Effects of solar radiation on photosynthetic physiology of barren stalk differentiation in maize.

Barren stalks and kernel abortion are the major obstacles that hinder maize production. After many years of inbreeding, our group produced a pair of barren stalk/non-barren stalk near-isogenic lines SN98A/SN98B. Under weak light stress, the barren stalk rate is up to 98 % in SN98A but zero in SN98B. Therefore, we consider that SN98A is a weak light-sensitive inbred line whereas SN98B is insensitive. In the present study, the near-isogenic lines SN98A/SN98B were used as test materials to conduct cytological and photosynthetic physiological analyses of the physiological mechanism associated with the differences in maize barren stalk induced by weak light stress. The results showed that weak light stress increased the accumulation of reactive oxygen species (ROS), decreased the function of chloroplasts, destroyed the normal rosette structure, inhibited photosynthetic electron transport, and enhanced lipid peroxidation. The actual photochemical quantum efficiency for PSI (Y(I)) and PSII (Y(II)), relative electron transfer rate for PSI (ETR(I)) and PSII (ETR(II)), and the P700 activities decreased significantly in the leaves of SN98A and SN98B under weak light stress, where the decreases were greater in SN98A than SN98B. After 10 days of shading treatment, the O2·- production rate, H2O2 contents, the yield of regulated energy dissipation (Y(NPQ)), the donor side restriction for PSI (Y(ND)) and the quantum efficiency of cyclic electron flow photochemistry were always higher in SN98A than SN98B, and the antioxidant enzyme activities were always lower in SN98A than those in SN98B. These results show that SN98B has a stronger ability to remove ROS at its source, and maintain the integrity of the structure and function of the photosynthetic system. This self-protection mechanism is an important physiological reason for its adaptation to weak light.

Modeling of Retinal Degeneration.

We developed a model of retinal degeneration in rabbits based on exposure to light with a wavelength of 405 nm. This model allows reproducing structural and functional disorders in the central parts of the retina, including primarily degeneration of the outer layers of the retina (retinal pigment epithelium and layer of photoreceptor cells), and is designed to study the mechanisms of formation, progression and effectiveness of new drugs and methods of treatment of degenerative diseases of the retina.

A Comprehensive Study of the Retinal Phenotype of Rpe65-Deficient Dogs.

The Rpe65-deficient dog has been important for development of translational therapies of Leber congenital amaurosis type 2 (LCA2). The purpose of this study was to provide a comprehensive report of the natural history of retinal changes in this dog model. Rpe65-deficient dogs from 2 months to 10 years of age were assessed by fundus imaging, electroretinography (ERG) and vision testing (VT). Changes in retinal layer thickness were assessed by optical coherence tomography and on plastic retinal sections. ERG showed marked loss of retinal sensitivity, with amplitudes declining with age. Retinal thinning initially developed in the area centralis, with a slower thinning of the outer retina in other areas starting with the inferior retina. VT showed that dogs of all ages performed well in bright light, while at lower light levels they were blind. Retinal pigment epithelial (RPE) inclusions developed and in younger dogs and increased in size with age. The loss of photoreceptors was mirrored by a decline in ERG amplitudes. The slow degeneration meant that sufficient photoreceptors, albeit very desensitized, remained to allow for residual bright light vision in older dogs. This study shows the natural history of the Rpe65-deficient dog model of LCA2.

Ignoring correlated activity causes a failure of retinal population codes.

From starlight to sunlight, adaptation alters retinal output, changing both the signal and noise among populations of retinal ganglion cells (RGCs). Here we determine how these light level-dependent changes impact decoding of retinal output, testing the importance of accounting for RGC noise correlations to optimally read out retinal activity. We find that at moonlight conditions, correlated noise is greater and assuming independent noise severely diminishes decoding performance. In fact, assuming independence among a local population of RGCs produces worse decoding than using a single RGC, demonstrating a failure of population codes when correlated noise is substantial and ignored. We generalize these results with a simple model to determine what conditions dictate this failure of population processing. This work elucidates the circumstances in which accounting for noise correlations is necessary to take advantage of population-level codes and shows that sensory adaptation can strongly impact decoding requirements on downstream brain areas.

