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The signalling protein Fringe (Fng) has a sequence homology to the glycosyltransferases. In Drosophila eye development is an early event is the eye disc division into dorsoventral domains. It is shown that Fng is specifically expressed in the ventral portion of the undifferentiated eye disc, creating a dorsoventral boundary. Equatorial expression of Notch signalling proteins is disrupted by lack of Fng boundary, and leads to failure of eye development.

The eyes face the challenge that they are constantly making small movements even when a fixed gaze is maintained. Position changes from large eye movements appear to be corrected by extraretinal signals and resulting motion response is switched off. A novel visual illusion is reported, that reveals a compensation mechanism based on visual motion signals. A model accounting for the illusion is proposed.

The human eye rotates with three degrees of freedom: horizontally, vertically, and torsionally (1, 2). With few exceptions, theories of vision and eye movement have ignored rotations about the line [...], Horizontal and vertical movements of the human eye bring new objects to the center of the visual field, but torsional movements rotate the visual world about its center. Ocular torsion stays near zero during head-fixed gaze shifts, and eye movements to visual targets are thought to be driven by purely horizontal and vertical commands. Here, analysis of eye-head gaze shifts revealed that gaze commands were three-dimensional, with a separate neural control system for torsion. Active torsion optimized gaze control as no two-dimensional system could have, stabilizing the retinal image as quickly as possible when it would otherwise have spun around the fixation point.

We have generated and characterized a Drosophila cyclin E hypomorphic mutation, [DmccycE.sup.JP], that is homozygous viable and fertile, but results in adults with rough eyes. The mutation arose from an internal deletion of an existing P[[w.sup.+]lacZ] element inserted 14 kb upstream of the transcription start site of the DmcycE zygotic mRNA. The presence of this deleted P element, but not the P[[w.sup.+]lacZ] element from which it was derived, leads to a decreased level of DmcycE expression during eye imaginal disc development. Eye imaginal discs from [DmcycE.sup.JP] larvae contain fewer S phase cells, both anterior and posterior to the morphogenetic furrow. This results in adults with small rough eyes, largely due to insufficient numbers of pigment cells. Altering the dosage of the Drosophila cdk2 homolog, cdc2c, retinoblastoma, or [p21.sup.CIP1] homolog dacapo, which encode proteins known to physically interact with Cyclin E, modified the [DmcycE.sup.JP] rough eye phenotype as expected. Decreasing the dosage of the S phase transcription factor gene, dE2F, enhanced the [DmcycE.sup.JP] rough eye phenotype. Surprisingly, mutations in G2/M phase regulators cyclin A and string (cdc25), but not cyclin B1, B3, or cdc2, enhanced the [DmcycE.sup.JP] phenotype without affecting the number of cells entering S phase, but by decreasing the number of cells entering mitosis. Our analysis establishes the [DmcycE.sup.JP] allele as an excellent resource for searching for novel cyclin E genetic interactors. In addition, this analysis has identified cyclin A and string as [DmcycE.sup.JP] interactors, suggesting a novel role for cyclin E in the regulation of Cyclin A and String function during eye development.

The ciliary body contains an epithelial bilayer consisting of an outer pigmented cell layer (PE) and an inner nonpigmented cell layer (NPE) responsible for aqueous humor secretion. Secretion may be mediated in part by cytosolic [Ca.sup.2+] concentration ([[[Ca.sup.2+]].sub.i]), but whether or how the two layers could coordinate their [Ca.sup.2+] signals to regulate secretion is unclear. To investigate interactions between PE and NPE, we examined [[[Ca.sup.2+]].sub.i] signaling in isolated intact ciliary epithelial bilayers using confocal microscopy. Phenylephrine selectively increased [[[Ca.sup.2+]].sub.i] in PE and acetylcholine increased [[[Ca.sup.2+].sub.i] in NPE, but epinephrine increased [[[Ca.sup.2+]].sub.i] in both layers. This increase spread from PE to NPE, and [[[Ca.sup.2+].sub.i] signaling across the bilayer remained coordinated during [[[Ca.sup.2+]].sub.i] oscillations. All epinephrine-induced [[[Ca.sup.2+].sub.i] signaling was blocked by the [[Alpha].sub.l]-adrenergic antagonist prazosin, whereas signaling in the NPE but not PE was blocked by the [Beta]-adrenergic antagonist propranolol, the gap junction blockers octanol and 18[Alpha]-glycyrrhetinic acid, or the A kinase inhibitor [R.sub.p] diastereomer of adenosine 3[prime],5[prime]-cyclic monophosphothioate. The [Beta]-adrenergic agonist isoproterenol failed to increase [Ca.sup.2+] by itself, but isoproterenol plus phenylephrine-induced [[[Ca.sup.2+].sub.i] signals across the bilayer similar to those induced by epinephrine. Finally, isoproterenol increased cell-to-cell spread of lucifer yellow via gap junctions, whereas cell-to-cell spread of [[[Ca.sup.2+].sub.i] signals could be induced by photorelease of caged inositol 1,4,5-trisphosphate. Thus, calcium signals are coordinated in the epithelial bilayer so that adrenergic stimulation can increase [[Ca.sup.2+]].sub.i] in NPE, but only if NPE are primed by activation of endogenous adenylyl cyclase, whereupon they receive stimulation from adjacent PE via gap junctions. This novel interplay between endocrine and paracrine pathways may coordinate [[[Ca.sup.2+].sub.i] signaling across the ciliary epithelial bilayer.

