EvoprintHD of sine oculis

Ensembl GeneView CG11121

BIOLOGICAL OVERVIEW

sine oculis and three other transcription factors are involved in early eye morphogenesis: eyeless, (a homeodomain protein), optimotor blind (the brachyury homolog) and eyes absent (the cell survival and differentiation gene). Sine oculis is present at the birth of the eye primordium, and has a direct role in this process. In mutants there is an increase in cell death in the region of the primordium. Movement of the primordium into the head is arrested at an early stage. optimotor blind continues to be expressed in the invagination-defective optic primordium of sine oculis mutants. Expressed prior to the development of the morphogenetic furrow, sine oculis may have a role in establishment of the furrow, or may influence the direction and polarity of furrow movement (Cheyette, 1994).

Sine oculis and Eyes absent have been found to form a complex and to regulate multiple steps in Drosophila eye development (see Specification of the eye disc primordium and establishment of dorsal/ventral asymmetry). So and Eya (1) regulate common steps in eye development including cell proliferation, patterning, and neuronal development; (2) they synergize in inducing ectopic eyes and (3) interact in yeast and in vitro through evolutionarily conserved domains. Clones of so and of eya mutant cells overproliferate and fail to differentiate into neurons. Mutant clones retain their epithelial organization and lead to abnormal folding of the disc. The previously reported cell death phenotype is a secondary result of cell overgrowth. It is concluded that both so and eya play a role in controlling proliferation in the eye primordium of the eye-antennal disc and may therefore contribute to regulating the size of the disc (Pignoni, 1997).

Morphogenetic furrow (MF) initiation does not occur in so and eya mutant clones. decapentaplegic expression is not detected in mutant so and eya clones. Development of eye tissue in the posterior and lateral regions but not the anterior region of so and eya mutant discs is rescued by ectopic expression of the respective genes. Rescue is restricted to the most posterior region of the mutant discs, leading to the conclusion that so and eyaare required during MF formation. so and eya are also required for neuronal development. Homozygous mutant cells were produced selectively posterior to the MF. These mutant clones result in absence of a significant number of photoreceptors, precisely those that are known to be born late under normal conditions, corresponding to the time of so and eya mutant clone induction (Pignoni, 1997).

Ectopic expression of so has little or no effect on antennal, wing, or leg disc development, while ectopic eya expression often causes mild growth alterations resulting in extra folds in the epithelium and, rarely, formation of small ectopic ommatidial arrays in the antennal disc. Coexpression of so and eya leads to a dramatic increase in the development of ectopic eye tissue in antennal discs. These ommatidial arrays lead to adult eye structures. Ectopic so/eya induce eyeless expression in the antennal disc. When expressed in eyeless mutant discs, ectopic so/eya produces growth alterations, but ectopic eyes are not observed (Pignoni, 1997).

So and Eya are able to physically interact through their evolutionarily conserved domains. The sequences responsible for interaction are localized to the N-terminal domain of Eya, while the So interaction domain is localized to the Six domain, a conserved sequence shared with vertebrate So homologs. Because of the multiple effects of the So/Eya interaction in MF induction, cell proliferation and neural induction, it is proposed that a So/Eya complex regulates multiple steps in eye development and functions within the context of a network of genes to specify eye tissue identity (Pignoni. 1997).

