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PubMed1992

Induction of experimental autoimmune uveoretinitis in Lewis rats with purified recombinant human retinal S-antigen fusion protein.

Full-length human retinal cDNA for S antigen (S-ag) and for the alpha subunit of transducin (alpha-Td) were subcloned into a bacterial expression plasmid vector to generate recombinant fusion proteins with glutathione-S-transferase (GST). The recombinant GST-S-ag and rGST-alpha-Td fusion proteins were purified from bacterial extracts by continuous flow preparative gel electrophoresis under denaturing conditions, and were assessed for their ability to induce experimental autoimmune uveoretinitis (EAU). Immunization of Lewis rats with single doses of 10 micrograms-100 micrograms rGST-S-ag in Freund's complete adjuvant supplemented with Bordetella pertussis readily induced clinical signs of EAU. Immunization with GST alone did not induce EAU indicating that disease activity was ascribable to the S-ag residues in the fusion protein. Although the alpha-Td shares limited sequence homology with S-ag, the rGST-alpha-Td fusion protein was also not uveitogenic in Lewis rats. The clinical severity of EAU in Lewis rats sensitized with rGST-S-ag was found to be milder than that induced with native S-ag preparations purified from human retina. However, humoral antibody responses to sensitization with the recombinant S-ag fusion protein were of a higher magnitude than with native S-ag. The availability of recombinant preparations of human S-ag protein will be of value in studying its processing and presentation to T cells derived from patients with autoimmune retinal vasculitis.

Animals↗
PubMed2005

Cone cGMP-gated channel mutations and clinical findings in patients with achromatopsia, macular degeneration, and other hereditary cone diseases.

Unrelated patients with achromatopsia, macular degeneration with onset under age 50 years, cone degeneration or dysfunction, cone-rod degeneration, or macular malfunction were screened for mutations in the three genes known to be associated with achromatopsia: the GNAT2 gene encoding the alpha subunit of cone transducin and the CNGA3 and CNGB3 genes encoding the alpha and beta subunits of the cone cGMP-gated cation channel. We found no examples of patients with GNAT2 mutations. Out of 36 achromats, 12 (33%) had mutations in CNGA3 (13 different mutations including five novel mutations) and 12 (33%) had mutations in CNGB3 (six different mutations including four novel mutations). All achromats with CNG mutations had residual, presumably cone function as determined by computer-averaged 30-Hz electroretinograms (ERGs). There was considerable variability in acuity and color vision, with most patients having acuities of 20/200-20/400 and complete absence of color perception, and others having acuities of 20/25-20/40 and some color vision. Two pseudodominant achromatopsia cases were uncovered, both with CNGA3 mutations, including one family in which some compound heterozygotes with achromatopsia mutations were clinically unaffected. We found two novel CNGB3 changes in three patients with juvenile macular degeneration, a phenotype not previously associated with mutations in the cone channel subunits. These patients had subnormal acuity (20/30-20/60), normal to subnormal color vision, and normal to subnormal full-field cone ERG amplitudes. Our results indicate that some patients with channel protein mutations retain residual foveal cone function. Based on our findings, CNGB3 should be considered as a candidate gene to be evaluated in patients with forms of cone dysfunction, including macular degeneration.

Adult↗
PubMed2006

Acute myelogenous leukemia-derived SMAD4 mutations target the protein to ubiquitin-proteasome degradation.

