scholarly journals Acclimation of Photosynthesis to Changes in the Environment Results in Decreases of Oxidative Stress in Arabidopsis thaliana

2021 ◽  
Vol 12 ◽  
Author(s):  
Mohd Fauzihan Karim ◽  
Giles N. Johnson

The dynamic acclimation of photosynthesis plays an important role in increasing the fitness of a plant under variable light environments. Since acclimation is partially mediated by a glucose-6-phosphate/phosphate translocator 2 (GPT2), this study examined whether plants lacking GPT2, which consequently have defective acclimation to increases in light, are more susceptible to oxidative stress. To understand this mechanism, we used the model plant Arabidopsis thaliana [accession Wassilewskija-4 (Ws-4)] and compared it with mutants lacking GPT2. The plants were then grown at low light (LL) at 100 μmol m−2 s−1 for 7 weeks. For the acclimation experiments, a set of plants from LL was transferred to 400 μmol m−2 s−1 conditions for 7 days. Biochemical and physiological analyses showed that the gpt2 mutant plants had significantly greater activity for ascorbate peroxidase (APX), guiacol peroxidase (GPOX), and superoxide dismutase (SOD). Furthermore, the mutant plants had significantly lower maximum quantum yields of photosynthesis (Fv/Fm). A microarray analysis also showed that gpt2 plants exhibited a greater induction of stress-related genes relative to wild-type (WT) plants. We then concluded that photosynthetic acclimation to a higher intensity of light protects plants against oxidative stress.

2001 ◽  
Vol 79 (6) ◽  
pp. 657-665 ◽  
Author(s):  
Quintin J Steynen ◽  
Dee A Bolokoski ◽  
Elizabeth A Schultz

We have identified three phases within the wild-type Arabidopsis thaliana (L.) Heynh. rosette, based on significant differences in leaf shape, size, vascular pattern, and presence of abaxial trichomes. To test the hypothesis that a single, central mechanism controls the progression through all plant phases and that conditions that alter the time to flowering will also alter the progression through vegetative phases, we analysed the rosette phases under such conditions. In support of our hypothesis, we determined that those conditions (loss of LEAFY activity, short days) that decelerate time to flowering show decelerated progression through the rosette phases, while those conditions (loss of TERMINAL FLOWER, overexpression of LEAFY, low light) that accelerate time to flowering show accelerated progression through the rosette phases. In all conditions except short days, the length of the first phase was unaffected, indicating that this phase is less susceptible to influences of the central mechanism. Progression through the subsequent two rosette phases was accelerated differentially, such that the second phase was affected more strongly than the first. This supports the idea that, in the rosette, as in the inflorescence, the inhibition of phase transition by the central mechanism is gradually decreasing.Key words: phase change, flowering time, Arabidopsis thaliana, LEAFY, TERMINAL FLOWER, heteroblasty.


2011 ◽  
Vol 301 (5) ◽  
pp. R1400-R1407 ◽  
Author(s):  
Lisa M. Larkin ◽  
Carol S. Davis ◽  
Catrina Sims-Robinson ◽  
Tatiana Y. Kostrominova ◽  
Holly Van Remmen ◽  
...  

An association between oxidative stress and muscle atrophy and weakness in vivo is supported by elevated oxidative damage and accelerated loss of muscle mass and force with aging in CuZn-superoxide dismutase-deficient ( Sod1−/−) mice. The purpose was to determine the basis for low specific force (N/cm2) of gastrocnemius muscles in Sod1−/− mice and establish the extent to which structural and functional changes in muscles of Sod1−/− mice resemble those associated with normal aging. We tested the hypothesis that muscle weakness in Sod1−/− mice is due to functionally denervated fibers by comparing forces during nerve and direct muscle stimulation. No differences were observed for wild-type mice at any age in the forces generated in response to nerve and muscle stimulation. Nerve- and muscle-stimulated forces were also not different for 4-wk-old Sod1−/− mice, whereas, for 8- and 20-mo-old mice, forces during muscle stimulation were 16 and 30% greater, respectively, than those obtained using nerve stimulation. In addition to functional evidence of denervation with aging, fiber number was not different for Sod1−/− and wild-type mice at 4 wk, but 50% lower for Sod1−/− mice by 20 mo, and denervated motor end plates were prevalent in Sod1−/− mice at both 8 and 20 mo and in WT mice by 28 mo. The data suggest ongoing denervation in muscles of Sod1−/− mice that results in fiber loss and muscle atrophy. Moreover, the findings support using Sod1−/− mice to explore mechanistic links between oxidative stress and the progression of deficits in muscle structure and function.