Ambient light conditions affect the morphology of synaptic elements within the cone pedicle and modulate the spatial properties of the horizontal cell receptive field. We describe here that the effects of retinoic acid on these properties are similar to those of light adaptation. Intraorbital injection of retinoic acid into eyes of dark-adapted carp that subsequently were kept in complete darkness results in the formation of numerous spinules at the terminal dendrites of horizontal cells, a typical feature of light-adapted retinae. The formation of these spinules during light adaptation is impaired in the presence of citral, a competitive inhibitor of the dehydrogenase responsible for the generation of retinoic acid in vivo. Intracellularly recorded responses of horizontal cells from dark-adapted eyecup preparations superfused with retinoic acid reveal typical light-adapted spatial properties. Retinoic acid thus appears to act as a light-signaling modulator. Its activity appears not to be at the transcriptional level because its action was not blocked by actinomycin.

Mutations in the gene encoding rhodopsin, the visual pigment in rod photoreceptors, lead to retinal degeneration in species from Drosophila to man. The pathogenic sequence from rod cell-specific mutation to degeneration of rods and cones remains unclear. To understand the disease process in man, we studied heterozygotes with 18 different rhodopsin gene mutations by using noninvasive tests of rod and cone function and retinal histopathology. Two classes of disease expression were found, and there was allele-specificity. Class A mutants lead to severely abnormal rod function across the retina early in life; topography of residual cone function parallels cone cell density. Class B mutants are compatible with normal rods in adult life in some retinal regions or throughout the retina, and there is a slow stereotypical disease sequence. Disease manifests as a loss of rod photoreceptor outer segments, not singly but in microscopic patches that coalesce into larger irregular areas of degeneration. Cone outer segment function remains normal until > 75% of rod outer segments are lost. The topography of cone loss coincides with that of rod loss. Most class B mutants show an inferior-nasal to superior-temporal retinal gradient of disease vulnerability associated with visual cycle abnormalities. Class A mutant alleles behave as if cytotoxic; class B mutants can be relatively innocuous and epigenetic factors may play a major role in the retinal degeneration.

Introduction Hydrothermal vents are generally found in the region of tectonic plate boundaries such as the mid-Atlantic ridge and the Galapagos rift. The emission of super-heated water (350 ° C) [...], The structure and ultrastructure of the eyes of postlarval vent shrimps provisionally designated 'Alvinocaris' and 'Chorocaris' are described. The eyes of the postlarval 'Alvinocaris' are cylindrical, borne on short stalks, and contain closely packed rhabdoms. The ommatidia lack dioptric apparatus and have rhabdoms extending almost to the cornea. The rhabdoms consist of orthogonal layers of microvilli typical of crustacean rhabdoms. The eyes of the 'Chorocaris' are similar, but the rhabdom layer extends back through the reduced eyestalks and covers some of the dorsal surface of the cephalothorax. The rhabdoms from both the anterior and the thoracic regions consist of layered microvilli. The eyes of a slightly smaller postlarval vent shrimp, termed 'Type A', differ. Although clearly related to the other vent shrimps, Type A has stalked eyes held at an angle to the head. The eye displays a gradient of ommatidial development, with the older ommatidia closely resembling those seen in the other postlarval types. Between the cornea and the rhabdom layer, the youngest ommatidia possess quadripartite crystalline cones similar to those seen in related families of caridean shrimps; these are absent in the more mature ommatidia. The external structure of the anterior and thoracic eyes of juvenile Rimicaris exoculata (after settlement at the vent site) is also described. Juveniles up to 9 mm in carapace length have anterior corneas similar to those seen in postlarvae, whereas in larger specimens the corneas are progressively replaced by an ocular plate.