Disruption of transforming growth factor-beta (TGFB1/TGF-beta) signaling contributes to the formation of human hematological malignancies. Smad4, a tumor suppressor, functions as an essential intracellular signal transducer of the TGF-beta signaling pathway. Recent studies have demonstrated that some tumor-derived mutations of Smad4 are associated with protein instability; however, the precise mechanism by which mutated Smad4 proteins undergo rapid degradation remains to be elucidated. A missense mutation of the SMAD4 gene in the Mad homology 1 (MH1) domain (c.305C>T, Pro102Leu) and one frameshift mutation resulting in termination in the Mad homology 2 (MH2) domain (c.1447_1448insAATA, Delta483-552) have been identified in acute myelogenous leukemia. It is not known whether protein instability of these SMAD4 mutants is one of the contributors to TGF-beta signaling disruption in acute myelogenous leukemia. Here we report that these two acute myelogenous leukemia-derived SMAD4 mutants are degraded rapidly when compared to their wild-type counterpart. We have demonstrated that both mutated proteins exhibit enhanced polyubiquitination (or polyubiquitylation) and proteasomal degradation. Importantly, we found that beta-transducin-repeat-containing protein 1 (beta-TrCP1), an F-box protein in the ubiquitin E3 ligase Skp1-Cullin-F-box protein (SCF) complex, directly interacts with and acts as a critical determinant for degradation of both mutated SMAD4 proteins. In addition, small interference RNA (siRNA)-triggered endogenous beta-TrCP1 suppression increased the protein expression level of both overexpressed SMAD4 mutants and endogenous mutated SMAD4 protein in acute myelogenous leukemia cells. These data suggest that mutated SMAD4 proteins undergo rapid degradation in acute myelogenous leukemia cells via SCF(beta-TrCP1) E3 ligase-mediated protein ubiquitination (or ubiquitylation) and subsequent proteasomal degradation.

Animals↗
PubMed2002

Molecular genetic analysis of malignant melanomas for aberrations of the WNT signaling pathway genes CTNNB1, APC, ICAT and BTRC.

Aberrant activation of the Wnt signaling pathway has been reported in different human tumor types, including malignant melanomas. We investigated 37 malignant melanomas (15 primary tumors and 22 metastases) for alterations of 4 genes encoding members of this pathway, i.e., CTNNB1 (beta-catenin gene, 3p22.1), APC (adenomatous polyposis coli gene, 5q22.2), BTRC (beta-transducin repeat-containing protein gene, 10q24.3) and ICAT (inhibitor of beta-catenin and Tcf-4, 1p36.2). Mutational analysis of CTNNB1 identified somatic mutations in 1 primary melanoma and 1 melanoma metastasis from 2 different patients (5%). Both mutations affected the N-terminal degradation box of beta-catenin, which is important for the regulation of beta-catenin homeostasis. Another primary melanoma carried a somatic APC missense mutation within the known mutation cluster region in exon 15. Fourteen tumors (40%) showed LOH at microsatellite markers on 1p36. None of the tumors had lost both copies of the ICAT gene, but 1 melanoma metastasis carried a somatic point mutation altering the translation start codon of ICAT. Real-time RT-PCR showed markedly reduced ICAT transcript levels (<or=20% relative to normal skin and benign melanocytic nevi) in 28/36 malignant melanomas (78%), including 13/14 tumors with LOH on 1p36. Allelic loss on 10q was detected in 15 tumors (44%). We found neither mutations nor complete loss of expression of the BTRC gene in our melanoma series. Taken together, our results indicate that the Wnt pathway may be altered in malignant melanomas by different mechanisms, including rare somatic mutations in CTNNB1, APC or ICAT, as well as low or absent expression of ICAT transcripts.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Regulation of lung cancer cell growth and invasiveness by beta-TRCP.

Beta-transducin-repeat-containing protein (beta-TRCP) serves as a substrate-recognition subunit of Skp1/Cullin/F-box (SCF)(beta-TRCP) E3 ligases, involved in regulation of several important signaling molecules. SCF(beta-TRCP) E3 ligases play a critical role in cell mitosis as well as in various signaling pathways. Here, we provide evidence to support that beta-TRCP negatively regulates cell growth and motility of lung cancer cells. With specific antibodies, we detect loss of beta-TRCP1 protein in several lung cancer cell lines. One cell line contains an inactivated mutation of the beta-TRCP1 gene. Loss of beta-TRCP1 protein is also found in subsets of lung cancer specimens. We observe that retrovirus-mediated stable expression of beta-TRCP1 in beta-TRCP1 negative cells inhibits cell growth in soft-agar and tumor formation in nude mice. Furthermore, expression of beta-TRCP1 alters cell motility, as indicated by morphological changes and a reduced level of active matrix metalloproteinase (MMP)11. Conversely, inactivation of beta-TRCP1 by specific siRNA accelerates cell invasion. Of the 10 known substrates of SCF(beta-TRCP) E3 ligases, the protein level of cell division cycle 25 (CDC25)A is clearly affected in these lung cancer cells. Cells treated with CDC25A inhibitors become less invasive. Thus, loss of beta-TRCP1 may promote both growth and cell motility of lung cancer cells, possibly through regulation of CDC25A and the MMP11 level.

