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PubMed2004

Retinal cell fate determination and bHLH factors.

Retinal development is controlled antagonistically by multiple basic helix-loop-helix (bHLH) transcriptional activators and repressors. bHLH repressors suppress bHLH activators and promote maintenance of progenitors and generation of glial cells. In contrast, bHLH activators override activities of bHLH repressors and promote neuronal differentiation. However, bHLH activators alone are not sufficient but homeodomain factors are additionally required for neuronal subtype specification. It is likely that homeodomain factors regulate the layer specificity but not the neuronal fate while bHLH activators determine the neuronal fate within the homedomain factor-specified layers. Thus, combinations of proper bHLH and homeodomain factors are required for neuronal subtype specification.

Amacrine Cells↗
PubMed1993

Transcriptional downregulation of the retina-specific QR1 gene by pp60v-src and identification of a novel v-src-responsive unit.

The embryonic avian neuroretina (NR) is part of the central nervous system and is composed of various cell types: photoreceptors and neuronal and Müller (glial) cells. These cells are derived from proliferating neuroectodermal precursors which differentiate after terminal mitosis and become organized in cell strata. Proliferation of differentiating NR cells can be induced by infection with Rous sarcoma virus (RSV) and requires the expression of a functional v-src gene. To understand the mechanisms involved in the regulation of neural cell growth and differentiation, we studied the transcriptional regulation of QR1, a gene specifically expressed in postmitotic NR cells. Transcription of this gene is detected primarily in Müller cells and is strongly downregulated by the v-src gene product. Moreover, QR1 expression takes place only during the late phase of retinal development and is shut off abruptly at hatching. We have isolated a promoter region(s) of the QR1 gene that confers v-src responsiveness. By transfection of QR1-CAT constructs into quail NR cells infected with the temperature-sensitive mutant of RSV, PA101, we have identified a v-src-responsive region located between -1208 and -1161 upstream of the transcription initiation site. This sequence is able to form two DNA-protein complexes, C1 and C2. Formation of complex C2 is specifically induced in cells expressing an active v-src product, while formation of C1 is detected mainly in nonproliferating quail NR cells upon pp60v-src inactivation. C1 is also a target for regulation during development. We have identified the DNA binding site for the C1 complex, a repeated GCTGAC sequence, and shown that mutations in this element abolish binding of this factor as well as transcription of the gene at the nonpermissive temperature. Neither formation of C1 nor that of C2 seems to involve factors known to be targeted in the pp60v-src cascade. Our data suggest that C1 could be a novel target for both developmental control and oncogene-induced cell growth regulation.

Actins↗
PubMed2006

SOCS3 is required to temporally fine-tune photoreceptor cell differentiation.

Suppressor of cytokine signaling 3 (SOCS3) is an intracellular, ligand-induced negative feedback modulator of STAT3 activation that acts during inflammation. Here, we demonstrate that SOCS3 expression is important for normal retinal development in the perinatal period. STAT3 is highly activated in the late-embryonic retina, then downregulated at postnatal day 0 (P0), presumably by the depletion of upstream ligands. We found that SOCS3 was required after P0 to shut down the residual STAT3 activation; this loss of activated STAT3 leads to Rhodopsin expression and rod photoreceptor cell differentiation. SOCS3 deficiency failed to terminate STAT3 activation, thereby delaying expression of Rhodopsin and its upstream transcription factor, crx. Development subsequently continued, but its course was temporally erratic, probably because of faulty compensation. Interestingly, SOCS3 protein expression was first detected postnatally, after STAT3 activation was mostly downregulated. It initially appeared in some of the presumptive photoreceptor cells and gradually spread. SOCS3 mRNA level was constant from the late-embryonic to early-postnatal period. Post-transcriptional inhibition of SOCS3 protein expression maintains a high STAT3 activation during late embryogenesis, and after P0, releasing from the inhibition promptly terminates STAT3 activation. Thus, SOCS3 can act as a temporal fine-tuner of STAT3 activation during photoreceptor cell differentiation.

