Pest and disease management by red light.

Light is essential for plant life. It provides a source of energy through photosynthesis and regulates plant growth and development and other cellular processes, such as by controlling the endogenous circadian clock. Light intensity, quality, duration and timing are all important determinants of plant responses, especially to biotic stress. Red light can positively influence plant defence mechanisms against different pathogens, but the molecular mechanism behind this phenomenon is not fully understood. Therefore, we reviewed the impact of red light on plant biotic stress responses against viruses, bacteria, fungi and nematodes, with a focus on the physiological effects of red light treatment and hormonal crosstalk under biotic stress in plants. We found evidence suggesting that exposing plants to red light increases levels of salicylic acid (SA) and induces SA signalling mediating the production of reactive oxygen species, with substantial differences between species and plant organs. Such changes in SA levels could be vital for plants to survive infections. Therefore, the application of red light provides a multidimensional aspect to developing innovative and environmentally friendly approaches to plant and crop disease management.

Veinal necrosis induced by turnip mosaic virus infection in Arabidopsis is a form of defense response accompanying HR-like cell death.

In the pathosystems of Turnip mosaic virus (TuMV) with Brassicaceae crops, various symptoms, including mosaic and necrosis, are observed. We previously reported a necrosis-inducing factor TuNI in Arabidopsis thaliana, a model species. In this study, we show that the necrotic symptom induced by TuNI, observed along the veins, was actually a form of defense response accompanying a hypersensitive reaction (HR)-like cell death in the veinal area. The virus is often localized in the necrotic region. The necrotic response is associated with the production of H2O2, accumulation of salicylic acid (SA), emission of ethylene, and subsequent expression of defense-related genes. Additionally, this HR-like cell death is eased or erased by a shading treatment. These features are similar to the HR-associated resistance reaction to pathogens. However, unlike HR, two phytohormones--SA and ethylene--are involved in the necrosis induction, and both SA- and ethylene-dependent pathogenesis-related genes are activated. We concluded that the veinal necrosis induced by TuMV is regulated by a complex and unique network of at least two signaling pathways, which differs from the signal transduction for the known HR-associated resistance.

Influence of Irradiance and Temperature on the Virus MpoV-45T Infecting the Arctic Picophytoplankter Micromonas polaris.

Arctic marine ecosystems are currently undergoing rapid changes in temperature and light availability. Picophytoplankton, such as Micromonas polaris, are predicted to benefit from such changes. However, little is known about how these environmental changes affect the viruses that exert a strong mortality pressure on these small but omnipresent algae. Here we report on one-step infection experiments, combined with measurements of host physiology and viability, with 2 strains of M. polaris and the virus MpoV-45T under 3 light intensities (5, 60 and 160 µmol quanta m-2 s-1), 2 light period regimes (16:8 and 24:0 h light:dark cycle) and 2 temperatures (3 and 7 °C). Our results show that low light intensity (16:8 h light:dark) delayed the decline in photosynthetic efficiency and cell lysis, while decreasing burst size by 46%. In contrast, continuous light (24:0 h light:dark) shortened the latent period by 5 h for all light intensities, and even increased the maximum virus production rate and burst size under low light (by 157 and 69%, respectively). Higher temperature (7 °C vs 3 °C) led to earlier cell lysis and increased burst size (by 19%), except for the low light conditions. These findings demonstrate the ecological importance of light in combination with temperature as a controlling factor for Arctic phytoplankton host and virus dynamics seasonally, even more so in the light of global warming.

Plant responses to UV radiation and links to pathogen resistance.

Increased incident ultraviolet (UV) radiation due to ozone depletion has heightened interest in plant responses to UV because solar UV wavelengths can reduce plant genome stability, growth, and productivity. These detrimental effects result from damage to cell components including nucleic acids, proteins, and membrane lipids. As obligate phototrophs, plants must counter the onslaught of cellular damage due to prolonged exposure to sunlight. They do so by attenuating the UV dose received through accumulation of UV-absorbing secondary metabolites, neutralizing reactive oxygen species produced by UV, monomerizing UV-induced pyrimidine dimers by photoreactivation, extracting UV photoproducts from DNA via nucleotide excision repair, and perhaps transiently tolerating the presence of DNA lesions via replicative bypass of the damage. The signaling mechanisms controlling these responses suggest that UV exposure also may be beneficial to plants by increasing cellular immunity to pathogens. Indeed, pathogen resistance can be enhanced by UV treatment, and recent experiments suggest DNA damage and its processing may have a role.

Radiation genetics in microorganisms and evolutionary considerations.

Recent knowledge of UV-resistance mechanisms in microorganisms is reviewed in perspective, with emphasis on E. coli. Dark-repair genes are classified into "excision" and "tolerance" (ability to produce a normal copy of DNA from damaged DNA). The phenotype of DNA repair is rather common among the microorganisms compared, and yet their molecular mechanisms are not universal. In contrast, DNA photoreactivation is the simplest and the most general among these three repair systems. It is proposed that DNA repair mechanisms evolved in the order: photoreactivation, excision repair, and tolerance repair. The UV protective capacity and light-inducible RNA photoreactivation possessed by some plant viruses are interpreted to be the result of solar UV selection during a rather recent era of evolution.

Spectral quality may be used to alter plant disease development in CELSS.