Humans↗
PubMed1993

A yeast antiviral protein, SKI8, shares a repeated amino acid sequence pattern with beta-subunits of G proteins and several other proteins.

SKI8 is a yeast antiviral gene, essential for controlling the propagation of M double-stranded RNA (dsRNA) and thus for preventing virus-induced cytopathology. Our DNA sequence of SKI8 shows that it encodes a 397 amino acid protein containing two copies of a 31 amino acid repeat pattern first identified in mammalian beta-transducin and Cdc4p of yeast. There are also four copies of this repeat in yeast Mak11p, necessary for M dsRNA propagation, and three copies in the putative product of the Dictyostelium AAC3 gene. Analysis of 36 cases of the repeat unit shows they have a consensus predicted structure: N-helix-sheet-turn-sheet-turn-sheet-helix-C.

Amino Acid Sequence↗
PubMed1995

A cell-cycle nuclear autoantigen containing WD-40 motifs expressed mainly in S and G2 phase cells.

Recently a novel nuclear protein mainly expressed in S and G2 phase cells was characterized using autoantibodies from a cancer patient (Exp. Cell Res., 212, 255-261, 1994). cDNA clones were isolated by immunoscreening, and sequence analysis revealed that the cDNA clones encoded a 713-amino acid residue polypeptide which is provisionally named SG2NA (S/G2 nuclear antigen). In the carboxyl terminal half of SG2NA, there are 6 copies of WD-40 motifs characteristic of a large family of proteins of which the prototype is beta-transducin/enhancer of split (TLE). In addition, there are nuclear localization sequence and phosphorylation sites related to the TLE proteins. Autoantibodies occurring spontaneously in certain cancer patients have been useful reagents for identifying cellular proteins and this is the first report of a novel WD-40 protein which is the target of an autoimmune response.

Adenocarcinoma↗
PubMed1995

Binding of pleckstrin homology domains to WD40/beta-transducin repeat containing segments of the protein product of the Lis-1 gene.

In previous experiments we demonstrated an interaction between certain pleckstrin homology (PH) domains and regions containing the so-called WD40 (or beta-transducin) repeats of the beta subunit of trimeric G-proteins (G beta), a finding we here extend to the PH domains of the src-related tyrosine kinase TecIIa and the GTPase dynamin. To examine the possibility that WD40 repeats in molecules other than G beta might also bind PH domains we examined PAFAH-45, the protein product of the Lis-1 gene, which contains 7 WD40 repeats. We found that 1) Purified PAFAH-45 binds PH domain constructs in vitro. 2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45 but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing hierarchy of affinities than that seen with G beta. 3). PAFAH-45 WD40 repeats will reduce the binding of PH domains to brain G beta and brain G beta gamma will reduce the binding of PH domains to PAFAH-45. These data support the hypothesis that PH domain/WD40 interactions are involved in a wide variety of important protein/protein interactions.

Animals↗
PubMed2001

Molecular evidence that human ocular ciliary epithelium expresses components involved in phototransduction.

Here we report the expression, in the human ocular ciliary epithelium and in a human nonpigmented (NPE) ciliary epithelial cell line, of genes usually restricted to cone and rod photoreceptor cells of the retina. By RT-PCR and DNA sequencing we identified the expression of rhodopsin and components linked to its deactivation, including rhodopsin kinase, recoverin, and visual arrestin. We also detected the expression of transducin (T-alpha), phosphodiesterase (PDE-alpha), and cGMP-gated channel alpha-subunits. Cultured NPE cells responded to treatment with phorbol ester by enhancing the expression of rhodopsin mRNA three- to fourfold. Indirect immunofluorescence of the intact ciliary epithelium with monoclonal antibodies (MAbs) against rhodopsin, rhodopsin kinase, and visual arrestin revealed labeling preferentially restricted to the NPE cells. Furthermore, Western blot analysis of whole lysates from the pars plicata region of the human ciliary epithelium with MAbs demonstrated immunochemical cross-reactivity with proteins of molecular mass similar to rhodopsin (36 kDa), rhodopsin kinase (64 to 66 kDa), and arrestin (48-52 kDa) from the human retina. These results provide the first molecular evidence that components of a non-visual phototransduction pathway are expressed in the human ocular NPE ciliary epithelium, which may be linked to circadian entrainment tasks.