Animals↗
PubMed1997

Pax-6, Prox 1, and Chx10 homeobox gene expression correlates with phenotypic fate of retinal precursor cells.

PURPOSE: To study the expression patterns of the homeobox genes Pax-6, Prox 1, and Chx10 during chick retinal development in vivo and in vitro. METHODS: Sections of paraformaldehyde-fixed, paraffin-embedded eyes were obtained at a range of developmental stages. In situ hybridization was carried out on tissue sections using digoxigenin-labeled sense and antisense RNA probes that recognize chicken Pax-6 and Prox 1 (whose sequences were already available), and chicken Chx10 (which was cloned and sequenced as part of this study). Selected developmental stages were also studied by immunocytochemistry with antibodies against Pax-6 and Prox 1, and by Northern blot analysis using 32P-labeled probes. RESULTS: Until embryonic day (ED) 5, in situ hybridization shows widespread, diffuse distribution of all three genes. Between ED 6 and ED 8, however, they acquire distinct, topographically specific patterns of expression. The Prox 1 signal is predominantly expressed in the prospective horizontal cell layer of the neuroepithelium, decreases vitreally, and is absent from ganglion cells and the prospective photoreceptor layer. Pax-6 is strongly expressed only in the prospective ganglion-cell and amacrine-cell regions at the same stages, and is not detected in prospective photoreceptors. Chx10 expression becomes concentrated in the future bipolar-cell region of the inner nuclear layer. Similar patterns are maintained by ED 15 through ED 18, after cell differentiation has taken place. Pax-6 and Prox 1 immunoreactive materials showed nuclear localization and a pattern of laminar distribution equivalent to that seen by in situ hybridization. CONCLUSIONS: These results suggest that the differentiated fate of retinal precursor cells may be influenced by Pax-6, Prox 1, or Chx10, this hypothesis is now being tested using dissociated chick embryo retinal cell cultures.

Amino Acid Sequence↗
PubMed1996

Interphotoreceptor retinoid-binding protein (IRBP): expression in the adult and developing Xenopus retina.

Apposition of the neural retina and pigment epithelium is critical to photoreceptor development and function. Interphotoreceptor retinoid-binding protein (IRBP) is a major component of the extracellular matrix separating these epithelia in the African clawed frog Xenopus laevis (Gonzalez-Fernandez et al., [1993], J. Cell Sci. 105:7-21). In the adult retina, IRBP appears to mediate the transport of hydrophobic molecules, particularly retinoids and fatty acids, within the hydrophilic extracellular domain. In this paper, we compare the distribution of IRBP and its mRNA in adult and embryonic Xenopus retina. Xenopus IRBP antisense RNA, labeled with tritium or digoxigenin, was used for in situ hybridizaton studies. For immunohistochemistry, we used an antiserum against Xenopus IRBP expressed in Escherichia coli. In the adult, we found that IRBP is synthesized at similar levels by both rods and cones. The protein is restricted to the interphotoreceptor matrix, with lesser amounts in the pigment epithelial cytoplasm. In the embryo, expression of the mRNA for IRBP is restricted to the central retina, where photoreceptor differentiation has taken place. By contrast, the protein is distributed throughout the embryonic subretinal space. Therefore, the presence of IRBP precedes photoreceptor differentiation. In summary, IRBP is synthesized by both rods and cones and may be internalized by the pigment epithelium. In the embryo, IRBP is synthesized by the central retina and diffuses through the matrix, reaching the undifferentiated peripheral retina. In view of its ligand-binding properties, diffusion of IRBP may provide the peripheral neural retina with a vehicle to transport retinoids and docosahexaenoic acid (molecules critical to normal retinal development) from the pigment epithelium.

Animals↗
PubMedDate not supplied

Increasing toxoplasma seropositivity in women with bad obstetric history and in newborns.

