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At least 685 records · Page 38Linked to original sources
PubMed1998

Induction of Fos expression in the circadian system by unsignaled light is attenuated as a result of previous experience with signaled light: a role for Pavlovian conditioning.

A circadian clock responsive to light is located in the hypothalamic suprachiasmatic nucleus. In rodents, light induces the expression of the transcription factor Fos in cells of the suprachiasmatic nucleus and this effect is associated with light-induced resetting of the circadian clock. Until recently, it was thought that the induction of Fos in the suprachiasmatic nucleus was mediated by a mechanism uniquely sensitive to photic cues. We have shown, however, using Pavlovian conditioning procedures, that a nonphotic stimulus that has been repeatedly paired with light can, in the absence of light, induce Fos expression in the suprachiasmatic nucleus. In the present study we asked whether, as a result of conditioning, the ability of light alone to induce Fos expression in the suprachiasmatic nucleus might be altered. We suspected that once the mechanism mediating Fos expression in the suprachiasmatic nucleus had become tuned to receiving light signaled by a conditioned stimulus, the response to presentation of light alone would be diminished. To study this possibility we investigated whether induction of Fos expression in the suprachiasmatic nucleus by unsignaled light would be altered as a result of previous experience with signaled light. Consistent with our hypothesis, we found that a series of conditioning trials not only confers upon a nonphotic stimulus the ability to activate the mechanism mediating Fos expression in the suprachiasmatic nucleus, but also reduces the efficacy of light itself to activate this mechanism.

Circadian Rhythm↗
PubMed2005

Epidermal growth factor receptor signaling is partially responsible for the increased matrix metalloproteinase-1 expression in ocular epithelial cells after UVB radiation.

Pterygia are inflammatory, invasive, and proliferative lesions of the human ocular surface in which the matrix metalloproteinase (MMP) collagenase-1 (MMP-1) is highly expressed. Pterygia development may involve MMP-1 activity against interstitial fibrillar collagen, an abundant extracellular matrix component of the cornea, and its induction by ultraviolet light (UVB). We examined the pathways responsible for enhanced expression of MMP-1 in pterygium epithelial cells after UVB exposure and/or treatment with chemical inhibitors of mitogen-activated protein kinases or epidermal growth factor receptor. The induction of MMP-1 by UVB was comparable to that mediated by heparin-binding epidermal growth factor-like growth factor and epidermal growth factor. The epidermal growth factor receptor inhibitor PD153035 partially blocked the UVB-mediated induction of MMP-1 and totally abrogated its production after stimulation with either heparin-binding epidermal growth factor-like growth factor or epidermal growth factor. UVB exposure enhanced the phosphorylated form of ERK1/2 in a time-dependent manner whereas the ERK1/2 inhibitor PD98059 decreased this induction by at least fivefold. Transcripts for c-jun and c-fos were detected as early as 2 hours after UVB exposure and were suppressed by PD98059. The identification of a specific intracellular signaling pathway responsible for the enhanced production of a key enzyme that denatures intact fibrillar collagen has important implications for understanding the pathophysiology and future therapy for pterygia.

Blotting, Western↗
PubMed1990

Expression of a stilbene synthase gene in Nicotiana tabacum results in synthesis of the phytoalexin resveratrol.

A gene from groundnut (Arachis hypogaea) coding for stilbene synthase was transferred together with a chimaeric kanamycin resistance gene. It was found to be rapidly expressed after induction with UV light and elicitor in tobacco cells (Nicotiana tabacum). Comparative studies of stilbene synthase mRNA synthesis in groundnut and transgenic tobacco suspension cultures revealed the same kinetics of gene expression. Stilbene synthase specific mRNA was detectable 30 minutes after elicitor induction and 10 minutes after UV irradiation. The maximum of mRNA accumulation was between 2 and 8 hours post induction. 24 hours after induction stilbene synthase mRNA accumulation ceased. Furthermore, in transgenic tobacco plants, the gene was found to be inducible in sterile roots, stems and leaves. Stilbene synthase was demonstrated in crude protein extracts from transgenic tobacco cell cultures using specific antibodies. Resveratrol, the product of stilbene synthase, was identified by HPLC and antisera raised against resveratrol.

Acyltransferases↗
PubMed2005

Peroxisomal monodehydroascorbate reductase. Genomic clone characterization and functional analysis under environmental stress conditions.