Animals↗
PubMed1993

Synthesis and stability of retinal photoreceptor mRNAs are coordinately regulated during bovine fetal development.

Steady state photoreceptor specific mRNA levels in bovine retina were studied during fetal maturation for five gene transcripts, including rhodopsin, arrestin (S-antigen), rod alpha-subunit of transducin, interphotoreceptor retinoid-binding protein (IRBP) and rod alpha-subunit of cGMP phosphodiesterase in order to understand mechanisms of gene regulation during photoreceptor development. A 10-15-fold increase in each transcript level begins between 5.5 and 6 months of gestation for each gene, suggesting a single coordinate induction event at this time. Quantitative analysis of transcriptional rates for each gene by nuclear run-on also reveals a coordinate increase at approximately the same time, demonstrating that induction is achieved by transcriptional activation. Interestingly, however, gene specific transcription rates in the pre-induction retina do not appear to parallel mRNA steady state levels. During fetal development neither the transcript level of each gene relative to the others nor relative mRNA turnover rates change substantially after the induction event at 5.5-6.0 months. However, at earlier times all genes exhibit higher mRNA turnover, implying that differential mRNA stability may also play an important role in determining steady-state levels.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2002

Distribution and density of medium- and short-wavelength selective cones in the domestic pig retina.

The topography of medium (M)- and short (S)-wavelength sensitive cone photoreceptors was studied in the domestic pig retina. Antisera specific for M or S opsin as well as cone photoreceptor proteins arrestin and alpha-transducin were used to label cone types. Retinal wholemounts and their blood vessel patterns were drawn and specific regions removed. The wholemounts were immunocytochemically labelled to detect both M and S cones, and the specific regions labelled to detect S cones. Cones were counted in a 1 mm grid pattern, using the drawings as a guide. Pig retina has a high cone density retinal streak extending across the retina covering the optic disc (OD) and horizontal meridian. Densities in the streak are 20,000-35,000 mm(-2). Two higher peaks occur in the streak, one in temporal retina near the OD (39,000 mm(-2)) and the other in nasal retina 5-7 mm from the OD (40,500 mm(-2)). The lowest cone density is in far peripheral inferior retina (7000 mm(-2)). The total number of cones in pig retina is 17-20 million. Both types of cones are found throughout the retina, with S cone percentages ranging from 7.4 to 17.5% in no consistent topographical pattern. S cones have an irregular local distribution which can vary from a regular hexagonal pattern to small clusters of adjacent S cones to small areas lacking S cones. Double-label immunocytochemistry found that virtually all S cone outer segments (OS) contain some M opsin. M cone OS do not label at detectible levels for S opsin. Domestic pig retina is widely available, large, has a high cone density and has two types of cones. This tissue should be an excellent source for biochemical analysis of cone proteins, and for in vitro approaches to understanding cone survival factors.

Animals↗
PubMed1992

Genes expressed selectively in plasmacytomas: markers of differentiation and transformation.

We have analyzed a murine plasmacytoma minus highly differentiated B lymphoma subtractive cDNA library and identified eight genes that are expressed in most plasmacytomas but at a much lower level, or not at all, in most B lymphomas. Four of the genes are markers of the terminal differentiation of B lymphocytes into plasma cells: placental alkaline phosphatase, also expressed in pre-B lymphomas xlr-3, a new X-linked member of the xlr multi-gene family EGP314, a pan-epithelial glycoprotein with sequence features of an adhesion molecule PC315, a gene that is up-regulated by IL6, but without obvious sequence homologies. Two of the genes are not clearly related to normal B cell differentiation, appearing to be associated with malignant transformation of plasma cells: PC326 is a new member of the beta-transducin mosaic protein gene family. It is an X-linked gene, expressed at a very low level in testis, but in no other normal tissue, including LPS- or IL6-induced plasma cells. It has a high level of expression (apparently dysregulated) in most (> 85%) mineral oil induced plasmacytomas. However the likelihood that PC326 is expressed decreases as the tumor latency decreases when different retroviral agents are used to accelerate mineral oil induced plasmacytomagenesis. This suggests that PC326 expression may be a late event in a multi-step process of tumorigenesis. PC251 a new member of the hematopoietic growth factor receptor family, most homologous to IL5R alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1991

Molecular interactions between the photoreceptor G protein and rhodopsin.