[New lighting technology and our eyes]. / Les nouveaux éclairages et nos yeux.

The retina is the neurosensitive layer of the eye. In this tissue, photoreceptors convert light into nerve signals to be relayed to the brain. Despite retinal specialization in the treatment of light, excessive exposure can cause retinal damage, called retinal phototoxicity. In recent years, lighting devices rich in wavelengths of high energy (blue light) appeared, raising new concerns about retinal protection against light damage. We focus here on light-induced ocular diseases and the possible influence on visual health of new lighting technologies.

TITLE: Les nouveaux éclairages et nos yeux. ABSTRACT: Dans la rétine, couche neurosensorielle de l'œil, les photorécepteurs transforment le signal lumineux en influx nerveux interprétable par le cerveau. Malgré sa spécialisation dans le traitement des signaux lumineux, la rétine peut subir des dommages, à la suite d'une exposition excessive à la lumière ; on parle alors de phototoxicité rétinienne. Ces dernières années, l'apparition de dispositifs d'éclairage riches en longueurs d'onde de forte énergie (ce que l'on nomme lumière bleue), remet le problème de la phototoxicité rétinienne à l'ordre du jour. Nous discutons des pathologies oculaires induites par la lumière et de la possible influence des nouvelles technologies d'éclairage sur notre santé visuelle.

Interplay between differentially expressed enzymes contributes to light color acclimation in marine Synechococcus.

Marine Synechococcus, a globally important group of cyanobacteria, thrives in various light niches in part due to its varied photosynthetic light-harvesting pigments. Many Synechococcus strains use a process known as chromatic acclimation to optimize the ratio of two chromophores, green-light-absorbing phycoerythrobilin (PEB) and blue-light-absorbing phycourobilin (PUB), within their light-harvesting complexes. A full mechanistic understanding of how Synechococcus cells tune their PEB to PUB ratio during chromatic acclimation has not yet been obtained. Here, we show that interplay between two enzymes named MpeY and MpeZ controls differential PEB and PUB covalent attachment to the same cysteine residue. MpeY attaches PEB to the light-harvesting protein MpeA in green light, while MpeZ attaches PUB to MpeA in blue light. We demonstrate that the ratio of mpeY to mpeZ mRNA determines if PEB or PUB is attached. Additionally, strains encoding only MpeY or MpeZ do not acclimate. Examination of strains of Synechococcus isolated from across the globe indicates that the interplay between MpeY and MpeZ uncovered here is a critical feature of chromatic acclimation for marine Synechococcus worldwide.

Sustained Melanopsin Photoresponse Is Supported by Specific Roles of ß-Arrestin 1 and 2 in Deactivation and Regeneration of Photopigment.

Melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs) are indispensable for non-image-forming visual responses that sustain under prolonged illumination. For sustained signaling of ipRGCs, the melanopsin photopigment must continuously regenerate. The underlying mechanism is unknown. We discovered that a cluster of Ser/Thr sites within the C-terminal region of mammalian melanopsin is phosphorylated after a light pulse. This forms a binding site for ß-arrestin 1 (ßARR1) and ß-arrestin 2. ß-arrestin 2 primarily regulates the deactivation of melanopsin; accordingly, ßαrr2-/- mice exhibit prolonged ipRGC responses after cessation of a light pulse. ß-arrestin 1 primes melanopsin for regeneration. Therefore, ßαrr1-/- ipRGCs become desensitized after repeated or prolonged photostimulation. The lack of either ß-arrestin attenuates ipRGC response under prolonged illumination, suggesting that ß-arrestin 2-mediated deactivation and ß-arrestin 1-dependent regeneration of melanopsin function in sequence. In conclusion, we discovered a molecular mechanism by which ß-arrestins regulate different aspects of melanopsin photoresponses and allow ipRGC-sustained responses under prolonged illumination.

