scholarly journals Lhx1 in the proximal region of the optic vesicle permits neural retina development in the chicken

Biology Open ◽  
2012 ◽  
Vol 1 (11) ◽  
pp. 1083-1093 ◽  
Author(s):  
T. Kawaue ◽  
M. Okamoto ◽  
A. Matsuyo ◽  
J. Inoue ◽  
Y. Ueda ◽  
...  
Development ◽  
2001 ◽  
Vol 128 (24) ◽  
pp. 5051-5060 ◽  
Author(s):  
Shulei Zhao ◽  
Fang-Cheng Hung ◽  
Jennifer S. Colvin ◽  
Andrew White ◽  
Weilie Dai ◽  
...  

During vertebrate embryogenesis, the neuroectoderm differentiates into neural tissues and also into non-neural tissues such as the choroid plexus in the brain and the retinal pigment epithelium in the eye. The molecular mechanisms that pattern neural and non-neural tissues within the neuroectoderm remain unknown. We report that FGF9 is normally expressed in the distal region of the optic vesicle that is destined to become the neural retina, suggesting a role in neural patterning in the optic neuroepithelium. Ectopic expression of FGF9 in the proximal region of the optic vesicle extends neural differentiation into the presumptive retinal pigment epithelium, resulting in a duplicate neural retina in transgenic mice. Ectopic expression of constitutively active Ras is also sufficient to convert the retinal pigment epithelium to neural retina, suggesting that Ras-mediated signaling may be involved in neural differentiation in the immature optic vesicle. The original and the duplicate neural retinae differentiate and laminate with mirror-image polarity in the absence of an RPE, suggesting that the program of neuronal differentiation in the retina is autonomously regulated. In mouse embryos lacking FGF9, the retinal pigment epithelium extends into the presumptive neural retina, indicating a role of FGF9 in defining the boundary of the neural retina.


Development ◽  
2001 ◽  
Vol 128 (20) ◽  
pp. 3987-3994 ◽  
Author(s):  
Gilbert Bernier ◽  
Wolfgang Vukovich ◽  
Lorenz Neidhardt ◽  
Bernhard G. Herrmann ◽  
Peter Gruss

The transcription factor Pax6 is required for eye morphogenesis in humans, mice and insects, and can induce ectopic eye formation in vertebrate and invertebrate organisms. Although the role of Pax6 has intensively been studied, only a limited number of genes have been identified that depend on Pax6 activity for their expression in the mammalian visual system. Using a large-scale in situ hybridization screen approach, we have identified a novel gene expressed in the mouse optic vesicle. This gene, Necab, encodes a putative cytoplasmic Ca2+-binding protein and coincides with Pax6 expression pattern in the neural ectoderm of the optic vesicle and in the forebrain pretectum. Remarkably, Necab expression is absent in both structures in Pax6 mutant embryos. By contrast, the optic vesicle-expressed homeobox genes Rx, Six3, Otx2 and Lhx2 do not exhibit an altered expression pattern. Using gain-of-function experiments, we show that Pax6 can induce ectopic expression of Necab, suggesting that Necab is a direct or indirect transcriptional target of Pax6. In addition, we have found that Necab misexpression can induce ectopic expression of the homeobox gene Chx10, a transcription factor implicated in retina development. Taken together, our results provide evidence that Necab is genetically downstream of Pax6 and that it is a part of a signal transduction pathway in retina development.


Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 1053-1061 ◽  
Author(s):  
A.P. Monaghan ◽  
D.R. Davidson ◽  
C. Sime ◽  
E. Graham ◽  
R. Baldock ◽  
...  

The mouse Hox-7.1 gene has previously been shown to be related to the Drosophila Msh homeobox-containing gene. Here we report the isolation of a new member of this family which resides at an unlinked chromosomal location and has been designated Hox-8.1. Both Hox-7.1 and Hox-8.1 are expressed in the mouse embryo during the early stages of eye development in a distinct spatial and temporal relationship. Hox-8.1 is expressed in the surface ectoderm and in the optic vesicle before invagination occurs in regions corresponding to the prospective corneal epithelium and neural retina, respectively. Hox-7.1 is expressed after formation of the optic cup, marking the domain that will give rise to the ciliary body. The activity of these genes indicates that the inner layer of the optic cup is differentiated into three distinct compartments before overt cellular differentiation occurs. Our results suggest that these genes are involved in defining the region that gives rise to the inner layer of the optic cup and in patterning this tissue to define the iris, ciliary body and retina.


