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Results for “Light Signal Transduction”

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PubMed2004

Control of photosynthetic and high-light-responsive genes by the histidine kinase DspA: negative and positive regulation and interactions between signal transduction pathways.

We have deleted a gene for a sensor histidine kinase, dspA (or hik33), in the cyanobacterium Synechocystis sp. strain PCC6803. In low and moderate light, the mutant grew slowly under photoautotrophic conditions, with a doubling time of approximately 40 h, and had severely reduced photosynthetic oxygen evolution. When the mutant was maintained in low or moderate light in the presence of glucose, its growth rate was only somewhat lower than that of wild-type cells. However, the mutant was light sensitive and rapidly died in high light. Furthermore, levels of many transcripts encoding genes associated with photosynthesis were altered in the mutant relative to wild-type Synechocystis sp. strain PCC6803 both in low light and following exposure to high light. There was constitutive expression of several high-light-inducible genes, including hli, psbAIII, and gpx2; there was little increased accumulation of sodB mRNA in high light; and the cells failed to accumulate cpcBA and psaAB mRNAs in low light in the presence of glucose, although a normal decline in the levels of these mRNAs was observed during exposure to high light. These results suggest that DspA is involved in controlling sets of photosynthetic and high-light-responsive genes, either directly or indirectly. These and other results, some of which are presented in a companion paper (C.-J. Tu, J. Shrager, R. Burnap, B. L. Postier, and A. R. Grossman, J. Bacteriol. 186:3889-3902, 2004), suggest that DspA acts as a global regulator that helps coordinate cellular metabolism with growth limitations imposed by environmental conditions.

Bacterial Proteins↗
PubMed2004

Mitochondrial signal transduction in accelerated wound and retinal healing by near-infrared light therapy.

Photobiomodulation by light in the red to near infrared range (630-1000 nm) using low energy lasers or light-emitting diode (LED) arrays has been shown to accelerate wound healing, improve recovery from ischemic injury in the heart and attenuate degeneration in the injured optic nerve. Recent evidence indicates that the therapeutic effects of red to near infrared light result, in part, from intracellular signaling mechanisms triggered by the interaction of NIR light with the mitochondrial photoacceptor molecule cytochrome c oxidase. We have demonstrated that NIR-LED photo-irradiation increases the production of cytochrome oxidase in cultured primary neurons and reverses the reduction of cytochrome oxidase activity produced by metabolic inhibitors. We have also shown that NIR-LED treatment prevents the development of oral mucositis in pediatric bone marrow transplant patients. Photobiomodulation improves wound healing in genetically diabetic mice by upregulating genes important in the promotion of wound healing. More recent studies have provided evidence for the therapeutic benefit of NIR-LED treatment in the survival and functional recovery of the retina and optic nerve in vivo after acute injury by the mitochondrial toxin, formic acid generated in the course of methanol intoxication. Gene discovery studies conducted using microarray technology documented a significant upregulation of gene expression in pathways involved in mitochondrial energy production and antioxidant cellular protection. These findings provide a link between the actions of red to near infrared light on mitochondrial oxidative metabolism in vitro and cell injury in vivo. Based on these findings and the strong evidence that mitochondrial dysfunction is involved in the pathogenesis of numerous diseases processes, we propose that NIR-LED photobiomodulation represents an innovative and non-invasive therapeutic approach for the treatment of tissue injury and disease processes in which mitochondrial dysfunction is postulated to play a role including diabetic retinopathy, age-related macular degeneration, Leber's hereditary optic neuropathy and Parkinson's disease.

Journal Article↗
PubMed1989

Biosynthesis of the two halobacterial light sensors P480 and sensory rhodopsin and variation in gain of their signal transduction chains.

The two retinal-containing photoreceptors of halobacteria, P480 and sensory rhodopsin, are formed constitutively and inducibly, respectively. Both photoreceptors are synthesized as apoproteins in cells with nicotine-inhibited retinal synthesis and are reconstituted as chromoproteins by the addition of all-trans retinal to cell membrane preparations. The decrease in photoreceptor-mediated photophobic response at the stationary growth phase of cells is not due to photoreceptor degradation but due to a deficiency of the signal transduction chain in the cell.

Bacterial Proteins↗
PubMed2002

Phytochromes control photomorphogenesis by differentially regulated, interacting signaling pathways in higher plants.