In plant cells, ascorbate is a major antioxidant that is involved in the ascorbate-glutathione cycle. Monodehydroascorbate reductase (MDAR) is the enzymatic component of this cycle involved in the regeneration of reduced ascorbate. The identification of the intron-exon organization and the promoter region of the pea (Pisum sativum) MDAR 1 gene was achieved in pea leaves using the method of walking polymerase chain reaction on genomic DNA. The nuclear gene of MDAR 1 comprises nine exons and eight introns, giving a total length of 3,770 bp. The sequence of 544 bp upstream of the initiation codon, which contains the promoter and 5' untranslated region, and 190 bp downstream of the stop codon were also determined. The presence of different regulatory motifs in the promoter region of the gene might indicate distinct responses to various conditions. The expression analysis in different plant organs by northern blots showed that fruits had the highest level of MDAR. Confocal laser scanning microscopy analysis of pea leaves transformed with Agrobacterium tumefaciens having the binary vectors pGD, which contain the autofluorescent proteins enhanced green fluorescent protein and enhanced yellow fluorescent protein with the full-length cDNA for MDAR 1 and catalase, indicated that the MDAR 1 encoded the peroxisomal isoform. The functional analysis of MDAR by activity and protein expression was studied in pea plants grown under eight stress conditions, including continuous light, high light intensity, continuous dark, mechanical wounding, low and high temperature, cadmium, and the herbicide 2,4-dichlorophenoxyacetic acid. This functional analysis is representative of all the MDAR isoforms present in the different cell compartments. Results obtained showed a significant induction by high light intensity and cadmium. On the other hand, expression studies, performed by semiquantitative reverse transcription-polymerase chain reaction demonstrated differential expression patterns of peroxisomal MDAR 1 transcripts in pea plants grown under the mentioned stress conditions. These findings show that the peroxisomal MDAR 1 has a differential regulation that could be indicative of its specific function in peroxisomes. All these biochemical and molecular data represent a significant step to understand the specific physiological role of each MDAR isoenzyme and its participation in the antioxidant mechanisms of plant cells.

2,4-Dichlorophenoxyacetic Acid↗
PubMed2006

Optical induction of synaptic plasticity using a light-sensitive channel.

We have combined millisecond activation of channelrhodopsin-2 (ChR2), a light-gated ion channel, with two-photon calcium imaging to investigate active synaptic contacts in rat hippocampal slice cultures. Calcium influx was larger during light-induced action potentials than during action potentials induced by somatic current injection, leading to highly reproducible synaptic transmission. Pairing of light stimulation with postsynaptic depolarization induced long-term potentiation, making this technique ideal for genetic and pharmacological dissection of synaptic plasticity.

Action Potentials↗
PubMed2005

Induction of p19INK4d in response to ultraviolet light improves DNA repair and confers resistance to apoptosis in neuroblastoma cells.

The genetic instability driving tumorigenesis is fueled by DNA damage and by errors made by the DNA replication. Upon DNA damage the cell organizes an integrated response not only by the classical DNA repair mechanisms but also involving mechanisms of replication, transcription, chromatin structure dynamics, cell cycle progression, and apoptosis. In the present study, we investigated the role of p19INK4d in the response driven by neuroblastoma cells against DNA injury caused by UV irradiation. We show that p19INK4d is the only INK4 protein whose expression is induced by UV light in neuroblastoma cells. Furthermore, p19INK4d translocation from cytoplasm to nucleus is observed after UV irradiation. Ectopic expression of p19INK4d clearly reduces the UV-induced apoptosis as well as enhances the cellular ability to repair the damaged DNA. It is clearly shown that DNA repair is the main target of p19INK4d effect and that diminished apoptosis is a downstream event. Importantly, experiments performed with CDK4 mutants suggest that these p19INK4d effects would be independent of its role as a cell cycle checkpoint gene. The results presented herein uncover a new role of p19INK4d as regulator of DNA-damage-induced apoptosis and suggest that it protects cells from undergoing apoptosis by allowing a more efficient DNA repair. We propose that, in addition to its role as cell cycle inhibitor, p19INK4d is involved in maintenance of DNA integrity and, therefore, would contribute to cancer prevention.