Convergent evolution of SWS2 opsin facilitates adaptive radiation of threespine stickleback into different light environments.

Repeated adaptation to a new environment often leads to convergent phenotypic changes whose underlying genetic mechanisms are rarely known. Here, we study adaptation of color vision in threespine stickleback during the repeated postglacial colonization of clearwater and blackwater lakes in the Haida Gwaii archipelago. We use whole genomes from 16 clearwater and 12 blackwater populations, and a selection experiment, in which stickleback were transplanted from a blackwater lake into an uninhabited clearwater pond and resampled after 19 y to test for selection on cone opsin genes. Patterns of haplotype homozygosity, genetic diversity, site frequency spectra, and allele-frequency change support a selective sweep centered on the adjacent blue- and red-light sensitive opsins SWS2 and LWS. The haplotype under selection carries seven amino acid changes in SWS2, including two changes known to cause a red-shift in light absorption, and is favored in blackwater lakes but disfavored in the clearwater habitat of the transplant population. Remarkably, the same red-shifting amino acid changes occurred after the duplication of SWS2 198 million years ago, in the ancestor of most spiny-rayed fish. Two distantly related fish species, bluefin killifish and black bream, express these old paralogs divergently in black- and clearwater habitats, while sticklebacks lost one paralog. Our study thus shows that convergent adaptation to the same environment can involve the same genetic changes on very different evolutionary time scales by reevolving lost mutations and reusing them repeatedly from standing genetic variation.

Luminance-dependent long-term chromatic adaptation.

There is theoretical and empirical support for long-term adaptation of human vision to chromatic regularities in the environment. The current study investigates whether relationships of luminance and chromaticity in the natural environment could drive chromatic adaptation independently and differently for bright and dark colors. This is motivated by psychophysical evidence of systematic difference shifts in red-green chromatic sensitivities between contextually bright- versus dark-colored stimuli. For some broad classes of scene content, consistent shifts in chromaticity are found between high and low light levels within images. Especially in those images in which sky and terrain are juxtaposed, this shift has direction and magnitude consistent with the observed psychophysical shifts in the red-green balance between bright and dark colors. Taken together, these findings suggest that relative weighting of M- and L-cone signals could be adapted, in a luminance-dependent fashion, to regularities in the natural environment.

A simple principled approach for modeling and understanding uniform color metrics.

An important goal in characterizing human color vision is to order color percepts in a way that captures their similarities and differences. This has resulted in the continuing evolution of "uniform color spaces," in which the distances within the space represent the perceptual differences between the stimuli. While these metrics are now very successful in predicting how color percepts are scaled, they do so in largely empirical, ad hoc ways, with limited reference to actual mechanisms of color vision. In this article our aim is to instead begin with general and plausible assumptions about color coding, and then develop a model of color appearance that explicitly incorporates them. We show that many of the features of empirically defined color order systems (those of Munsell, Pantone, NCS, and others) as well as many of the basic phenomena of color perception, emerge naturally from fairly simple principles of color information encoding in the visual system and how it can be optimized for the spectral characteristics of the environment.

Signaling and Adaptation Modulate the Dynamics of the Photosensoric Complex of Natronomonas pharaonis.