In this review the kinetic properties of both phytochrome A and B measured by in vivo spectroscopy in Arabidopsis are described. Inactivation of phyA is mediated by destruction and that of phyB by fast dark reversion. Recent observations, describing a complex interaction network of various phytochromes and cryptochromes, are also discussed. The review describes recent analysis of light-dependent nuclear translocation of phytochromes and genetic and molecular dissection of phyA- and phyB-mediated signal transduction. After nuclear transport, both phyA- and phyB-mediated signal transduction probably include the formation of light-dependent transcriptional complexes. Although this hypothesis is quite attractive and probably true for some responses, it cannot account for the complex network of phyA-mediated signaling and the interaction with the circadian clock. In addition, the biological function of phytochromes localized in the cytosol remains to be elucidated.

Morphogenesis↗
PubMed1995

Phytochromes: photosensory perception and signal transduction.

The phytochrome family of photoreceptors monitors the light environment and dictates patterns of gene expression that enable the plant to optimize growth and development in accordance with prevailing conditions. The enduring challenge is to define the biochemical mechanism of phytochrome action and to dissect the signaling circuitry by which the photoreceptor molecules relay sensory information to the genes they regulate. Evidence indicates that individual phytochromes have specialized photosensory functions. The amino-terminal domain of the molecule determines this photosensory specificity, whereas a short segment in the carboxyl-terminal domain is critical for signal transfer to downstream components. Heterotrimeric GTP-binding proteins, calcium-calmodulin, cyclic guanosine 5'-phosphate, and the COP-DET-FUS class of master regulators are implicated as signaling intermediates in phototransduction.

Photoreceptor Cells↗
PubMed1987

A structural model for the alpha-subunit of transducin. Implications of its role as a molecular switch in the visual signal transduction mechanism.

Transducin is a GTP-binding protein which mediates the light activation signal from photolyzed rhodopsin to cGMP phosphodiesterase and is pivotal in the visual excitation process. Biochemical studies suggest that the T alpha subunit of transducin is composed of three functional domains, one for rhodopsin/T beta gamma interaction, another for guanine nucleotide binding, and a third for the activation of phosphodiesterase. The integration of the primary sequence of T alpha along with secondary structure, hydropathy and folding topology predictions, and a comparison with homologous proteins have led to the construction of a three-dimensional model of the T alpha subunit. A molecular mechanism which underlies the coupling action of T alpha is suggested on the basis of this model.

Enzyme Activation↗
PubMed1981

The pathway of photosensory transduction in Physarum polycephalum.

Irradiation of the plasmodia of Physarum with blue and white light results in a transient change of theie oscillatory contraction frequency. This reaction to light decreases with increasing distance from the illuminated area (Block and Wohlfarth-Bottermann, 1981). The first local appearance of light response in non-illuminated parts of the plasmodia was used to analyse the sensory pathway of the light stimulus modulating the contractile apparatus. Different experimental assays revealed that the direction of photosensory transduction is determined by the momentary direction of protoplasmic shuttle streaming. The endoplasmic flow carriers the signal responsible for photosensory transduction and light reaction to the force generating ectoplasmic tube.

Cytoplasm↗
PubMed1995

Phytochrome signal-transduction: characterization of pathways and isolation of mutants.

The study of phytochrome signalling has yielded a wealth of data describing both the perception of light by the receptor, and the terminal steps in phytochrome-regulated gene expression by a number of transcription factors. We are now focusing on establishing the intervening steps linking phytochrome photoactivation to gene expression, and the regulation and interactions of these signalling pathways. Recent work has utilized both a pharmacological approach in phototrophic soybean suspension cultures and microinjection techniques in tomato to establish three distinct phytochrome signal-transduction pathways: (i) a calcium-dependent pathway that regulates the expression of genes encoding the chlorophyll a/b binding protein (CAB) and other components of photosystem II; (ii) a cGMP-dependent pathway that regulates the expression of the gene encoding chalcone synthase (CHS) and the production of anthocyanin pigments; and (iii) a pathway dependent upon both calcium and cGMP that regulates the expression of genes encoding components of photosystem I and is necessary for the production of mature chloroplasts. To study the components and the regulation of phytochrome signal-transduction pathways, mutants with altered photomorphogenic responses have been isolated by a number of laboratories. However, with several possible exceptions, little real progress has been made towards the isolation of mutants in positive regulatory elements of the phytochrome signal-transduction pathway. We have characterized a novel phytochrome A (PhyA)-mediated far-red light (FR) response in Arabidopsis seedlings which we are currently using to screen for specific phyA signal-transduction mutants.