Plants were grown under light emitting diode (LED) arrays with different spectral qualities to determine the effects of light on the development of tomato mosaic virus (ToMV) in peppers and powdery mildew on cucumbers. One LED array supplied 100% of the photosynthetic photon flux (PPF) at 660 nm, a second array supplied 90% of the PPF at 660 nm and 10% at 735 nm, and a third array supplied 98% of the PPF at 660 nm with 2% in the blue region (380-500 nm) supplied by blue fluorescent lamps. Control plants were grown under metal halide (MH) lamps. Pepper plants inoculated with ToMV and grown under 660 and 660/735 LED arrays showed marked increases in both the rate and the severity of symptoms as compared to inoculated plants grown under the MH lamp or 660/blue array. Pepper plants grown under the 660/blue array did not develop symptoms as rapidly as inoculated plants grown under the 660 or 660/735 arrays, but they did develop symptoms faster than inoculated plants grown under the MH lamp. The numbers of colonies of powdery mildew per leaf and the size of each colony were greatest on inoculated cucumber plants grown under the MH lamp.

[Difference in the mechanism of self-assembly in vitro in tobacco mosaic virus and potato virus X]. / Razlichiia v mekhanizmakh samosborki in vitro virusa tabachnoi mozaiki i X-virusa kartofelia.

The effects of 254 nm UV-irradiation of tobacco mosaic virus (TMV) and potato virus X (PVX) RNA preparations on the RNA ability to self-assembly in vitro with the viral coat proteins were studied. It was found that while TMV RNA ability to assemble with the homologous protein is rapidly inactivated by the UV-irradiation, PVX RNA ability to be encapsidated by the PVX coat protein is quite resistant to the irradiation. More than that, the irradiation of TMV RNA with the dose strongly inhibiting its assembly with the homologous protein, did not result in any significant inhibition of this RNA ability to be coated with the PVX protein. The results testify to the profound differences in the mechanisms of RNA-protein interactions in the processes of self-assembly in vitro of tobamoviruses and potexviruses.

Photoreactivation of ultraviolet irradiated blue-green alga: Anacystis nidulans and cyanophage AS-1.

Ultraviolet (UV) inactivation and photoreactivation of Anacystis nidulans and cyanophage AS-1 was studied at different wavelengths. UV inactivation of free phage particles and one and two hour host-phage complexes (intracellular phages) were exponential. UV resistance of plaque forming units was attained at the latter phase of latent period. Black, blue and white lights were able to photoreactivate the UV irradiated A. nidulans whereas green, yellow and red lights were not. However, incubation of A. nidulans for more than 2 hours in black light resulted in loss of viability but shift to red light caused significant recovery. This suggests the involvement of two types of photoreactivation, i.e. of photoenzymatic repair of DNA and of the repair of the photosynthetic apparatus of A. nidulans.

Photoreactivation of UV-irradiated blue-green algae and algal virus LPP-1.

Ultraviolet (UV) sensitivity and photoreactivation of blue-green algae Cylindrospermum sp., Plectonema boryanum, spores of Fischerella muscicola and algal virus (cyanophage) LPP-1 were studied. The survival value after UV irradiation of filaments of Cylindrospermum sp. and Virus LPP-1 showed exponential trend and these were comparatively sensitive towards UV than F.muscicola and P.boryanum. Photoreactivation of UV-induced damage occurred in black, blue, green, yellow, red and white light in Cylindrospermum sp., however only black, blue and white light were capable of photorepair of UV-induced damage in P.boryanum, spores of F.muscicola and virus LPP-1 in infected host alga. Pre-exposure to yellow and black light did not show photoprotection. The non-heterocystous and nitrogen fixation-less mutants of Cylindrospermum sp. were not induced by UV and their spontaneous mutation frequency was not affected after photoreactivation. The short trichome mutants of P.boryanum were more resistant towards UV. The occurrence of photoreactivation of UV-induced killing wide range of light in Cylindrospermum sp. is the first report in organisms.

Sensitization of algal virus to UV by the incorporation of 5-bromouracil and mutations of host alga Plectonema boryanum.

Ultraviolet light (UV) sensitivity and photoreactivation of algal virus (cyanophage) LPP-1 were studied after multiplication in host alga Plectonema boryanum in presence of 5-bromouracil (5-BU) alone and in conjunction with sulfanilamide. Virus particles containing 5-BU were more sensitive towards UV and also showed low photoreactivation. There was less incorporation of 5-BU in virus without pretreatment of host alga with sulfanilamide, an inhibitor of thymine synthesis. 5-BU-induced short trichome mutants of Plectonema boryanum were isolated. These mutants grew slowly in liquid medium as well as on agar plates and differed in other morphological characters. Reversion of short trichome mutants was observed with a frequency of about 10(-3), but revertants were different from parent alga. The short trichome mutants were sensitive to virus LPP-1 and resistant towards UV.

Ultraviolet light inactivation and photoreactivation of AS-1 cyanophage in Anacystis nidulans.

Black light effected photorecovery of AS-1 cyanophage and wild-type cells. However, only partial photoreactivation of AS-1 was observed in a partially photoreactivable mutant of Anacystis nidulans.

LPP-1 infection of the blue-green alga Plectonema boryanum. 3. Protein synthesis.

The structural proteins of mature LPP-1 particles and the patterns of protein synthesis after LPP-1 infection have been examined by electrophoresis on sodium dodecyl sulfate polyacrylamide gels. Structural proteins account for 35% of the LPP-1 genome, and proteins that would require about 65% of the total coding capacity have been detected after infection. The major head proteins have molecular weights of 39,000 and 13,000, whereas the major tail protein is an 80,000-molecular-weight species. Host protein synthesis is depressed soon after infection and appears to be entirely shut off by 5 hr. Three classes of viral proteins are distinguished in infected cells, based on their time course of synthesis and their presence in mature virions.