2002 ◽  
Vol 282 (4) ◽  
pp. L719-L726 ◽  
Author(s):  
Russell P. Bowler ◽  
Mike Nicks ◽  
Karrie Warnick ◽  
James D. Crapo

Bleomycin administration results in well-described intracellular oxidative stress that can lead to pulmonary fibrosis. The role of alveolar interstitial antioxidants in this model is unknown. Extracellular superoxide dismutase (EC-SOD) is the primary endogenous extracellular antioxidant enzyme and is abundant in the lung. We hypothesized that EC-SOD plays an important role in attenuating bleomycin-induced lung injury. Two weeks after intratracheal bleomycin administration, we found that wild-type mice induced a 106 ± 25% increase in lung EC-SOD. Immunohistochemical staining revealed that a large increase in EC-SOD occurred in injured lung. Using mice that overexpress EC-SOD specifically in the lung, we found a 53 ± 14% reduction in bleomycin-induced lung injury assessed histologically and a 17 ± 6% reduction in lung collagen content 2 wk after bleomycin administration. We conclude that EC-SOD plays an important role in reducing the magnitude of lung injury from extracellular free radicals after bleomycin administration.


2020 ◽  
Vol 12 (2) ◽  
pp. 150-155
Author(s):  
Inna Buzduga ◽  
Tetiana Tkachuk ◽  
Irina Panchuk

High temperature negatively affects the plants. In particular, under the heat stress he production of reactive oxygen species increases in the plant cell. It leads to the development of oxidative stress. The formation of carbonyl groups in proteins is a marker of oxidative damage of plant cells. Plants have a defense system that consists of soluble carbohydrates such as sucrose and glucose and antioxidant enzymes, including catalase. Carbohydrates have protective mechanisms and can activate different signaling pathways with following changes in gene expression. Despite the data available, information on the effects of sucrose and glucose on the oxidative modification of proteins under heat stress is insufficient. The aim of our work was to study the role of sucrose and glucose for the carbonyl groups content in cat2cat3 knockout plants of A. thaliana under heat stress. We used 7-week-old Arabidopsis thaliana plants of wild-type and knockout cat2cat3 line, which lacks the expression of two catalase genes – cat2 and cat3. Plants were grown under 16-hour light day at a temperature of + 20°C and an illumination of 2.5 kL. Heat treatment was performed on a water bath in glass flasks with 15-20 leaves which were incubated in 1 mm potassium phosphate buffer without carbohydrates and with addition of sucrose or glucose (1% final concentration) during 2 and 4 hours at the +37°C and +44° C. The content of carbonyl groups and total protein was determined photometrically. It has been shown that intact knockout cat2cat3 plants have a higher content of carbonyl groups, which indicates chronic oxidative stress. Addition of exogenous sucrose or glucose to the incubation buffer had a protective effect during 4 hours of stress. Carbonyl groups formation in wild type decreased under the +37ºС and +44ºС, while in the cat2сat3 line only under the moderate (+37ºС) heat stress. In the knockout mutant alternative ways of defense are exhausted under +44ºC.


2015 ◽  
Vol 309 (3) ◽  
pp. C169-C178 ◽  
Author(s):  
Guiming Liu ◽  
Rania A. Elrashidy ◽  
Nan Xiao ◽  
Michael Kavran ◽  
Yexiang Huang ◽  
...  

Manganese superoxide dismutase (MnSOD) is considered a critical component of the antioxidant systems that protect against oxidative damage. We are interested in the role of oxidative stress in bladder detrusor smooth muscle (SM) in different disease states. In this study, we generated an inducible, SM-specific Sod2−/− mouse model to investigate the effects of MnSOD depletion on the function of the bladder. We crossbred floxed Sod2 ( Sod2lox/lox) mice with mice containing heterozygous knock-in of a gene encoding a tamoxifen-activated Cre recombinase in the SM22α promoter locus [SM-CreERT2(ki)Cre/+]. We obtained Sod2lox/lox,SM-CreERT2(ki)Cre/+ mice and injected 8-wk-old males with 4-hydroxytamoxifen to induce Cre-mediated excision of the floxed Sod2 allele. Twelve weeks later, SM-specific deletion of Sod2 and depletion of MnSOD were confirmed by polymerase chain reaction, immunoblotting, and immunohistochemistry. SM-specific Sod2−/− mice exhibited normal growth with no gross abnormalities. A significant increase in nitrotyrosine concentration was found in bladder SM tissue of SM-specific Sod2−/− mice compared with both wild-type mice and Sod2+/+, SM-CreERT2(ki)Cre/+ mice treated with 4-hydroxytamoxifen. Assessment of 24-h micturition in SM-specific Sod2−/− mice revealed significantly higher voiding frequency compared with both wild-type and SM-specific Cre controls. Conscious cystometry revealed significantly shorter intercontraction intervals and lower functional bladder capacity in SM-specific Sod2−/− mice compared with wild-type mice. This novel model can be used for exploring the mechanistic role of oxidative stress in organs rich in SM in different pathological conditions.