1. The visual transduction system of the vertebrate retina is a well-studied model for biochemical and molecular studies of signal transduction. The structure and function of rhodopsin, a prototypical G protein-coupled receptor, and transducin or Gt, the photoreceptor G protein, have been particularly well studied. Mechanisms of rhodopsin-Gt interaction are discussed in this review. 2. The visual pigment rhodopsin contains a chromophore, and thus conformational changes leading to activation can be monitored spectroscopically. A model of the conformational changes in the activated receptor is presented based on biophysical and biochemical data. 3. The current information on sites of interaction on receptors and cognate G proteins is summarized. Studies using synthetic peptides from amino acid sequences corresponding to Gt and rhodopsin have provided information on the sites of rhodopsin-Gt interaction. Synthetic peptides from the carboxyl terminal region of alpha t mimic Gt by stabilizing the active conformation of rhodopsin, Metarhodopsin II. 4. The conformation of one such peptide when it is bound to Metarhodopsin II was determined by 2D NMR. The model based on the NMR data was tested using peptide analogs predicted to stabilize or break the structure. These studies yield molecular insight into why toxin-treated and mutant G proteins are uncoupled from receptors.

Amino Acid Sequence↗
PubMed1998

Probing functional interfaces of rod PDE gamma-subunit using scanning fluorescent labeling.

In the dark, the activity of the rod cGMP phosphodiesterase (PDE) catalytic alpha- and beta-subunits (P alpha beta) is inhibited by two gamma-subunits (P gamma). On light stimulation of the photoreceptor cells, the GTP-bound alpha-subunit of visual G-protein transducin (GtaGTP) displaces the P gamma-subunits from their inhibitory sites on P alpha beta, leading to the effect or enzyme activation. We designed a number of P gamma mutants, each with a single cysteine residue evenly distributed at a different position along the P gamma polypeptide chain. These cysteine residues served as sites for the introduction of the environmentally sensitive fluorescent probe, 3-(bromoacetyl)-7-diethyl aminocoumarin (BC). Analysis of the interactions of P alpha beta and Gta with the fluorescently labeled P gamma mutants suggests two distinct functional interfaces of P gamma. The P alpha beta/P gamma interface is formed essentially by the C-terminus of P gamma and by the N-terminal portion of the P gamma polycationic region, P gamma-24-45, whereas the P gamma/Gta interface includes the C-terminal portion of P gamma-24-45 and the region surrounding P gamma Cys68. Such functional organization of P gamma may represent an important element for the PDE activation mechanism during transduction of visual signals.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1997

Morphine and muscle relaxants are receptor-independent G-protein activators and cromolyn is an inhibitor of stimulated G-protein activity.

Morphine and muscle relaxants are classical mast cell activators and cromolyn is a mast cell inhibitor. However, the mechanisms underlying the effects of these drugs are obscure. We asked the question whether morphine and muscle relaxants may activate heterotrimeric guanine nucleotide-binding proteins (G-proteins), and whether cromolyn may prevent this activation. Morphine activated Gi-proteins in HL-60 membranes and purified transducin (TD) at concentrations above 1 mM, but the effects on morphine did not reach saturation up to 10 mM. d-Tubocurarine activated Gi-proteins and TD in a saturable manner, with EC50 values of 0.3 mM and 4.2 mM, respectively. Gallamine and succinylcholine were less effective activators of TD than d-tubocurarine, Morphine and d-tubocurarine were about similarly effective activators of Gi-proteins, whereas d-tubocurarine was a more effective activator of TD than morphine. Cromolyn at 10 microM and 100 microM had little effect on TD activity but reduced the stimulatory effect of morphine by 50% and 80%, respectively. Our data suggest the following: (1) Receptor-independent G-protein activation by morphine and muscle relaxants presumably accounts for their mast cell-activating properties. (2) Cromolyn may act by preventing G-protein activation. (3) The variability in responsiveness of mast cells towards morphine and muscle relaxants could be due to differential expression of G-proteins with different sensitivity to activation by these drugs.