Motile bacteria and archaea respond to chemical and physical stimuli seeking optimal conditions for survival. To this end transmembrane chemo- and photoreceptors organized in large arrays initiate signaling cascades and ultimately regulate the rotation of flagellar motors. To unravel the molecular mechanism of signaling in an archaeal phototaxis complex we performed coarse-grained molecular dynamics simulations of a trimer of receptor/transducer dimers, namely NpSRII/NpHtrII from Natronomonas pharaonis. Signaling is regulated by a reversible methylation mechanism called adaptation, which also influences the level of basal receptor activation. Mimicking two extreme methylation states in our simulations we found conformational changes for the transmembrane region of NpSRII/NpHtrII which resemble experimentally observed light-induced changes. Further downstream in the cytoplasmic domain of the transducer the signal propagates via distinct changes in the dynamics of HAMP1, HAMP2, the adaptation domain and the binding region for the kinase CheA, where conformational rearrangements were found to be subtle. Overall these observations suggest a signaling mechanism based on dynamic allostery resembling models previously proposed for E. coli chemoreceptors, indicating similar properties of signal transduction for archaeal photoreceptors and bacterial chemoreceptors.

Slow Cone Reflectance Changes during Bleaching Determined by Adaptive Optics Scanning Laser Ophthalmoscope in Living Human Eyes.

To investigate the changes in the reflectance of human cone photoreceptors by an adaptive optics scanning laser ophthalmoscope (AO-SLO) during photobleaching. A custom-built AO-SLO with an observation light of 840-nm was used to measure the cone densities and the reflectance changes during bleaching by 630 nm red light emitting diodes. Measurements were made at 1° and 3° temporal to the fovea within an area of 1° × 1° in 8 eyes of 8 normal subjects. After dark-adaptation, images of the cone mosaics were recorded continuously for 5-min before, 5-min during, and after 5-min of light stimulation with a sampling rate of 5-Hz. The first positive peak (P1) was observed at 72.2 ± 15.0-s and a second positive peak (P2) at 257.5 ± 34.5-s at 1°. The increase of the reflectance of P1 was significantly larger at 1° (34.4 ± 13.9%) than at 3° (26.0 ± 10.5%; P = 0.03, Wilcoxon's signed rank test). The average cone density at 1° (51123.13 ± 1401.23 cells/mm2) was significantly larger than that at 3° (30876.13 ± 1459.28 cells/mm2; P <0.001, Wilcoxon's signed rank test). The changes in the reflectance of the cones during bleaching by red light had two peaks. The two peaks may be caused by regeneration of cone photopigment during bleaching.

Plasticity in the growth of the chick eye: emmetropization achieved by alternate morphologies.

Both refractive properties of the eyes and ambient light conditions affect emmetropization during growth. Exposure to constant light flattens the cornea making chicks hyperopic. To discover whether and how growing chick eyes restore emmetropia after exposure to constant light (CL) for 3, 7, or 11weeks, we returned chicks to normal (N) conditions with 12h. of light alternating with 12h. of darkness (designated the "R", or recovery, condition) for total periods of 4, 7, 11, or 17weeks. The two control groups were raised in CL conditions or raised in N conditions for the same length of time. We measured anterior chamber depths and lens thicknesses with an A-scan ultrasound machine. We measured corneal curvatures with an eight-axis keratometer, and refractions with conventional retinoscopy. We estimated differences in optical powers of CL, R and N chicks of identical age by constructing ray-tracing models using the above measurements and age-adjusted normal lens curvatures. We also computed the sensitivity of focus for small perturbations of the above optical parameters. Full refractive recovery from CL effects always occurred. Hyperopic refractive errors were absent when R chicks were returned to N for as little as 1week after 3weeks CL treatment. In R chicks exposed to CL for 11weeks and returned to N, axial lengths, vitreous chamber depths and radii of corneal curvatures did not return to normal, although their refractions did. While R chicks can usually recover emmetropia, after long periods of exposure to CL, they cannot recover normal ocular morphology. Emmetropization following CL exposure is achieved primarily by adjusting the relationship between corneal curvature and axial length, resulting in normal refractions.

Adaptation to changes in higher-order stimulus statistics in the salamander retina.

