Induction of Abiotic Stress Tolerance by Salicylic Acid Signaling

The role of salicylic acid (SA) as a key molecule in the signal transduction pathway of biotic stress responses has already been well described. Recent studies indicate that it also participates in the signaling of abiotic stresses. The application of exogenous SA could provide protection against several types of stresses such as high or low temperature, heavy metals, and so on. Although SA may also cause oxidative stress to plants, partially through the accumulation of hydrogen peroxide, the results published so far show that the preliminary treatment of plants with low concentrations of SA might have an acclimation-like effect, causing enhanced tolerance toward most kinds of abiotic stresses due primarily to enhanced antioxidative capacity. The effect of exogenous SA depends on numerous factors such as the species and developmental stage of the plant, the mode of application, and the concentration of SA and its endogenous level in the given plant. Recent results show that not only does exogenous SA application moderate stress effects, but abiotic stress factors may also alter the endogenous SA levels in the plant cells. This review compares the roles of SA during different abiotic stresses.     

Salicylic acid may indirectly influence the photosynthetic electron transport

Salicylic acid (SA) is a phenolic phytohormone with important roles in plant development, transpiration, endogenous signaling and defense against pathogens. One of the pathways of SA biosynthesis is located in the chloroplasts. The aim of the present work was to investigate the possible regulatory effects of SA on photosynthetic electron transport processes. Here we show that SA also affects leaf photosynthesis, via inducing stomatal closure and also by slowing down Photosystem II (PS II) electron transport. Photosynthetic CO? incorporation and stomatal conductivity (measured with an infrared gas analyzer) were much lower in SA-infiltrated tobacco leaves than in untreated or water-infiltrated controls. PS II electron transport (calculated from PAM chlorophyll fluorescence data) was more sensitive to SA than Photosystem I (PS I) (measured with far red absorption). Direct probing of PS II charge separation and stabilization (measured with thermoluminescence), however, showed that these events were less affected in isolated thylakoid membranes than in leaves, suggesting that the effect of SA on PS II is indirect and different from similar effects of phenolic herbicides.     

Non-invasive monitoring of the light-induced cyclic photosynthetic electron flow during cold hardening in wheat leaves

The effect of irradiance during low temperature hardening was studied in a winter wheat variety. Ten-day-old winter wheat plants were cold-hardened at 5 degrees C for 11 days under light (250 micromol m(-2) S(-1)) or dark (20 micromol m(-2) s(-1)) conditions. The effectiveness of hardening was significantly lower in the dark, in spite of a slight decrease in the Fv/Fm chlorophyll fluorescence induction parameter, indicating the occurrence of photoinhibition during the hardening period in the light. Hardening in the light caused a downshift in the far-red induced AG (afterglow) thermoluminescence band. The faster dark re-reduction of P700+, monitored by 820-nm absorbance, could also be observed in these plants. These results suggest that the induction of cyclic photosynthetic electron flow may also contribute to the advantage of frost hardening under light conditions in wheat plants.     

The Histidine Decarboxylase (HDC) Gene of Tetrahymena Pyriformis is Similar to the Mammalian One. A Study of HDC Expression

RNA was isolated from Tetrahymena pyriformis GL and using human histidine decarboxylase (HDC) gene primers, the RT-PCR product was sequenced. A fraction containing 207 base pairs was compared to the published sequences of prokaryotic and mammalian (rat, mouse and human) HDC cDNA (exons). The HDC-cDNA fraction of Tetrahymena was similar to the mammalian cDNA-s and it was completely different from the prokaryotic HDC-gene. The results indicate the presence of a mammalian-like HDC-gene already in a unicellular eukaryote organism and demonstrates also that the divergence of the prokaryotic–eukaryotic common gene took place already at this low evolutionary level.     

Relationship between the tumor necrosis factor alpha polymorphism and the serum C-reactive protein levels in inflammatory bowel disease

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract, including ulcerative colitis (UC) and Crohn's disease (CD). The aim of the study was to determine the prevalence of the tumor necrosis factor alpha (TNF-) promoter polymorphisms at positions –238 and –308, and to measure the serum CRP levels in CD and UC patients and in a healthy population. The TNF- gene polymorphisms were determined by the PCR-RFLP method. Samples of 74 CD and 50 UC patients and 138 healthy Hungarian volunteers were examined. The GA substitution at position –308 (designated the TNF2 allele) was significantly less frequent among IBD patients than in the control group (P=0.0009); 15% of the CD patients and 18% of the UC patients carried the mentioned allele, which was significantly less frequent compared with the healthy population (33%, P=0.0035 and P=0.036, respectively). No difference in the GA substitution at position –238 was observed. We found the median CRP levels to be significantly higher in the active phase of the disease than in the inactive phase among the –308A allele carriers (P=0.002), while this difference was not significant when the CRP levels in the active and inactive phases were compared among the –308GG homozygous patients (P=0.084). The decreased frequency of the TNF2 allele (known to be associated with elevated TNF- production) in IBD may determine the severity of IBD through its interaction with plasma CRP levels, and may modify the pathogenesis of this chronic inflammatory disease.     