BACKGROUND: Most infants with congenital Toxoplasma gondii infection have no symptoms at birth but few may develop retinal diseases or neurological abnormalities later in life. The presence of significant titres of antitoxoplasma antibodies in women in the reproductive age group indirectly indicates that Toxoplasma gondii is the cause of such congenital abnormalities and also sporadic abortions in some women. METHODS: We did a retrospective analysis of antitoxoplasma antibodies detected by indirect haemagglutination assay, in women with bad obstetrical history and in newborns clinically suspected of congenital toxoplasmosis during 1981-91. RESULTS: A significant increase in seropositivity in women and newborns was seen during 1989-91 as compared to 1981-88. More seropositive patients were recorded between April-June and October-December. However, no significant correlation could be observed between rising incidence of seropositivity and the seasonal distribution or age of women. CONCLUSION: Epidemiological studies are required to ascertain the reason for the increasing trend of toxoplasma seropositivity and to suggest appropriate control strategies as it is possible to prevent congenital infection.

Adolescent↗
PubMed1995

Developmental control of transcription of a retina-specific gene, QR1, during differentiation: involvement of factors from the POU family.

Developmental control of gene expression often results from the coupling of growth arrest with the establishment of differentiation programs. QR1 is a gene specifically expressed in retinas during the late phase of embryogenesis. At this stage neuroectodermal precursors have reached terminal mitosis and are undergoing differentiation into distinct cell types. Transcription of the QR1 gene is tightly regulated during retinal development: this gene is expressed between embryonic day 9 (ED9) and ED17 and is completely repressed at hatching in quail. Moreover, QR1 transcription is downregulated when postmitotic neural retina cells are induced to proliferate by pp60v-src. We studied the stage-dependent transcriptional control of this gene during quail neural retina (QNR) cell development. Transient transfection experiments with QR1/CAT constructs at various stages of development showed that a region located between -935 and -1265 bp upstream of the transcription start site is necessary to promote transcription in retina cells during the late phase of embryonal development (QNR9, corresponding to ED9). By in vivo footprinting assays we identified at least two elements that are occupied by DNA-protein complexes in QNR cells: the A and B boxes. The A box allows formation of several biochemically distinct complexes: C1, C2, C3, and C4. Formation of the C2 complex mainly during early stages (ED7) and of C2, C3, and C4 complexes during postnatal life correlates with repression of QR1 transcription, whereas the C1 complex is strongly induced at ED11 when the QR1 gene is expressed. We previously showed that C1 was involved in downregulation of QR1 transcription by pp60v-src. Several complexes are also formed on the B box. We show that these complexes are exclusively present in neural tissues and that they involve members of the POU family of transcription factors. Mutations of each one of the two regions which abolish the binding of the C1 factor(s) on the A box and of the POU factor(s) on the B box also prevent stimulation of QR1 transcription in QNR9. Therefore, both elements appear to be required for the stage-specific transcription of the QR1 gene. We also show that the regulatory region from position -1265 to position -935 is able to confer stage-specific transcription upon a heterologous promoter (thymidine kinase). Indeed, this region stimulates transcription in differentiating retinas (QNR9) and represses transcription in terminally differentiated retinas (QNR17, corresponding to postnatal life). Our results suggest that cell growth regulation and developmental control are coordinated through the A and B boxes in regulating QR1 transcription during retinal differentiation.

Animals↗
PubMed2002

Different RPGR exon ORF15 mutations in Canids provide insights into photoreceptor cell degeneration.