The cellular and subcellular sites of aquaporin (AQP) water transport proteins in the eye are defined using immuno-blotting, high-resolution immunocytochemistry and immuno-electron microscopy of intact human and rat tissues. Results reveal selective expression of AQP1, AQP3, AQP4 and AQP5 in distinct epithelia while assigning specific roles for each one in the complex network through which water movements take place in the eye.

Byline: C. Kemner (1), M. N. Verbaten (2), J. M. Cuperus (1), G. Camfferman (2), H. van Engeland (1) Keywords: Saccadic eye movement; autism Abstract: The saccadic eye movements, generated during a visual oddball task, of autistic children, normal children, children with attention deficit disorder and hyperactivity (ADDH), and dyslexic children were examined to determine whether autistic children differed from these other groups in saccadic frequency. Autistic children made more saccades during the presentation of frequent stimuli (than normals and ADDH children), and between stimulus presentations. Also, unlike the normal and dyslexic groups, their saccadic frequency did not depend on stimulus type. This abnormal pattern of saccades may negatively influence the ability to attend to stimuli, and thereby learning processes. Suggestions are made with respect to possible abnormalities in subcortical mechanisms involved in saccade generation. Author Affiliation: (1) Department of Child and Adolescent Psychiatry, Utrecht University, Utrecht, The Netherlands (2) Department of Psychoparmacology, Utrecht University, Utrecht, The Netherlands Article History: Registration Date: 29/09/2004

Sine oculus (so) and eyes absent (eya) are needed for Drosophila eye development, and are members of the mammalian Six and Eya gene families. The genes are thought to act with eyeless (Pa6) in regulating eye development in vertebrates and invertebrates. It is demonstrated the So and Eya regulate steps in eye development such as cell proliferation, neuronal development and patterning.

In urodele amphibians, lens induction during development and regeneration occurs through different pathways. During development, the lens is induced from the mutual interaction of the ectoderm and the optic vesicle, whereas after lentectomy the lens is regenerated through the transdifferentiation of the iris-pigmented epithelial cells. Given the known role of fibroblast growth factors (FGFs) during lens development, we examined whether or not the expression and the effects of exogenous FGF during urodele lens regeneration were conserved. In this paper, we describe expression of FGF-1 and its receptors, FGFR-2 (KGFR and bek variants) and FGFR-3, in newts during lens regeneration. Expression of these genes was readily observed in the dedifferentiating pigmented epithelial cells, and the levels of expression were high in the lens epithelium and the differentiating fibers and lower in the retina. These patterns of expression implied involvement of FGFs in lens regeneration. To further elucidate this function, we examined the effects of exogenous FGF-1 and FGF-4 during lens regeneration. FGF-1 or FGF-4 treatment in lentectomized eyes resulted in the induction of abnormalities reminiscent to the ones induced during lens development in transgenic mice. Effects included transformation of epithelial cells to fiber cells, double lens regeneration, and lenses with abnormal polarity. These results establish that FGF molecules are key factors in fiber differentiation, polarity, and morphogenesis of the lens during regeneration even though the regenerating lens is induced by a different mechanism than in lens development. In this sense, FGF function in lens regeneration and development should be regarded as conserved. Such conservation should help elucidate the mechanisms of lens regeneration in urodeles and its absence in higher vertebrates.

Random mixed pro- and antisaccade research trials show that spatial selectivity remains constant in visual and movement neurons of the eye. Evidence suggests that voluntary antisaccade instructions take precedence over reflexive glances. The dorsolateral prefrontal cortex, primary frontal eye field and supplementary eye field are thought to result in antisaccade initiation through different mechanisms.

Neural research shows a cyclic allosteric mechanism activates the retinal and olfactory cyclic-nucleotide-gated channels in ligand-independent and ligand-dependent channel openings. An amino-terminal domain other than the pore and ligand-binding motifs is involved in the allosteric gating transition which in turn tunes the physiological response of ligand-binding proteins in biological signals.

Exposure to light causes the rods and cones of the two lateral eyes of vertebrates to hyperpolarize. This can be attributed to a cyclic GMP cascade that results in cGMP hydrolysis and the consequent closure of cGMP-gated cation channels that open in the dark. In contrast, the parietal or third eye of lizards and other lower vertebrates depolarize when illuminated. Despite these opposite reactions, evidence is found indicating that both lateral eyes and parietal eyes use a cGMP signalling cascade for phototransduction without the involvement of inositol-1,4,5-trisphosphate.