Animals↗
PubMed2003

Absence of detectable alterations in the putative tumor suppressor gene BTRC in cerebellar medulloblastomas and cutaneous basal cell carcinomas.

The sonic hedgehog signal transduction pathway is aberrantly activated in the majority of cutaneous basal cell carcinomas and a subset of cerebellar medulloblastomas. The latter tumors may also show activation of the wingless (Wnt) signaling pathway. In Drosophila, the F-box/WD40-repeat containing protein Slimb has been shown to function as an intracellular negative regulator of both pathways. The BTRC gene (beta-transducin repeat-containing protein) is a human homolog of Slimb that is located at 10q24.3, a chromosome region frequently deleted in medulloblastomas. Here, we report on the mutational analysis of BTRC in 91 human tumors, including 66 primitive neuroectodermal tumors (PNETs) of the central nervous system (62 medulloblastomas and 4 supratentorial PNETs) and 25 cutaneous basal cell carcinomas (BCCs). These analyses revealed no tumor-associated BTRC mutations. BTRC transcripts were expressed in non-neoplastic brain tissue, normal skin, as well as in all PNETs and BCCs analyzed by real-time reverse transcription-PCR. Two novel BTRC transcript variants were expressed at higher levels in non-neoplastic brain tissue than in normal skin and the investigated tumors. Taken together, our results indicate that PNETs and BCCs neither show mutations nor loss of mRNA expression of BTRC. Therefore, BTRC alteration does not appear to be involved in the pathogenesis of these neoplasms.

Base Sequence↗
PubMed1998

Complete physical map of the common deletion region in Williams syndrome and identification and characterization of three novel genes.

Williams syndrome (WS) is a contiguous gene deletion disorder caused by haploinsufficiency of genes at 7q11.23. We have shown that hemizygosity of elastin is responsible for one feature of WS, supravalvular aortic stenosis (SVAS). We have also implicated LIM-kinase 1 hemizygosity as a contributing factor to impaired visual-spatial constructive cognition in WS. However, the common WS deletion region has not been completely characterized, and genes for additional features of WS, including mental retardation, infantile hypercalcemia, and unique personality profile, are yet to be discovered. Here, we present a physical map encompassing 1.5 Mb DNA that is commonly deleted in individuals with WS. Fluorescence in situ hybridization analysis of 200 WS individuals shows that WS individuals have the consistent deletion interval. In addition, we identify three novel genes from the common deletion region: WS-betaTRP, WS-bHLH, and BCL7B. WS-betaTRP has four putative beta-transducin (WD40) repeats, and WS-bHLH is a novel basic helix-loop-helix leucine zipper (bHLHZip) gene. BCL7B belongs to a novel family of highly conserved genes. We describe the expression profile and genomic structure for each of these genes. Hemizygous deletion of one or more of these genes may contribute to developmental defects in WS.

Amino Acid Sequence↗
PubMed2000

Colocalization of pinopsin with two types of G-protein alpha-subunits in the chicken pineal gland.

Pinopsin is a photoreceptive molecule present in the outer segments of chicken pinealocytes. In this paper, the localization of alpha-subunits of G-proteins, rod transducin (Gt1) and Gq/11, was examined by immunoelectron microscopy to investigate whether these G-proteins colocalize with pinopsin in the outer segments. Ultrathin sections of the chicken pineal gland were double-immunolabeled with antibodies to pinopsin and either Gt1alpha or Gq/11alpha. As shown previously, the outer segments around the follicular lumen exhibited divergent morphology with ciliary, bulbous, or lamellate shapes, and most of them displayed pinopsin immunoreactivity. The majority (>90%) of pinopsin-immunopositive outer segments were labeled by anti-Gt1alpha and/or anti-Gq/11alpha antibodies. Application of double-immunolabeling to serial sections demonstrated that a large number of the pinopsin-immunopositive outer segments contained both Gt1alpha and Gq/11alpha immunoreactivities. These results suggest that Gt1alpha and Gq/11alpha are functionally coupled with light-activated pinopsin within a single outer segment.

Animals↗