The canine disease, X-linked progressive retinal atrophy (XLPRA), is similar to human RP3, an X-linked form of retinitis pigmentosa, and maps to the same region in the X chromosome. Analysis of the physical map of the XLPRA and RP3 intervals shows a high degree of conservation in terms of genes and their order. We have found different mutations in exon ORF15 of the RPGR gene in two distinct mutant dog strains (XLPRA1, XLPRA2). Microdeletions resulting in a premature stop or a frameshift mutation result in very different retinal phenotypes, which are allele-specific and consistent for each mutation. The phenotype associated with the frameshift mutation in XLPRA2 is very severe and manifests during retinal development; the phenotype resulting from the XLPRA1 nonsense mutation is expressed only after normal photoreceptor morphogenesis. Splicing of RPGR mRNA transcripts in retina is complex, and either exon ORF15 or exon 19 can be a terminal exon. The retina-predominant transcript contains ORF15 as a terminal exon, and is expressed in normal and mutant retinas. The frameshift mutation dramatically alters the deduced amino acid sequence, and the protein aggregates in the endoplasmic reticulum of transfected cells. The cellular and molecular results in the two canine RPGR exon ORF15 mutations have implications for understanding the phenotypic variability found in human RP3 families that carry similar mutations.

Animals↗
PubMed2006

Induction of BIM(EL) following growth factor withdrawal is a key event in caspase-dependent apoptosis of 661W photoreceptor cells.

Apoptosis of photoreceptor cells in the early postnatal period is a normal feature of mammalian retinal development. The role of mitochondria and caspases in the process has been well established; however, the identification of key apoptotic mediators still remains elusive. Here we report that BIM(EL), a pro-apoptotic BCL-2 family member, may be one such molecule. Following growth factor deprivation, BIM(EL) was up-regulated in mouse 661W cone photoreceptors. This event correlated with the release of mitochondrial apoptogenic factors into the cytosol, the activation of caspases and apoptosis. Moreover, a similar behaviour was observed in response to UV radiation, ionomycin or H(2)O(2) treatments. We identified the PI3K-Akt-FKHRL1 signalling cascade as the main regulatory pathway of BIM(EL) expression in these cells. Finally, using RNA interference, we were able to silence BIM(EL) expression and subsequently suppress caspase-3 activation. In conclusion, we propose BIM(EL) as a critical factor in mitochondria-dependent apoptosis of 661W photoreceptors.

Animals↗
PubMed2000

Retinal dysfunction in basigin deficiency.

PURPOSE: To examine the retina of basigin (Bsg) knockout mice by electrophysiological and histologic methods and thereby to determine the possible function of Bsg in phototransduction and retinal development. METHODS: Scotopic and photopic electroretinograms (ERGs) were recorded from 11 wild-type, 12 heterozygous, and 8 homozygous Bsg gene knockout mice of different ages. The retinas were also examined by histologic and immunolabeling methods. RESULTS: Bsg knockout mice of 5 to 41 weeks of age showed a decrease in the amplitude of all components of both the photopic and scotopic ERGs. In contrast, the fundus and the fluorescein fundus angiography and morphology of the retina at the light microscopic level appeared to be normal until 8 weeks of age in Bsg knockout mice. Thereafter, the length of outer segment and outer nuclear layers decreased with increasing age. Immunohistochemical analysis localized Bsg protein in a variety of cells in the retina, especially in the pigment epithelium, the upper outer plexiform layer and the inner segments of photoreceptor cells. CONCLUSIONS: The results demonstrated that both rod and cone function were severely affected from an early age by the targeted disruption of the Bsg gene. In spite of abnormal ERGs, the photoreceptor cells maintained normal morphology up to 8 weeks. Thereafter, the photoreceptor cells degenerated gradually and were almost ablated by 41 weeks.

Animals↗
PubMed2000

Insulin-like growth factor-I protects axotomized rat retinal ganglion cells from secondary death via PI3-K-dependent Akt phosphorylation and inhibition of caspase-3 In vivo.

