Control ofDrosophilaRetinoid and Fatty Acid Binding Glycoprotein Expression by Retinoids and Retinoic Acid: Northern, Western and Immunocytochemical Analyses
“…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.…”
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,
“…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.…”
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,
“…By converting the mutation at position 838 in the ninaB P315 cDNA, the enzymatic activity of the encoded protein could be restored. Besides its role as the visual chromophore, vitamin A influences on opsin gene transcription, translation, and the maturation of the visual pigments have been reported (30)(31)(32) but are controversial. By using the ninaB mutants, which have a genetically caused vitamin A deficiency, we addressed this question and investigated the impact of this mutation on the regulation of the mRNA levels of the major opsin gene (ninaE) by semiquantitative RT-PCR.…”
Section: A Single Lys-to-glu Substitution In the Ninab P315 Allele Anmentioning
Visual pigments (rhodopsins) are composed of a chromophore (vitamin A derivative) bound to a protein moiety embedded in the retinal membranes. Animals cannot synthesize the visual chromophore de novo but rely on the uptake of carotenoids, from which vitamin A is formed enzymatically by oxidative cleavage. Despite its importance, the enzyme catalyzing the key step in vitamin A formation resisted molecular analyses until recently, when the successful cloning of a cDNA encoding an enzyme with ,-carotene-15,15-dioxygenase activity from Drosophila was reported. To prove its identity with the key enzyme for vitamin A formation in vivo, we analyzed the blind Drosophila mutant ninaB. In two independent ninaB alleles, we found mutations in the gene encoding the ,-carotene-15,15-dioxygenase. These mutations lead to a defect in vitamin A formation and are responsible for blindness of these flies.
“…The relatively slow onset of activation of TRP and TRPL might re¯ect an indirect action of PUFAs; however, other possible explanations are that access to the microvillar membrane might be restricted, or that PUFA concentrations could be controlled by endogenous inactivation mechanisms or buffered by a fatty-acidbinding glycoprotein found in the intra-ommatidial matrix 19 . We therefore also made recordings from TRPL channels heterologously expressed in Drosophila S2 cells; channel identity was con®rmed by the characteristic biophysical properties of the expressed channels (Table 1) which seem to be indistinguishable from the properties of native TRPL channels 20 , and by the absence of any such channels in untransfected cells.…”
Phototransduction in invertebrate microvillar photoreceptors is thought to be mediated by the activation of phospholipase C (PLC), but how this leads to gating of the light-sensitive channels is unknown. Most attention has focused on inositol-1,4,5-trisphosphate, a second messenger produced by PLC from phosphatidylinositol-4,5-bisphosphate; however, PLC also generates diacylglycerol, a potential precursor for several polyunsaturated fatty acids, such as arachidonic acid and linolenic acid. Here we show that both of these fatty acids reversibly activate native light-sensitive channels (transient receptor potential (TRP) and TRP-like (TRPL)) in Drosophila photoreceptors as well as recombinant TRPL channels expressed in Drosophila S2 cells. Recombinant channels are activated rapidly in both whole-cell recordings and inside-out patches, with a half-maximal effector concentration for linolenic acid of approximately 10 microM. Four different lipoxygenase inhibitors, which might be expected to lead to build-up of endogenous fatty acids, also activate native TRP and TRPL channels in intact photoreceptors. As arachidonic acid may not be found in Drosophila, we suggest that another polyunsaturated fatty acid, such as linolenic acid, may be a messenger of excitation in Drosophila photoreceptors.
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