Photoreceptor Outer Segment Development in Xenopus laevis: Influence of the Pigment Epithelium

Stiemke, Monica M.; Landers, Robert A.; Al‐Ubaidi, Muayyad R.; Rayborn, Mary E.; Hollyfield, Joe G.

doi:10.1006/dbio.1994.1076

Cited by 68 publications

(43 citation statements)

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“…Using a dual approach of embryo transfections and transgenesis, in vivo functional characterization of a rod-specific promoter has been performed in photoreceptors. This environment is permissive for photoreceptor cellspecific transcription, even though during transfection partial disruption of cell contacts prevents normal rod outer segment formation (34). The transfected heads are harvested at the onset of rhodopsin expression and photoreceptors express endogenous rhodopsin to levels similar to untreated heads at the same stage.…”

Section: Discussionmentioning

confidence: 99%

Xenopus Rhodopsin Promoter

Mani¹,

Batni²,

Whitaker³

et al. 2001

Journal of Biological Chemistry

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To understand the mechanisms that control the cellspecific visual pigment gene transcription, the Xenopus rhodopsin 5 regulatory region has been characterized in vivo using transient transfection of Xenopus embryos and transgenesis. The principal control sequences were located within ؊233/؉41, a region with significant conservation with mammalian rhodopsin genes. DNase footprinting indicated seven distinct regions that contain potential cis-acting elements. Sequences near the initiation site (؊45/؉41, basal region) were essential, but not sufficient, for rod-specific transcription. Two negative regulatory regions were found, one between ؊233 to ؊202, with no apparent similarity to known elements, and a second Ret-1-like CAAT (؊136/؊122) motif. Deletion of either sequence led to a 2-3-fold increase in expression levels, without a change in rod specificity. Sequences between ؊170 to ؊146, which contain an E-box motif, were necessary for high level expression in transgenic tadpoles but not in transient transfections. Sequences between ؊84 and ؊58, which contained an NRE-like consensus were found to be necessary for high level expression in both assays. Although expression levels were modulated by various proximal sequences in the rhodopsin promoter, none of the tested sequences were found to be necessary for rod specificity. Promoter constructs with a consensus BAT-1 sequence in conjunction with an NRE-like element upstream of the basal promoter directed low level green fluorescent protein expression in the central nervous system in transgenic tadpoles. These results suggest that rod cell-specific expression of rhodopsin is controlled by redundant elements in the proximal promoter.Phototransduction occurs in the photoreceptor layer of the vertebrate retina, which is composed of distinct cell types: rods and cones (1). These cells express a number of specific proteins that regulate the light-dependent currents mediating vision (2, 3). Among these cell-specific proteins are the visual pigments, which combine with 11-cis-retinal to form the light-sensitive component of the transduction cascade. The visual pigments are a large family of genes, which contain rod-specific rhodopsins and at least four classes of cone-specific opsins (4). Rhodopsin, required for nocturnal vision, is the most abundant opsin in many vertebrate retinae by virtue of the size of the rod outer segments, abundance of the rod cells, and the high level of transcription. As such, the regulation of rhodopsin expression has been a focus for understanding mechanisms of cellspecific gene expression in the retina (5).Transcription initiation has been identified as the major control point for rhodopsin gene expression (6, 7). A variety of studies using different approaches have demonstrated that important transcriptional control sequences lie within the 5Ј upstream regions of various rhodopsin genes. Functional assays using transgenic mice have shown that 2-4 kb 1 of upstream sequences from the mouse and bovine rhodopsin genes direct reporter gene express...