Recently we have shown that the majority of retinal ganglion cells (RGCs) dies via activation of caspase-3 after transection of the optic nerve (ON) in the adult rat. In the present study we investigated whether insulin-like growth factor-I (IGF-I), an important factor in retinal development, prevents secondary death of RGCs after axotomy. Moreover, we studied potential intracellular mechanisms of IGF-mediated neuroprotection in more detail. Our results indicate that intraocular application of IGF-I protects RGCs from death after ON transection in a dose-dependent manner. We show reduced caspase-3 activity as one possible neuroprotective mechanism of IGF-I treatment in vivo. Caspase-3 mRNA expression remained unchanged. Because caspase inhibition can be mediated by Akt in vitro, we examined phosphorylation of Akt after axotomy and under IGF treatment. Western blot analysis revealed decreased Akt phosphorylation after axotomy without treatment and an increased phosphorylation of Akt under treatment with IGF-I. This strong increase could be reduced by simultaneous injection of wortmannin (WM), a potent inhibitor of phosphatidylinositol 3-kinase (PI3-K). To prove the pathway suggested by these experiments as relevant for the in vivo situation, we assessed the number of RGCs 14 d after ON transection under a combined treatment strategy of IGF-I and WM. As expected, WM significantly reduced the neuroprotective effects of IGF-I. In summary, we show for the first time in vivo that IGF is neuroprotective via PI3-K-dependent Akt phosphorylation and by inhibition of caspase-3.

Androstadienes↗
PubMed1998

Immunocytochemical characterisation of proteins secreted by retinal pigment epithelium in retinas of normal and Royal College of Surgeons dystrophic rats.

In a previous study, an antigen consisting of proteins secreted by retinal pigment epithelial (RPE) cells was injected into a sheep and the specificity of the resulting antiserum was shown by Western blotting and its effects on retinal development were determined in vitro and in vivo. In the present study, the distribution of these secreted proteins was determined by light microscopy immunocytochemistry in cultured neonatal rat RPE cells and retinas of normal and Royal College of Surgeons (RCS) dystrophic rats and cerebrum of normal adult rats. Immunolabelling for these RPE-secreted proteins was detected in cytoplasmic vesicles surrounding nuclei and within processes of cultured normal and transformed rat RPE. In retinas of late postnatal and adult rats, dense immunostaining was found in the cytoplasm of RPE cells and ganglion cell bodies. In addition to RPE and ganglion cells, scattered photoreceptors within the thin outer nuclear layer and small structures within the debris zone were also densely immunoreactive in retinas of 2-mo-old RCS dystrophic rats. The numbers of immunostained ganglion cells appeared to decrease in retinas of older RCS rats, although the immunoreactivity within the RPE appeared to increase in density. No other neuron within the retina, i.e. bipolar, amacrine or horizontal, was immunoreactive for RPE-secreted proteins. In the cerebral cortex of adult rats, immunoreactivity for RPE-secreted proteins was primarily detected within large perikarya of pyramidal neurons and smaller granule neurons. In conclusion, we report an immunocytochemical analysis of an antiserum raised against secreted proteins of rat RPE. This antiserum recognised proteins within secretory-like vesicles of cultured neonatal normal and transformed rat RPE and showed a specificity for RPE and ganglion cells in normal rat retinas, that appeared to be developmentally regulated, and neuron perikarya in adult rat cerebrum.

Animals↗
PubMed2000

Partial rescue of the ocular retardation phenotype by genetic modifiers.

