Control ofDrosophilaOpsin Gene Expression by Carotenoids and Retinoic Acid: Northern and Western Analyses

Picking, Wendy L.; Chen, De‐Mao; Lee, Ronnie D.; Vogt, Matthew E.; Polizzi, Joseph L.; Marietta, Robert G.; Stark, William S.

doi:10.1006/exer.1996.0139

Cited by 24 publications

(24 citation statements)

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“…Although there are now some data on devel- opmental roles of RA signaling emerging from invertebrate chordates, there is still an obvious lack of information on the role(s) of RA in non-chordates. Even if low concentrations of 9-cis and all-trans RA have been observed in regenerating limb blastemas of the crab Uca pugilator (Hopkins, 2001) and effects of treatments with RA agonists or antagonists have been described in sea urchins (Sciarrino and Matranga, 1995;Kuno et al, 1999), mollusks (Créton et al, 1993) crustaceans (Chung et al, 1998;Hopkins, 2001;Söderhäll et al, 2006), insects (Picking et al, 1996;Shim et al, 1997;Sun et al, 1993), planarians (Romero and Bueno, 2001), cnidarians (Müller, 1984), and sponges (Imsiecke et al, 1994;Nikko et al, 2001;Wiens et al, 2003), the actual presence and putative roles of RA signaling during development in these taxa remain elusive. Thus, to fully understand the origin and evolution of RA signaling during embryonic development, we need to broaden the sampling of animal taxa and apply more sophisticated experimental tools to non-vertebrate model systems.…”

Section: Discussionmentioning

confidence: 99%

Retinoic acid signaling in development: Tissue‐specific functions and evolutionary origins

Campo-Paysaa

Marlétaz

Laudet

et al. 2008

Genesis

118

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Summary: Retinoic acid (RA) is a vitamin A-derived morphogen important for axial patterning and organ formation in developing vertebrates and invertebrate chordates (tunicates and cephalochordates). Recent analyses of genomic data have revealed that the molecular components of the RA signaling cascade are also present in other invertebrate groups, such as hemichordates and sea urchins. In this review, we reassess the evolutionary origins of the RA signaling pathway by examining the presence of key factors of this signaling cascade in different metazoan genomes and by comparing tissue-specific roles for RA during development of different animals. This discussion of genomic and developmental data suggests that RA signaling might have originated earlier in metazoan evolution than previously thought. On the basis of this hypothesis, we conclude by proposing a scenario for the evolution of RA functions during development, which highlights functional gains and lineage-specific losses during metazoan diversification. genesis 46:640-656,

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Section: Discussionmentioning

confidence: 99%

Retinoic acid signaling in development: Tissue‐specific functions and evolutionary origins

Campo-Paysaa

Marlétaz

Laudet

et al. 2008

Genesis

118

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“…) medium (Fig. 8 A, B) (Picking et al, 1996;Orem and Dolph, 2002b), and the Psd knockdown flies grown in retinoid-free medium showed neither intracellular accumulation of Rh1, nor retinal degeneration under light-exposed conditions, whereas flies cultured in normal medium showed severe retinal degeneration (Fig. 8 A).…”

Section: Kg07569mentioning

confidence: 96%

Autophagy-Dependent Rhodopsin Degradation Prevents Retinal Degeneration inDrosophila

Midorikawa

Yamamoto-Hino²,

Awano³

et al. 2010

J. Neurosci.

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Recent studies have demonstrated protective roles for autophagy in various neurodegenerative disorders, including the polyglutamine diseases; however, the role of autophagy in retinal degeneration has remained unclear. Accumulation of activated rhodopsin in some Drosophila mutants leads to retinal degeneration, and although it is known that activated rhodopsin is degraded in endosomal pathways in normal photoreceptor cells, the contribution of autophagy to rhodopsin regulation has remained elusive. This study reveals that activated rhodopsin is degraded by autophagy in collaboration with endosomal pathways to prevent retinal degeneration. Lightdependent retinal degeneration in the Drosophila visual system is caused by the knockdown or mutation of autophagy-essential components, such as autophagy-related protein 7 and 8 (atg-7/atg-8), or genes essential for PE (phosphatidylethanolamine) biogenesis and autophagosome formation, including Phosphatidylserine decarboxylase (Psd) and CDP-ethanolamine:diacylglycerol ethanolaminephosphotransferase (Ept). The knockdown of atg-7/8 or Psd/Ept produced an increase in the amount of rhodopsin localized to Rab7-positive late endosomes. This rhodopsin accumulation, followed by retinal degeneration, was suppressed by overexpression of Rab7, which accelerated the endosomal degradation pathway. These results indicate a degree of cross talk between the autophagic and endosomal/lysosomal pathways. Importantly, a reduction in rhodopsin levels rescued Psd knockdown-induced retinal degeneration. Additionally, the Psd knockdown-induced retinal degeneration phenotype was enhanced by Ppt1 inactivation, which causes infantile neuronal ceroid lipofuscinosis, implying that autophagy plays a significant role in its pathogenesis. Collectively, the current data reveal that autophagy suppresses light-dependent retinal degeneration in collaboration with the endosomal degradation pathway and that rhodopsin is a key substrate for autophagic degradation in this context.

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“…Retinoic acid does not serve as a chromophore precursor for rhodopsin synthesis but does activate opsin gene transcription (Picking et al, 1996 ;Sun et al, 1993). Several immunocytochemistry experiments utilized retinoid replacement for deprived flies with carrot juice, retinoic acid or β-carotene (Chen and Stark, 1992 ;Sun et al, 1993) ; carrot juice is especially useful for the rapid sensitivity recovery it elicits (Chen and Stark, 1992).…”

Section: Animals and Retinoid Manipulationsmentioning

confidence: 99%

“…Retinoid deprivation was achieved by rearing flies from egg to adult on Sang's medium without any retinoids (Stark, 1977). To determine the effects of various potential transcription activators (Picking et al, 1996), flies were reared from egg to adult on Sang's medium containing all-trans retinoic acid (Sigma, St. Louis, U.S.A.) at 0n125 mg ml −" . Beef Brain-Heart Infusion (Difco, Chicago, IL, U.S.A.) at 37 mg ml −" or β-carotene at 0n25 mg ml −" .…”

Section: Animals and Retinoid Manipulationsmentioning

confidence: 99%

“…† Present address : Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, U.S.A. (Picking et al, 1996 ;Schwemer and Spengler, 1992) suggested that retinoids control opsin gene transcription. Replacement or rearing with alternate retinoids or factors including retinoid acid results in the transcription of opsin's mRNA.…”

Section: Introductionmentioning

confidence: 98%

See 1 more Smart Citation

Control ofDrosophilaRetinoid and Fatty Acid Binding Glycoprotein Expression by Retinoids and Retinoic Acid: Northern, Western and Immunocytochemical Analyses

Shim

Picking

Kutty

et al. 1997

Experimental Eye Research

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Control ofDrosophilaOpsin Gene Expression by Carotenoids and Retinoic Acid: Northern and Western Analyses

Cited by 24 publications

References 0 publications

Retinoic acid signaling in development: Tissue‐specific functions and evolutionary origins

Retinoic acid signaling in development: Tissue‐specific functions and evolutionary origins

Autophagy-Dependent Rhodopsin Degradation Prevents Retinal Degeneration inDrosophila

Control ofDrosophilaRetinoid and Fatty Acid Binding Glycoprotein Expression by Retinoids and Retinoic Acid: Northern, Western and Immunocytochemical Analyses

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