Fc gamma Rs modulate cytotoxicity of anti-Fas antibodies: implications for agonistic antibody-based therapeutics

Development of anti-Fas Abs to treat diseases with insufficient Fas-mediated apoptosis has been limited by concern about hepatotoxicity. We report here that hepatotoxicity elicited by anti-Fas Ab Jo2 is dependent on FcgammaRIIB. Thus, following Jo2 treatment, all FcgammaRIIB(-/-) mice survived while 80% of wild-type and all FcR-gamma(-/-) mice died from acute liver failure. Microscopic examination suggests that FcgammaRIIB deficiency protects the hepatic sinusoidal endothelium, a cell type that normally coexpresses Fas and FcgammaRIIB. In vitro studies showed that FcgammaRIIB, but not FcgammaRI and FcgammaRIII, on neighboring macrophages substantially enhanced Jo2 mediated apoptosis of Fas expressing target cells. However, FcgammaRI and FcgammaRIII appeared essential for apoptosis-inducing activity of a non-hepatotoxic anti-Fas mAb HFE7A. These findings imply that by interacting with the Fc region of agonistic Abs, FcgammaRs can modulate both the desired and undesired consequences of Ab-based therapy. Recognizing this fact should facilitate development of safer and more efficacious agonistic Abs.     

Competitive binding of acetate and chloride in photosystem II.

The binding of chloride and acetate to photosystem II (PSII) was examined to elucidate the mechanism of acetate inhibition. The mode of inhibition was studied, and individual binding sites were assigned by steady-state O2 evolution measurements in correlation with electron paramagnetic resonance (EPR) results. Two binding sites were found for acetate, one chloride-sensitive on the electron donor side and one chloride-insensitive on the electron acceptor side. The respective binding constants were as follows: KCl = 0.5 +/- 0.2 mM (chloride binding to the donor side), KI = 16 +/- 5 mM (acetate binding to the donor side), and KI' = 130 +/- 40 mM (acetate binding to the acceptor side). When acetate was bound to the acceptor side of PSII, 200 K illumination induced a narrowed form of the QA-FeII EPR signal, the yield of which was independent of the chloride concentration. When acetate was bound to the donor side, room-temperature illumination produced the S2YZ* state. EPR measurements showed that both the yield and formation rate of this state increased with acetate concentration. Increasing chloride concentrations slowed the rate of formation of the S2YZ* state, but did not affect the steady-state yield of the S2YZ* state. These findings indicate that the light-induced reactions in acetate-inhibited PSII are modulated by both donor side and acceptor side binding of acetate, while the steady-state yield of the S2YZ* state at the high PSII concentrations used for EPR measurements depends primarily on acceptor side turnover. Our data further support a close proximity of chloride to YZ*, indicating a possible role for chloride in the electron-transfer mechanism at the O2-evolving complex.     

The virulence function of Streptococcus pneumoniae surface protein A involves inhibition of complement activation and impairment of complement receptor-mediated protection

Complement is important for elimination of invasive microbes from the host, an action achieved largely through interaction of complement-decorated pathogens with various complement receptors (CR) on phagocytes. Pneumococcal surface protein A (PspA) has been shown to interfere with complement deposition onto pneumococci, but to date the impact of PspA on CR-mediated host defense is unknown. To gauge the contribution of CRs to host defense against pneumococci and to decipher the impact of PspA on CR-dependent host defense, wild-type C57BL/6J mice and mutant mice lacking CR types 1 and 2 (CR1/2(-/-)), CR3 (CR3(-/-)), or CR4 (CR4(-/-)) were challenged with WU2, a PspA(+) capsular serotype 3 pneumococcus, and its PspA(-) mutant JY1119. Pneumococci also were used to challenge factor D-deficient (FD(-/-)), LFA-1-deficient (LFA-1(-/-)), and CD18-deficient (CD18(-/-)) mice. We found that FD(-/-), CR3(-/-), and CR4(-/-) mice had significantly decreased longevity and survival rate upon infection with WU2. In comparison, PspA(-) pneumococci were virulent only in FD(-/-) and CR1/2(-/-) mice. Normal mouse serum supported more C3 deposition on pneumococci than FD(-/-) serum, and more iC3b was deposited onto the PspA(-) than the PspA(+) strain. The combined results confirm earlier conclusions that the alternative pathway of complement activation is indispensable for innate immunity against pneumococcal infection and that PspA interferes with the protective role of the alternative pathway. Our new results suggest that complement receptors CR1/2, CR3, and CR4 all play important roles in host defense against pneumococcal infection.