Arabidopsis↗
PubMed2005

Disruption of Cryptochrome partially restores circadian rhythmicity to the arrhythmic period mutant of Drosophila.

The Drosophila melanogaster circadian clock is generated by interlocked feedback loops, and null mutations in core genes such as period and timeless generate behavioral arrhythmicity in constant darkness. In light-dark cycles, the elevation in locomotor activity that usually anticipates the light on or off signals is severely compromised in these mutants. Light transduction pathways mediated by the rhodopsins and the dedicated circadian blue light photoreceptor cryptochrome are also critical in providing the circadian clock with entraining light signals from the environment. The cry(b) mutation reduces the light sensitivity of the fly's clock, yet locomotor activity rhythms in constant darkness or light-dark cycles are relatively normal, because the rhodopsins compensate for the lack of cryptochrome function. Remarkably, when we combined a period-null mutation with cry(b), circadian rhythmicity in locomotor behavior in light-dark cycles, as measured by a number of different criteria, was restored. This effect was significantly reduced in timeless-null mutant backgrounds. Circadian rhythmicity in constant darkness was not restored, and TIM protein did not exhibit oscillations in level or localize to the nuclei of brain neurons known to be essential for circadian locomotor activity. Therefore, we have uncovered residual rhythmicity in the absence of period gene function that may be mediated by a previously undescribed period-independent role for timeless in the Drosophila circadian pacemaker. Although we do not yet have a molecular correlate for these apparently iconoclastic observations, we provide a systems explanation for these results based on differential sensitivities of subsets of circadian pacemaker neurons to light.

Animals↗
PubMed1998

Induction of reactive oxygen species without 8-hydroxydeoxyguanosine formation in DNA of initiated mouse keratinocytes treated with 12-O-tetradecanoylphorbol-13-acetate.

Evidence for the involvement of oxidative stress in 12-O-tetradecanoylphorbol-13-acetate (TPA)-mediated tumor promotion has focused on non-initiated immune cells, tumor cell lines and non-initiated epidermis treated in vivo. This paper reports the effects of TPA on 8-hydroxydeoxyguanosine (8OHdG) formation and the generation of reactive oxygen species (ROS) in cloned initiated mouse epidermal keratinocytes in order to determine whether TPA can directly damage DNA through ROS production within the keratinocytes. Using high performance liquid chromatography with electrochemical detection (HPLC-EC), TPA did not induce 8OHdG formation in DNA of initiated keratinocytes treated under a variety of conditions. The reliability of the HPLC-EC system is demonstrated by (i) the linearity of the 8OHdG standard curve; (ii) the consistency of 8OHdG measurements in calf thymus and cellular DNA; and (iii) the dose-dependent increase in 8OHdG in DNA of initiated keratinocytes treated with UVC in the presence and absence of H2O2. Though not DNA-damaging, TPA induced a 65% increase in ROS (P < 0.05) as detected by luminol-dependent chemiluminescence. These results support a mechanism for the role of oxidative stress in tumor promotion that does not involve direct DNA damage to the keratinocyte target cell. The relationship between ROS, signal transduction and tumor promotion is discussed in light of the above results which is consistent with the role of TPA-induced ROS as second messengers in signal transduction.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2001

Small changes in the regulation of one Arabidopsis profilin isovariant, PRF1, alter seedling development.

Profilin (PRF) is a low-molecular-weight actin binding protein encoded by a diverse gene family in plants. Arabidopsis PRF1 transcripts are moderately well expressed in all vegetative organs. A regulatory mutant in PRF1, prf1-1, was isolated from a library of T-DNA insertions. The insertion disrupted the promoter region of PRF1 100 bp upstream from the transcriptional start site. Although steady state levels of PRF1 transcripts appeared normal in mature prf1-1 plants, the levels in young seedlings were only one-half those observed in wild type. Reactions with a PRF1 isovariant-specific monoclonal antiserum and general anti-profilin antisera demonstrated that PRF1 protein levels also were one-half those found in wild-type seedlings, although total profilin levels were unaffected. Mutant seedlings no longer could downregulate PRF1 levels in the light, as did wild type. Consistent with their molecular phenotypes, young mutant seedlings displayed several morphological phenotypes but developed into apparently normal adult plants. Their initial germination rate and development were slow, and they produced excessive numbers of root hairs. Mutant seedlings had abnormally raised cotyledons, elongated hypocotyls, and elongated cells in the hypocotyl, typical of phenotypes associated with some defects in light and circadian responses. A wild-type PRF1 transgene fully complements the hypocotyl phenotypes in the prf1-1 mutant. The ability of profilin to regulate actin polymerization and participate directly in signal transduction pathways is discussed in light of the prf1-1 phenotypes.