Adaptation in the retina is thought to optimize the encoding of natural light signals into sequences of spikes sent to the brain. While adaptive changes in retinal processing to the variations of the mean luminance level and second-order stimulus statistics have been documented before, no such measurements have been performed when higher-order moments of the light distribution change. We therefore measured the ganglion cell responses in the tiger salamander retina to controlled changes in the second (contrast), third (skew) and fourth (kurtosis) moments of the light intensity distribution of spatially uniform temporally independent stimuli. The skew and kurtosis of the stimuli were chosen to cover the range observed in natural scenes. We quantified adaptation in ganglion cells by studying linear-nonlinear models that capture well the retinal encoding properties across all stimuli. We found that the encoding properties of retinal ganglion cells change only marginally when higher-order statistics change, compared to the changes observed in response to the variation in contrast. By analyzing optimal coding in LN-type models, we showed that neurons can maintain a high information rate without large dynamic adaptation to changes in skew or kurtosis. This is because, for uncorrelated stimuli, spatio-temporal summation within the receptive field averages away non-gaussian aspects of the light intensity distribution.

Adaptation to steady light by intrinsically photosensitive retinal ganglion cells.

Intrinsically photosensitive retinal ganglion cells (ipRGCs) are recently discovered photoreceptors in the mammalian eye. These photoreceptors mediate primarily nonimage visual functions, such as pupillary light reflex and circadian photoentrainment, which are generally expected to respond to the absolute light intensity. The classical rod and cone photoreceptors, on the other hand, mediate image vision by signaling contrast, accomplished by adaptation to light. Experiments by others have indicated that the ipRGCs do, in fact, light-adapt. We found the same but, in addition, have now quantified this light adaptation for the M1 ipRGC subtype. Interestingly, in incremental-flash-on-background experiments, the ipRGC's receptor current showed a flash sensitivity that adapted in background light according to the Weber-Fechner relation, well known to describe the adaptation behavior of rods and cones. Part of this light adaptation by ipRGCs appeared to be triggered by a Ca(2+) influx, in that the flash response elicited in the absence of extracellular Ca(2+) showed a normal rising phase but a slower decay phase, resulting in longer time to peak and higher sensitivity. There is, additionally, a prominent Ca(2+)-independent component of light adaptation not typically seen in rods and cones or in invertebrate rhabdomeric photoreceptors.

The modulatory role of taurine in retinal ganglion cells.

Taurine (2-aminoethylsuphonic acid) is present in nearly all animal tissues, and is the most abundant free amino acid in muscle, heart, CNS, and retina. Although it is known to be a major cytoprotectant and essential for normal retinal development, its role in retinal neurotransmission and modulation is not well understood. We investigated the response of taurine in retinal ganglion cells, and its effect on synaptic transmission between ganglion cells and their presynaptic neurons. We find that taurine-elicited currents in ganglion cells could be fully blocked by both strychnine and SR95531, glycine and GABA(A) receptor antagonists, respectively. This suggests that taurine-activated receptors might share the antagonists with GABA and glycine receptors. The effect of taurine at micromolar concentrations can effectively suppress spontaneous vesicle release from the presynaptic neurons, but had limited effects on light-evoked synaptic signals in ganglion cells. We also describe a metabotropic effect of taurine in the suppression of light-evoked response in ganglion cells. Clearly, taurine acts in multiple ways to modulate synaptic signals in retinal output neurons, ganglion cells.

Age-dependent pupillary light reflex parameters in children.

Pupillary light reflex (PLR) refers to the phenomenon where pupil size changes in response to stimulation with a flash of light. It is a simple functional test that can reveal dysfunctions associated with the PLR pathway. Although abnormal PLR responses have been reported in many neurological disorders, few studies investigated neurodevelopmental effects on PLR parameters. We studied the effect of age on PLR in a group of 6 to 17 year old children with typical development. A significant and consistent age effect was found on PLR latency in children younger than 10 years old. Age effects were also observed in resting pupil diameter and constriction amplitude. However such age related trends were not observed in children with neurodevelopment disorders. These results suggest that PLR has the potential to be used as a simple noninvasive tool for monitoring neurodevelopment in children.