The or(J) allele of the murine ocular retardation mutation is caused by a premature stop codon in the homeodomain of the Chx10 gene. When expressed on an inbred 129/Sv strain, the or(J) phenotype is characterized by microphthalmia and a thin, poorly differentiated retina in which the peripheral portion is affected to a greater extent than the central portion. Such mutant retinae lack differentiated bipolar cells and the optic nerve typically fails to form, leading to blindness. Here, we show that progeny from an outcrossed backcross between 129/Sv-or(J) /or(J) and Mus musculus castaneus produce animals that are homozygous for the or(J) mutation and exhibit a much ameliorated eye phenotype. Although not of normal size, such modified or(J) eyes are significantly larger than those in 129/Sv-or(J) /or(J) mice, and contain a better organized retina which includes bipolar cells. Furthermore, optic nerves are frequently present, and the eyes show a degree of function as reflected by electroretinogram and pupillary response. As in 129/Sv-or(J) /or(J) mice, however, modified or(J) eyes show incomplete growth and a lack of cell differentiation in the periphery of the retina. The selective, and apparently nonmodifiable, effect of the ocular retardation phenotype on the periphery of the retina indicates that Chx10 plays an important role in the central-to-peripheral gradient of retinal development. These findings demonstrate that the ocular retardation phenotype can be greatly modified by the genetic background, and help to define a role for Chx10 in ocular development.

Animals↗
PubMed1985

Chronic lymphocytic leukemia with hyperleukocytosis. The hyperviscosity syndrome.

A 47-year-old man with hyperleukocytic chronic lymphocytic leukemia progressively developed retinal hemorrhages, headache, diplopia, dysequilibrium, slurred speech, nystagmus, ataxic gait, and hearing loss as his leukocyte count rose to a maximum of 968,000/mm3. All of these symptoms and signs resolved promptly after leukapheresis. The authors reviewed records of 210 patients with chronic lymphocytic leukemia seen at our institution over a 12-year period, and found 16 patients with sustained hyperleukocytosis above 500,000/mm3, 3 of whom had features of the hyperviscosity syndrome. No laboratory values consistently predicted the occurrence or lack of occurrence of the hyperviscosity syndrome. The key to the management of hyperviscosity syndrome in the setting of hyperleukocytic chronic lymphocytic leukemia is to consider the diagnosis and to rapidly lower the lymphocyte count.

Adult↗
PubMed1990

A phase II trial of recombinant tumor necrosis factor in patients with advanced colorectal carcinoma.

Sixteen previously treated (with only one prior regimen) patients with histologically proven metastatic or locally recurrent colorectal carcinoma were treated with recombinant tumor necrosis factor (rTNF) administered by 30-minute i.v. infusions twice daily for 5 consecutive days every other week for 8 weeks. Patients received 100 micrograms/m2 twice daily on day 1 of cycle 1 with escalation to 150 micrograms/m2 twice daily thereafter. Patients were concomitantly treated with indomethacin 25 mg every 6 hours and acetaminophen 650 mg every 4 hours to obviate fever and chills. Toxicities included: nausea/vomiting (69%), headache (25%), chills (69%), pain at tumor sites (63%), hypotension (31%), and hypertension (38%). Hematologic toxicity included leukopenia less than 2000 cells/mm3 (38%) and thrombocytopenia less than 100,000 cells/mm3 (13%). Liver function abnormalities occurred independently of the site or extent of metastatic disease and inconsistently in each treatment cycle. Four patients developed bilirubinemia greater than 2.5 x baseline values (range, 2.5 to 10.3 U/L); five patients had greater than 2.5 x elevations in alkaline phosphatase (range, 624 to 1663 U/L). Two patients developed retinal vein thrombosis in the absence of hemostatic abnormalities. In both instances, this complication occurred several weeks after completion of therapy. No objective responses were noted in 14 evaluable patients (95% confidence interval: 0 to 0.23). Three patients had stable disease for a median duration of 4.5 months. In conclusion, i.v. rTNF at this dose and schedule has no demonstrable antitumor efficacy. Twice-daily i.v. administration of this agent is associated with more hepatotoxicity than previously reported in trials using subcutaneous or once daily i.v. administration. Retinal vein thrombosis may be a late complication of i.v. rTNF at this dose and schedule.

Aged↗
PubMed1982

Transplantation of reaggregates of embryonic neural retinae to neonatal rat brain: differentiation and formation of connections.