Arabidopsis↗
PubMed2002

Bestrophin interacts physically and functionally with protein phosphatase 2A.

Bestrophin is a 68-kDa basolateral plasma membrane protein expressed in retinal pigment epithelial cells (RPE). It is encoded by the VMD2 gene, which is mutated in Best macular dystrophy, a disease characterized by a depressed light peak in the electrooculogram. Recently it was proposed that bestrophin is a chloride channel responsible for generating the light peak. To investigate its function further, we immunoaffinity purified a bestrophin complex from RPE lysates and identified bestrophin and the beta-catalytic subunit of protein phosphatase 2A (PP2A) as members of the complex by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Protein-protein interaction between bestrophin and PP2Ac and the structural subunit of PP2A, PR65, was confirmed by reciprocal immunoprecipitation. The C-terminal cytoplasmic domain of bestrophin was sufficient for the interaction with PP2A as demonstrated by a pulldown assay using a fusion of this domain with glutathione S-transferase. Bestrophin was phosphorylated when expressed in RPE-J cells and this phosphorylation was sensitive to okadaic acid. Purified PP2A effectively dephosphorylated bestrophin in vitro. These data suggest that bestrophin is in the signal transduction pathway that modulates the light peak of the electrooculogram, that it is regulated by phosphorylation, and that phosphorylation of bestrophin is in turn regulated by PP2A.

Amino Acid Sequence↗
PubMed1999

poc1: an Arabidopsis mutant perturbed in phytochrome signaling because of a T DNA insertion in the promoter of PIF3, a gene encoding a phytochrome-interacting bHLH protein.

The phytochrome family of informational photoreceptors has a central role in regulating light-responsive gene expression, but the mechanism of intracellular signal transduction has remained elusive. In a genetic screen for T DNA-tagged Arabidopsis mutants affected in early signaling intermediates, we identified poc1 (photocurrent 1), which exhibits enhanced responsiveness to red light. This phenotype is absent in a phyB (phytochrome B) null mutant background, indicating that the poc1 mutation enhances phyB signal transduction. The T DNA insertion in poc1 was found to be located in the promoter region of PIF3, a gene encoding a basic helix-loop-helix protein. The mutant phenotype seems to result from insertion-induced overexpression of this gene in red-light-grown seedlings, consistent with PIF3 functioning as a positively acting signaling intermediate. These findings, combined with data from a separate yeast two-hybrid screen that identified PIF3 as a phytochrome-interacting factor necessary for normal signaling, provide evidence that phytochrome signal transduction may include a direct pathway to photoresponsive nuclear genes via physical interaction of the photoreceptor molecules with the potential transcriptional regulator PIF3.

Arabidopsis↗
PubMed1994

In vivo and in vitro characterization of the light-regulated cpcB2A2 promoter of Fremyella diplosiphon.

When exposed to different spectral qualities of light, many cyanobacteria dramatically alter their phycobilisome rod composition in a process termed complementary chromatic adaptation. In the cyanobacterium Fremyella diplosiphon, this response is associated with differential expression of the cpcB2A2, cpeBA, and cpeCDE operons, which code for the phycobiliproteins phycocyanin and phycoerythrin and the phycoerythrin linker polypeptides, respectively. To define components of the signal transduction pathway involved in light-regulated expression of genes encoding phycobilisome polypeptides, we have used in vivo and in vitro techniques to identify cis-acting sequences and trans-acting factors necessary for the regulation of the red-light-inducible cpcB2A2 operon. Deletion of the cpcB2A2 upstream sequences to -76 bp with respect to the transcription start site had no effect on red-light induction of a cpcB2A2-beta-glucuronidase (GUS) chimeric gene, while deletion to -37 bp abolished GUS expression. Furthermore, a fragment of the cpcB2A2 gene from -76 to +25 bp linked to the untranslated leader of cpcB1A1 (a constitutively expressed operon encoding phycocyanin) is sufficient to drive high-level GUS expression in red light. Therefore, the sequence between positions -76 and -37 is necessary for the expression of cpcB2A2, and the region extending from -76 to +25 is sufficient for red-light induction of the operon. Attempts were made to correlate the in vivo data with protein binding in the region upstream of the transcription start site of cpcB2A2. Using in vitro analysis, we detected two protein-binding sites in the cpcB2A2 promoter which were localized to positions -162 to -122 and -37 to +25. Proteins from both red- and green-light-grown cells interacted with the former site, while only proteins present in extracts from red-light-grown cells interacted with the latter site. The data from both the in vivo and in vitro analyses suggest that while two regions upstream of the cpcB2A2 transcription initiation site specifically bind proteins, only the binding site bordering the transcription start site is important for complementary chromatic adaptation.