Animals↗
PubMed1998

Induction of acclimative proteolysis of the light-harvesting chlorophyll a/b protein of photosystem II in response to elevated light intensities

Most plants have the ability to respond to fluctuations in light to minimize damage to the photosynthetic apparatus. A proteolytic activity has been discovered that is involved in the degradation of the major light-harvesting chlorophyll a/b-binding protein of photosystem II (LHCII) when the antenna size of photosystem II is reduced upon acclimation of plants from low to high light intensities. This ATP-dependent proteolytic activity is of the serine or cysteine type and is associated with the outer membrane surface of the stroma-exposed thylakoid regions. The identity of the protease is not known, but it does not correspond to the recently identified chloroplast ATP-dependent proteases Clp and FtsH, which are homologs to bacterial enzymes. The acclimative response shows a delay of 2 d after transfer of the leaves to high light. This lag period was shown to be attributed to expression or activation of the responsible protease. Furthermore, the LHCII degradation was found to be regulated at the substrate level. The degradation process involves lateral migration of LHCII from the appressed to the nonappressed thylakoid regions, which is the location for the responsible protease. Phosphorylated LHCII was found to be a poor substrate for degradation in comparison with the unphosphorylated form of the protein. The relationship between LHCII degradation and other regulatory proteolytic processes in the thylakoid membrane, such as D1-protein degradation, is discussed.

Journal Article↗
PubMed1983

Induction of epithelial tight junctions by a light chain protein isolated from a patient with Fanconi's syndrome.

Tight junctions have not been described in the adult human glomerulus. In a 22-year-old patient with kappa light chain proteinuria, tight junctions were observed between glomerular epithelial cell foot processes (kidney biopsy). The light chain isolated from urine proved to have a relatively high isoelectric point. When the light chain was exposed in vitro to the mucosal surface of a 'leaky' epithelium, the Necturus gallbladder, transepithelial resistance and potential difference increased in a concentration-dependent, reversible manner and NaCl dilution potentials decreased, consistent with a reduction in tight-junctional ionic permeability. Gallbladders fixed in situ and freeze-fractured during peak electrophysiological responses revealed an increase in tight-junctional depth. This report indicates that certain light chains, possibly by virtue of a positive charge, may induce changes in epithelial tight junction structure and/or permeability.

Adult↗
PubMed1981

Influence of superinfection on the photoreversible phase of UV induced lysogenic bacteria.

1. Lysogenic induction by UV light can be reversed by photoreactivation. UV-treated E. coli K12 (lambda)+ uvr+ and uvr cells are sensitive to photoreactivation for a given time after irradiation. This sensitivity suddenly disappears at the end of this time. 2. The photoreversible period of UV induction is more than twice as long in uvr cells as it is in uvr+ cells. 3. The photoreversible period can be reduced by superinfection with lambda c mutants after irradiation. This effect is positively correlated with the multiplicity of superinfection. Such a reduction does not occur when superinfection is carried out with wild-type phages or with heteroimmune derivatives. 4. We concluded that during the photoreversible period of UV induction oligonucleotides are excised or synthesized and gaps are formed during excision repair and post replication repair of UV damage; these might react with E. coli recA protein thereby activating it to induce its own synthesis, to cleave phage repressors and to exert its other SOS functions.

Bacteriophage lambda↗
PubMed1990

The induction of chromosomal aberrations and SCEs by visible light in combination with dyes. II. Cell cycle dependence, and the effect of hydroxyl radical scavengers during light exposure in cultures of Chinese hamster ovary cells sensitized with acridine orange.

Chinese hamster ovary (CHO) cells were synchronized by mitotic shake-off, treated with the fluorochrome acridine orange (AO; 0.5 micrograms/ml), washed free of excess dye and subsequently exposed to visible light (2 X 40 W/8 Wm-2). The light exposure was performed on cells in the G1, G1/S, S or G2 phase of the cell cycle. AO + light induced high frequencies of aberration in the S phase and even higher in the G1 phase. The aberrations observed were all of the chromatid type. The chromosome-type aberrations (dicentrics, rings) obtained when cells in the G1 phase were exposed to X-rays were not found after corresponding treatments with AO + light. With the exception of an increased frequency of gaps, no chromosomal aberrations were induced in G2-phase cells. Sister-chromatid exchanges were efficiently produced by the photodynamic system in the G1, G1/S and S phase of the cell cycle. In other experiments, AO-treated unsynchronized CHO cells were exposed to light in the presence of the hydroxyl radical scavengers mannitol (100 mM) and 5-dimethyl thiourea (100 mM). In parallel experiments these scavengers were found to reduce markedly the chromosome breaking effects by X-rays but had no influence on the photodynamic induction of chromosomal alterations. The results presented show that the visible light-induced chromosomal alterations in CHO cells sensitized with the fluorochrome AO are obtained by an S-dependent mechanism. Furthermore, the results indicate that the hydroxyl free radical does not play a major role in the production of chromosomal alterations by AO + light.