Photopigment quenching is Ca2+ dependent and controls response duration in salamander L-cone photoreceptors.

The time scale of the photoresponse in photoreceptor cells is set by the slowest of the steps that quench the light-induced activity of the phototransduction cascade. In vertebrate photoreceptor cells, this rate-limiting reaction is thought to be either shutoff of catalytic activity in the photopigment or shutoff of the pigment's effector, the transducin-GTP-phosphodiesterase complex. In suction pipette recordings from isolated salamander L-cones, we found that preventing changes in internal [Ca(2+)] delayed the recovery of the light response and prolonged the dominant time constant for recovery. Evidence that the Ca(2+)-sensitive step involved the pigment itself was provided by the observation that removal of Cl(-) from the pigment's anion-binding site accelerated the dominant time constant for response recovery. Collectively, these observations indicate that in L-cones, unlike amphibian rods where the dominant time constant is insensitive to [Ca(2+)], pigment quenching rate limits recovery and provides an additional mechanism for modulating the cone response during light adaptation.

Phosducin regulates transmission at the photoreceptor-to-ON-bipolar cell synapse.

The rate of synaptic transmission between photoreceptors and bipolar cells has been long known to depend on conditions of ambient illumination. However, the molecular mechanisms that mediate and regulate transmission at this ribbon synapse are poorly understood. We conducted electroretinographic recordings from dark- and light-adapted mice lacking the abundant photoreceptor-specific protein phosducin and found that the ON-bipolar cell responses in these animals have a reduced light sensitivity in the dark-adapted state. Additional desensitization of their responses, normally caused by steady background illumination, was also diminished compared with wild-type animals. This effect was observed in both rod- and cone-driven pathways, with the latter affected to a larger degree. The underlying mechanism is likely to be photoreceptor specific because phosducin is not expressed in other retina neurons and transgenic expression of phosducin in rods of phosducin knock-out mice rescued the rod-specific phenotype. The underlying mechanism functions downstream from the phototransduction cascade, as evident from the sensitivity of phototransduction in phosducin knock-out rods being affected to a much lesser degree than b-wave responses. These data indicate that a major regulatory component responsible for setting the sensitivity of signal transmission between photoreceptors and ON-bipolar cells is confined to photoreceptors and that phosducin participates in the underlying molecular mechanism.

Retinophilin is a light-regulated phosphoprotein required to suppress photoreceptor dark noise in Drosophila.

Photoreceptor cells achieve high sensitivity, reliably detecting single photons, while limiting the spontaneous activation events responsible for dark noise. We used proteomic, genetic, and electrophysiological approaches to characterize Retinophilin (RTP) (CG10233) in Drosophila photoreceptors and establish its involvement in dark-noise suppression. RTP possesses membrane occupation and recognition nexus (MORN) motifs, a structure shared with mammalian junctophilins and other membrane-associated proteins found within excitable cells. We show the MORN repeats, and both the N- and C-terminal domains, are required for RTP localization in the microvillar light-gathering organelle, the rhabdomere. RTP exists in multiple phosphorylated isoforms under dark conditions and is dephosphorylated by light exposure. An RTP deletion mutant exhibits a high rate of spontaneous membrane depolarization events in dark conditions but retains the normal kinetics of the light response. Photoreceptors lacking neither inactivation nor afterpotential C (NINAC) myosin III, a motor protein/kinase, also display a similar dark-noise phenotype as the RTP deletion. We show that NINAC mutants are depleted for RTP. These results suggest the increase in dark noise in NINAC mutants is attributable to lack of RTP and, furthermore, defines a novel role for NINAC in the rhabdomere. We propose that RTP is a light-regulated phosphoprotein that organizes rhabdomeric components to suppress random activation of the phototransduction cascade and thus increases the signaling fidelity of dark-adapted photoreceptors.