Amino Acid Sequence↗
PubMed1995

Involvement of cGMP and calcium in the photoresponse in vertebrate photoreceptor cells.

The biochemical and physiological events responsible for reaction of the rod photoreceptor cells in the vertebrate eye have provided insight into the mechanisms involved in signal transduction in other cells. The light-mediated changes in the photopigment, rhodopsin, in the photoreceptive region of these photoreceptors initiates a cascade of events that result in changes in conductance through a specific ligand-gated receptor. This process involves activation of a specific heterotrimeric GTP-binding protein, transducin, and is mediated by changes in the intracellular concentration of two intracellular second messengers, cGMP and calcium. The current hypotheses are discussed of the mechanisms involved in various aspects of the photoresponse, particularly photoexcitation, termination, and recovery.

Animals↗
PubMed1992

Signal transduction enzymes of vertebrate photoreceptors.

A flash of light initiates a cascade of biochemical reactions inside vertebrate photoreceptor cells, culminating in hydrolysis of intracellular cyclic GMP and hyperpolarization of the cell. The cell recovers by shutting down this cascade and resynthesizing cGMP. Many of the reactions responsible for the excitation and recovery phases of the photoresponse have been identified. Here I review some characteristics of the proteins that participate in these reactions.

Animals↗
PubMed2006

Modulation of photic response by the metabotropic glutamate receptor agonist t-ACPD.

Glutamate is the primary excitatory transmitter in the hypothalamus. It conveys photic information to the suprachiasmatic nucleus of the hypothalamus, thereby entraining the circadian clock to environmental light cycles. While ionotropic glutamate receptors have been implicated in the transduction of photic information in suprachiasmatic nucleus cells, there is evidence that metabotropic glutamate receptors play a significant modulatory role. We investigated the effects of the metabotropic glutamate agonist (+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (ACPD) on light-evoked phase responses in Syrian hamsters at three phase points: circadian time 6, a time when light has no effect on the circadian timing system; circadian time 13.5, when light evokes the maximum phase delay; circadian time 19, the maximum phase advance. We found that ACPD significantly increased the light-evoked phase shift at circadian time 13.5, and had no effect at other phase points tested. These data support a role for metabotropic glutamate receptors in the circadian photic signal transduction system.

Animals↗
PubMed1992

Different populations of cells in the suprachiasmatic nuclei express c-fos in association with light-induced phase delays and advances of the free-running activity rhythm in hamsters.

Circadian rhythmicity is controlled by a light-entrainable pacemaker located in the suprachiasmatic nuclei (SCN) of the mammalian hypothalamus. Brief light exposure during the subjective night causes phase shifts of the free-running activity rhythm and expression of c-fos-related proteins (Fos) among a population of cells in the hamster SCN. Light exposure (30 lux for 15 min) during the early subjective night (CT13) causes phase delays (-60 +/- 12 min), while exposure at mid-subjective night (CT18) causes phase advances (114 +/- 48 min) of the free-running activity rhythm. Light exposure at mid-subjective day (CT6) does not cause phase alterations of the rhythm. Similarly, only light exposure at CT13 or CT18 induces Fos expression in the SCN. The distribution of Fos-immunoreactive cells in the SCN is more widespread in animals stimulated with light at CT18. In addition, a group of cells located dorsal and anterior to the SCN express Fos only after stimulation at CT18. The data are consistent with the hypothesis that Fos expression represents an event in the signal transduction pathway leading to light-induced alterations in circadian pacemaker function. Furthermore, the data raise the possibility that different populations of cells in the suprachiasmatic hypothalamus may participate in light-induced phase advances and delays of the circadian pacemaker.

Animals↗