Evidence is provided for the existence of an extraocular light perception in Drosophila that does not use the same phototransduction cascade as the adult photoreceptors. The Drosophila larva modulates its pattern of locomotion when exposed to light. Modulation of locomotion can be measured as a reduction in the distance traveled and by a sharp change of direction when the light is turned on. When the light is turned off this change of direction, albeit significantly smaller than when the light is turned on, is still significantly larger than in the absence of light transition. Mutations that disrupt adult phototransduction disrupt a subset of these responses. In larvae carrying these mutations the magnitude of change of direction when the light is turned on is reduced to levels indistinguishable from that recorded when the light is turned off, but it is still significantly higher than in the absence of any light transition. Similar results were obtained when these responses were measured in strains where the larval photoreceptor neurons were ablated by mutations in the glass (gl) gene or by the targeted expression of the cell death gene head involution defective (hid). A mutation in the homeobox gene sine oculis (so) that ablates the larval visual system, or the targeted expression of the reaper (rpr) cell death gene, abolishes all responses to light detected as a change of direction. The existence of an extraocular light perception is suggested that does not use the same phototransduction cascade as the adult photoreceptors. These results indicate that this novel visual function depends on the blue-absorbing rhodopsin Rh1 and is specified by the so gene (Busto, 1999). The larval visual system was first described in the house fly Musca domestica by Bolwig and henceforth was named the Bolwig's organ. Similarly, in D. melanogaster, the larval visual system is composed of two bilateral groups of 12 photoreceptor cells located in the more anterior part of the head, juxtaposed to the mouth hooks. The axons of the photoreceptor cells form the larval optic nerve that innervates the optic lobe primordium area of the brain lobes. The early development and the establishment of connectivity in this system has been described previously. In the Drosophila larva a light stimulus modulates the direction of movement as well as quantitative aspects of locomotion such as path length and frequency of turning. Mutations that disrupt phototransduction in the adult eye disrupt aspects of the larval response to light measured in this assay. These results suggest that the larval and adult visual systems are similar from the functional point of view. These mutations, however, fail to abolish all perception of light, suggesting the existence of a light detection mechanism that does not require these gene products. The analysis of developmental mutants and of strains where the cell death genes are ectopically expressed suggests that this novel light detection mechanism is not located in the Bolwig's organ (Busto, 1999).

In the wild-type strains tested, change of direction when the light is turned off is greater than in the absence of light transitions, suggesting that turning off the light is a transition perceived by the animal. This observation supports the notion that a simple mechanism for the perception of light exists in the Drosophila larva that distinguishes changes in light conditions from absence of light transitions but is unable to distinguish whether the light is being turned on or off. This light response is mediated by the blue-absorbing rhodopsin (Rh1) because it is abolished in part by mutations in the ninaE gene. Interestingly, it does not rely on the same phototransduction pathway as that of the adult visual system as seen by the wild-type response of norpA and ninaC mutant larvae. The results indicate that these hypothetical photoreceptors are not housed within the Bolwig's organ, defined as the larval photoreceptors that depend on the gl gene function for differentiation. However, the observation that the function of this visual system is impaired in larvae where the cell death gene rpr is expressed under the control of the gl promoter demonstrates that these are cells in which the gl transcription factor is functional. Thus it is possible that this novel function is performed by a small number of cells that express Rh1 and the gl gene product but whose differentiation and Rh1 expression are not under the control of the gl gene (Busto, 1999).

Two different groups of cells are likely to be involved in this novel light perception. The observation that the ability of these cells to register this type of light perception is dependent on the so gene function but not gl suggests that these cells are included in the optic lobe primordium. The ablation of this proposed function by expression of the cell death gene rpr under the gl promoter suggests that the central brain neurons that express the gl gene are also involved in this behavior. A precedent for a light detector that does not rely on known elements of the phototransduction machinery in adults is the photic input pathway required for the entrainment of the circadian rhythm. The novel visual system function proposed in this paper presents other parallels with cells involved in the control and generation of circadian rhythms. Mutations in the gl gene do not abolish circadian rhythms. However, the expression of the period (per) gene under the control of the gl promoter is sufficient to restore circadian rhythmicity in per mutant flies. These results strongly suggest that the gl-expressing cells that are not the photoreceptors house the circadian pacemaker. It is possible that this novel visual function, which distinguishes changes in light condition from absence of light transitions but is unable to distinguish whether light is being turned on or off, is also involved in the control of pacemaker oscillation (Busto, 1999). .

GENE STRUCTURE

Genomic length - 16 kb

cDNA clone length - 2861

Bases in 5' UTR -870

Exons - eight

Bases in 3' UTR - 742

PROTEIN STRUCTURE

Amino Acids - 416

Structural Domains

There is a central homeodomain, a C-terminal stretch rich in glutamine, and an N terminal rich in asparagine (Cheyette, 1994).

date revised: 15 July 98

Home page: The Interactive Fly © 1998 Thomas B. Brody, Ph.D.

The Interactive Fly resides on the
Society for Developmental Biology's Web server.