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Section: Discussionmentioning

confidence: 99%

Xenopus Rhodopsin Promoter

Mani¹,

Batni²,

Whitaker³

et al. 2001

Journal of Biological Chemistry

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“…Morphological observations of the initial elaboration of the outer segment and disc membranes from the tip of the connecting cilium have suggested that this initiation process is dependent on motive and fusion forces generated by the photoreceptor itself rather than the RPE (Obata and Usukura, 1992). When retinal explants are grown without RPE, short disorganized outer segments were observed budding off the connecting cilium, but not elongated stacked outer segments (Holly®eld and Witkovsky, 1974;Akagawa et al, 1987;Sparrow et al, 1990;Stiemke et al, 1994;Watanabe et al, 1997). Grown in isolation without the RPE, cone photoreceptors also form rudimentary outer segments (Saga et al, 1996) which argues that the RPE is not a critical component of outer segment initiation.…”

Section: Discussionmentioning

confidence: 99%

“…In amphibian, chick, and mammalian retinal explants cultured without the RPE, outer segment formation appears stalled at the initiation phase. Expansions of disorganized disc like pro®les were formed at the tip of the connecting cilia, but organized elongated stacked disc membranes were not observed (Holly®eld and Witkovsky, 1974;Akagawa, Hicks and Barnstable, 1987;Sparrow, Hicks and Barnstable, 1990;Stiemke et al, 1994;Saga, Scheurer and Adler, 1996;Watanabe et al, 1997).…”

Section: Introductionmentioning

confidence: 97%

Defects in the MITFmi / miApical Surface are Associated with a Failure of Outer Segment Elongation

Bumsted

Rizzolo

Barnstable

2001

Experimental Eye Research

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“…Retinal pigment epithelium disruption was found with altered retinal cell growth and differentiation (Lu et al 1998, Stiemke et al 1994) especially through secreting factors that promote both endothelial and photoreceptor survival and differentiation (Adamis et al 1993, Behling et al 2002, King & Suzuma 2000, Sheedlo et al 1998. Thickened Bruch's membrane was influenced in disturbing nutrient transport and subsequent pigmented cells distortion especially the apical microvilli which in turn caused vacuolation and degeneration of stacked membranes of the growing outer segments of photoreceptors.…”

Section: Fris and Midelfartmentioning

confidence: 99%

Effects of maternal phenylketonuria on the development of the offspring's eye

et al. 2009

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Phenylketonuria (PKU) is an autosomal recessive disease caused by phenylalanine‐4‐hydroxylase (P‐4‐H) deficiency, which is a liver‐specific enzyme that catalyzes the hydroxylation of l‐phenylalanine (Phe) to l‐tyrosine (Tyr). The deficiency of this enzyme leads to the accumulation of Phe in the tissues and plasma of patients. Among the clinical symptoms of this disease are mental retardation and other neurological features. The mechanisms of retinal cell damage are still poorly understood. In order to evaluate the damage in offspring of PKU mothers, fifty pregnant rats were used and arranged into two main groups, i.e., a control group and a group consisting of rats with experimentally induced PKU. Induction of PKU was carried out by daily intragastrical administration of 30 mg DL–alpha methylphenylalanine/150 g b.w. plus 60 mg/kg b.w. Phe at 12 h intervals throughout pregnancy till parturition as well as throughout lactation period till 14 days post‐partum. Morphometric analysis of retina in 1, 7 and 14‐day‐old pups of PKU mothers revealed a marked reduction of retinal thickness. Histological observations revealed numerical reduction of pigment cells. Apoptic cell death of retinal pigment cells, and of nuclear layer and ganglionic cells were observed. The nerve layer showed apparent vacuolar degeneration. At transmission electron microscope (TEM) level, pigment epithelium showed distortion of apical microvilli, vacuolation of cytoplasm and reduction of cytoplasm organelles. The Brush's membrane showed apparent thickening. In 7‐day‐old pups of PKU mothers, photoreceptor inner segment showed apparent degeneration. In 14‐day‐old pups of PKU mothers, both the inner and outer photoreceptor segment were degenerated and the stacked membrane of the outer segment appeared vacuolated and degenerated.

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Photoreceptor Outer Segment Development in Xenopus laevis: Influence of the Pigment Epithelium

Cited by 68 publications

References 0 publications

Xenopus Rhodopsin Promoter

Xenopus Rhodopsin Promoter

Defects in the MITFmi / miApical Surface are Associated with a Failure of Outer Segment Elongation

Effects of maternal phenylketonuria on the development of the offspring's eye

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