2006 ◽  
Vol 188 (24) ◽  
pp. 8586-8592 ◽  
Author(s):  
Ju-Sim Kim ◽  
Sang Ho Choi ◽  
Jeong K. Lee

ABSTRACT Lysine decarboxylase expression by Vibrio vulnificus, which is up-regulated by CadC in response to acid stress, is also induced by SoxR in response to superoxide stress. SoxR binds to the promoter region of the cadBA operon, coding for a lysine-cadaverine antiporter (CadB) and a lysine decarboxylase (CadA). The induction of cadBA transcription by SoxR is independent of CadC. Cadaverine, which neutralizes the external medium, also appears to scavenge superoxide radicals, since increasing cellular cadaverine by elevating the gene dosage of cadBA significantly diminished the induction of Mn-containing superoxide dismutase under methyl viologen-induced oxidative stress. Consistently, a lack of cadaverine caused by mutation in cadA resulted in low tolerance to oxidative stress compared with that of the wild type.


2013 ◽  
Vol 26 (4) ◽  
pp. 431-441 ◽  
Author(s):  
Liangsheng Xu ◽  
Weidong Chen

Agrobacterium-mediated transformation (AMT) was used to identify potential virulence factors in Sclerotinia sclerotiorum. Screening AMT transformants identified two mutants showing significantly reduced virulence. The mutants showed growth rate, sclerotial formation, and oxalate production similar to that of the wild type. The mutation was due to a single T-DNA insertion at 212 bp downstream of the Cu/Zn superoxide dismutase (SOD) gene (SsSOD1, SS1G_00699). Expression levels of SsSOD1 were significantly increased under oxidative stresses or during plant infection in the wild-type strain but could not be detected in the mutant. SsSOD1 functionally complemented the Cu/Zn SOD gene in a Δsod1 Saccharomyces cerevisiae mutant. The SOD mutant had increased sensitivity to heavy metal toxicity and oxidative stress in culture and reduced ability to detoxify superoxide in infected leaves. The mutant also had reduced expression levels of other known pathogenicity genes such as endo-polygalacturanases sspg1 and sspg3. The functions of SsSOD1 were further confirmed by SsSOD1-deletion mutation. Like the AMT insertion mutant, the SsSOD1-deletion mutant exhibited normal growth rate, sclerotial formation, oxalate production, increased sensitivity to metal and oxidative stress, and reduced virulence. These results suggest that SsSOD1, while not being required for saprophytic growth and completion of the life cycle, plays critical roles in detoxification of reactive oxygen species during host–pathogen interactions and is an important virulence factor of Sclerotinia sclerotiorum.


1999 ◽  
Vol 37 (5) ◽  
pp. 307-314 ◽  
Author(s):  
S. Ito-Kuwa ◽  
K. Nakamura ◽  
S. Aoki ◽  
T. Osafune ◽  
V. Vidotto ◽  
...  

2001 ◽  
Vol 69 (6) ◽  
pp. 4034-4040 ◽  
Author(s):  
Richard W. Seyler ◽  
Jonathan W. Olson ◽  
Robert J. Maier

ABSTRACT Superoxide dismutase (SOD) is a nearly ubiquitous enzyme among organisms that are exposed to oxic environments. The single SOD ofHelicobacter pylori, encoded by the sodB gene, has been suspected to be a virulence factor for this pathogenic microaerophile, but mutations in this gene have not been reported previously. We have isolated mutants with interruptions in thesodB gene and have characterized them with respect to their response to oxidative stress and ability to colonize the mouse stomach. The sodB mutants are devoid of SOD activity, based on activity staining in nondenaturing gels and quantitative assays of cell extracts. Though wild-type H. pylori is microaerophilic, the mutants are even more sensitive to O2 for both growth and viability. While the wild-type strain is routinely grown at 12% O2, growth of the mutant strains is severely inhibited at above 5 to 6% O2. The effect of O2 on viability was determined by subjecting nongrowing cells to atmospheric levels of O2 and plating for survivors at 2-h time intervals. Wild-type cell viability dropped by about 1 order of magnitude after 6 h, while viability of the sodBmutant decreased by more than 6 orders of magnitude at the same time point. The mutants are also more sensitive to H2O2, and this sensitivity is exacerbated by increased O2 concentrations. Since oxidative stress has been correlated with DNA damage, the frequency of spontaneous mutation to rifampin resistance was studied. The frequency of mutagenesis of ansodB mutant strain is about 15-fold greater than that of the wild-type strain. In the mouse colonization model, only 1 out of 23 mice inoculated with an SOD-deficient mutant of a mouse-adapted strain became H. pylori positive, while 15 out of 17 mice inoculated with the wild-type strain were shown to harbor the organism. Therefore, SOD is a virulence factor which affects the ability of this organism to colonize the mouse stomach and is important for the growth and survival of H. pylori under conditions of oxidative stress.


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