Acridine Orange↗
PubMed1988

Multiple, small exposures of far-ultraviolet or mid-ultraviolet light change the sensitivity to acute ultraviolet exposures measured by cell lethality and mutagenesis in V79 Chinese hamster cells.

Chinese hamster V79 cells (subline MI2G) were exposed repeatedly to fractionated doses of germicidal 254 nm light (far-uv) at 6 J.m-2/fraction/day or sunlight-simulating 290-330 nm (mid-uv) at 150 J.m-2/fraction/day and sensitivities to cell killing action and mutation of far-uv and mid-uv were examined. As the number of exposure fractions increased, the cell cultures became resistant to cell killing induced by both far-uv and mid-uv. Increases in both Do and Dq were observed. Treatment with exposures of 6 J.m-2 far-uv is more efficient in yielding cell cultures that are resistant than exposures of 150 J.m-2 mid-uv. In contrast to the cells exposed to repeated far-uv, the cells exposed to repeated mid-uv were relatively more resistant to cell killing effects of mid-uv than far-uv, suggesting a possible role of photolesions other than pyrimidine dimers. When mutants resistant to 6-thioguanine were assayed during repeated exposure to far- or mid-uv light, the yield was initially linear with accumulating dose. At high total accumulated doses, the frequency decreased gradually (6 J.m-2 mid-uv) or reached a plateau (150 J.m-2 mid-uv). The sensitivity of N80 cells (exposed to 80 fractions of mid-uv) to mutation induction by uv light is higher than that of the original MI2G cells, whereas U81 cells (exposed to 81 fractions of far-uv) have a sensitivity similar to that of the original cells. Although an initial decrease in resistance to cell killing was observed, resistant cells retained their characteristics after 100 days in culture without further exposure. Cross-resistance to X rays was not shown. The data in this paper suggest that the capacity for repair of photolesions in DNA by repair processes was enhanced in cell cultures by repeated exposure to far-uv or mid-uv and that this altered the cells' ability to cope with lethal and mutagenic lesions. It remains to be seen if these changes in cell sensitivity were brought about by selective or inductive processes or a combination of both.

Animals↗
PubMed2000

Gene expression in the mouse retina: the effect of damaging light.

PURPOSE: High levels of visible light induce apoptotic cell death of photoreceptors, a process depending on the activation of the transcription factor AP-1. This suggests that regulation of gene expression might be important for light-induced photoreceptor cell death. We measured expression of AP-1 family members and of several apoptosis-related genes to test their potential involvement in photoreceptor apoptosis. METHODS: Wildtype and c-fos-/- mice were exposed to low (roomlight) or high levels of visible light for up to two hours. Total RNA was prepared from isolated retinas during and after light exposure. Relative mRNA levels were determined semiquantitatively using either competitive or exponential RT-PCR. RESULTS: Expression of c-fos-/- was upregulated by intense light as early as 15 min after lights on. Highest levels (6-fold induction) were detected at 2 h after lights off declining thereafter to basal levels 20 h after the end of exposure. c-jun mRNA was induced at 30 min after lights on and high expression levels (fourfold induction) persisted at least for 8 h. Similarly, expression of caspase-1 was six to 9-fold increased at 6 to 8 h after light exposure in wildtype but not in c-fos knockout mice. The latter mice are protected against light-induced photoreceptor apoptosis. Expression of other apoptosis-related genes (bcl-2, bcl-XL, bax, bad, caspase-3) was not affected by light exposure or the lack of c-Fos in knockout mice. CONCLUSIONS: Expression of c-fos and c-jun mRNA is transiently induced by exposure to damaging light. Induced expression of c-jun persists longer than expression of c-fos. Among the apoptosis-related genes, only caspase-1 expression was upregulated by light exposure and Caspase-1 might therefore be involved in light-induced retinal degeneration.

Animals↗