Embryonic day 14 neural retinae were dissociated into single cells and reaggregated prior to transplantation over the superior colliculi of newborn rats. One month after transplantation, the brains of the host rats were examined for transplant differentiation and the formation of projections from the transplant to the host brain. All reaggregated retinal transplants differentiated in the host brain, showing normal lamination and cellular morphology. Electron microscopic examination demonstrated normal synaptology with the transplanted retinal neuropil. Horseradish peroxidase injections into the host superior colliculus retrogradely filled cells within the transplant. These cells were found in the lamina corresponding to the ganglion cell layer and displayed a morphology characteristic of normal ganglion cells. Lesions of the transplants confirmed the projection of the reaggregated retinal transplants to superior colliculus. Degeneration was also traced into a number of ther nuclei that are normally retinorecipient. The presence of degenerating synaptic terminals resembling those seen after eye removal in control rats was confirmed by electron microscopic examination. It appears that despite disruption of initial cell-cell associations early in retinal development and prior to transplantation, the reaggregated transplants retain the ability to differentiate and form appropriate connection with the host brain.

Animals↗
PubMed1990

Photoreceptor mosaic: number and distribution of rods and cones in the rhesus monkey retina.

Video-enhanced differential interference contrast optics was used to determine the number and distribution of photoreceptors across the entire retinal surface of 9 eyes obtained from 7 adult rhesus monkeys. We found that the retina of this primate contains an average of 3,100,000 cones (+/- 130,000) and 61,000,000 rods (+/- 7,500,000). Variation among animals in the number of rods and cones cannot be accounted for by differences in sex, age, or retinal surface area, nor is there a correlation between the number of rods and cones (a retina with a high number of rods does not typically have a high number of cones). Cone density peaks at 141,000 cones/mm2 in the foveola and decreases about 100-fold toward the periphery. Rod density in a central annulus around the fovea is 130,000/mm2 and decreases 6-8-fold toward the periphery. In all 9 retinae, we found that an area 4-5 mm dorsal to the fovea had the highest rod density at 184,000 rods/mm2. The functional significance of this area, which we term the dorsal rod peak (DRP), may be related to high sensitivity vision under scotopic conditions. Outside of the DRP, rod density is symmetrical around the major axes of the retina, whereas cone density is elevated in nasal retina. Among animals, both rods and cones display a 2-fold individual difference in receptor density at any given eccentricity. Although rods and cones differ in absolute number, the location and magnitude of their peak densities, and their central to peripheral density gradients, the ratio of the density of rods to cones (15-30:1) is remarkably stable from 3 mm to 15 mm eccentricity. The relative consistency in the proportion of rods and cones in extrafoveal retina may be related to mechanisms of retinal development and functional interactions between scotopic and photopic systems.

Animals↗
PubMed1994

Restricted expression of a new paired-class homeobox gene in normal and regenerating adult goldfish retina.

We describe the cloning and expression pattern of a new paired-class homeobox gene, Vsx-1, in the continuously growing retina of the goldfish. Vsx-1 belongs to a subset of paired-class homeobox genes that lack a second DNA binding domain, the paired-domain, and is closely related to the C. elegans ceh-10 gene. In the adult goldfish, Vsx-1 expression is restricted to the neural retina. In the central, mature retina, Vsx-1 mRNA is synthesized in a subset of differentiated cells in the inner nuclear layer in a pattern suggestive of bipolar cells. In immature retina, adjacent to the retinal margin, Vsx-1 is expressed in a relatively broader subset of newly postmitotic cells but is downregulated in some of these cells to form the mature expression pattern. Following retinal injury, during the early phase of regeneration, Vsx-1 mRNA synthesis appears to be upregulated in cells in the inner nuclear layer and is expressed de novo in cells outside this layer. By virtue of its identity as a transcriptional regulatory gene and its patterns of expression, we speculate that Vsx-1 may stabilize the differentiated state of a subset of cells in the inner nuclear layer and may be involved in cellular differentiation during retinal development and regeneration.

Amino Acid Sequence↗