1982 ◽  
Vol 5 (1) ◽  
pp. 40-53 ◽  
Author(s):  
Arnold G. Hyndman ◽  
Ruben Adler

2019 ◽  
Vol 61 (3) ◽  
pp. 252-262
Author(s):  
Misaki Shirahama ◽  
Ichie Steinfeld ◽  
Akari Karaiwa ◽  
Shigeru Taketani ◽  
Astrid Vogel‐Höpker ◽  
...  

1969 ◽  
Vol 47 (1) ◽  
pp. 142-143 ◽  
Author(s):  
D. E. Wedlock ◽  
D. J. McCallion

The optic vesicle of the young chick embryo explanted to the chorioallantois of host embryos induces the formation of scleral cartilage in the chorioallantoic mesenchyme. The part of the optic vesicle responsible for the induction of cartilage is the pigmented retina. Neural retina does not induce cartilage formation.


Development ◽  
1972 ◽  
Vol 28 (1) ◽  
pp. 117-132
Author(s):  
Takeo Mizuno

1. Dissociation and recombination experiments in vitro were found useful for analysing inductive tissue interactions involved in lens differentiation in the chick.2. When the presumptive cephalic region (epiblast plus hypoblast) of the embryo at predefinitive streak to one-somite stage is cultivated in vitro combined with the dermis isolated either from the dorsal skin of 6·5-day embryo or from the 13·5-day tarsometatarsal skin, a lens with fibres or lentoid is produced in the epiblast. In no case is there an optic vesicle present in the explant. 3. When the presumptive cephalic region (epiblast plus hypoblast) is cultivated without dermis, the lens is no longer formed. 4. If the epiblast alone, dissociated from the hypoblast of the presumptive cephalic region, is recombined with the dermis of the 6·5-day dorsal skin, lenses or lentoids fail to develop. 5. Cultivation of the epiblast alone cannot cause differentiation of the lens or lentoid. 6. The dermis can be replaced by other mesenchymes or embryonic organs: gizzard mesenchyme, mesonephros, sclerotome, liver and neural retina, though they are less effective than the dermis in producing lenses or lentoids in the epiblast. 7. It may therefore be concluded that the lens is induced in vitro by the actions of at least two factors: the epiblast first becomes competent under the specific influence of the hypoblast of the cephalic region. The lens will then differentiate from the competent epiblast by the non-specific action of various tissues such as the skin dermis, mesonephros, or sclerotome. 8. The primary stage of lens induction (action of the hypoblast on the epiblast) seems not yet completed by streak stage.


2003 ◽  
Vol 23 (13) ◽  
pp. 4637-4648 ◽  
Author(s):  
Xiaohong Fan ◽  
Andrei Molotkov ◽  
Shin-Ichi Manabe ◽  
Christine M. Donmoyer ◽  
Louise Deltour ◽  
...  

ABSTRACT Genetic studies have shown that retinoic acid (RA) signaling is required for mouse retina development, controlled in part by an RA-generating aldehyde dehydrogenase encoded by Aldh1a2 (Raldh2) expressed transiently in the optic vesicles. We examined the function of a related gene, Aldh1a1 (Raldh1), expressed throughout development in the dorsal retina. Raldh1−/− mice are viable and exhibit apparently normal retinal morphology despite a complete absence of Raldh1 protein in the dorsal neural retina. RA signaling in the optic cup, detected by using a RARE-lacZ transgene, is not significantly altered in Raldh1−/− embryos at embryonic day 10.5, possibly due to normal expression of Aldh1a3 (Raldh3) in dorsal retinal pigment epithelium and ventral neural retina. However, at E16.5 when Raldh3 is expressed ventrally but not dorsally, Raldh1−/− embryos lack RARE-lacZ expression in the dorsal retina and its retinocollicular axonal projections, whereas normal RARE-lacZ expression is detected in the ventral retina and its axonal projections. Retrograde labeling of adult Raldh1−/− retinal ganglion cells indicated that dorsal retinal axons project to the superior colliculus, and electroretinography revealed no defect of adult visual function, suggesting that dorsal RA signaling is unnecessary for retinal ganglion cell axonal outgrowth. We observed that RA synthesis in liver of Raldh1−/− mice was greatly reduced, thus showing that Raldh1 indeed participates in RA synthesis in vivo. Our findings suggest that RA signaling may be necessary only during early stages of retina development and that if RA synthesis is needed in dorsal retina, it is catalyzed by multiple enzymes, including Raldh1.


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