchi et al, 2000), bts1 (Tallafu␤ et al, 2001), gta3 (Neave et al, 1995), her5 (Mü ller et al, 1996), hgg1 (Thisse et al, 1994), hlx1 (Seo et al, 1999), hoxa1a (McClintock et al, 2001), nkx2.2 (Barth and, pax6.1 (Nornes et al, 1998), six3 (Seo et al, 1998), sox17 (Alexander and Stainier, 1999), zash1a and zash1b (Allende and Weinberg, 1994), zcoe2 (Bally-Cuif et al, 1998), antiinfected 4D9 antibody (recognizing all zebrafish Eng proteins; DHSB; dilution 1/8), and anti-HNK1 (DHSB zn12; dilution 1/500). X-Gal staining was performed by incubation in 4 mM Kferrocyanide, 4 mM Kferricyanide, 4 mM MgCl 2 , 400 ng/ l Xgal in phosphate buffered saline, after 25 min fixation in 2% paraformaldehyde; 0.2% glutaraldehyde at room temperature.…”

Section: Staining For Marker Expressionmentioning

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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“…Mutation of the Six6 gene leads to reduction of the pituitary in mice (20) and humans (23). The hypophyseal placode and adjacent ectoderm also expresses the other so-called ''placode genes,'' Six1, Six4, and Eya, and this coexpression pattern is conserved in amphibians (24), fish (25,26), and lower chordates such as ascidians (27,28). In mice, the anterior pituitary is reduced in size in the double mutant of Eya1 and Six1 (29), and in zebrafish, Eya1 is essential for differentiation of all pituitary cell types except for prolactin-expressing cells (25).…”

mentioning

confidence: 99%