Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:1.3.5.1 (
succinate dehydrogenase
)
8,177
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
An inducer of acquired disease resistance in plants, benzo (1,2,3) thiadiazole-7-carbothioic acid S-methyl ester, exhibited direct, concentration-dependent inhibition of the NADH:ubiquinone oxidoreductase activity of complex I of the mitochondrial electron transport chain of cultured tobacco cells. The complex I activity was less sensitive to inhibition by
salicylic acid
, an endogenous activator of acquired disease resistance. Using a dichlorodihydrofluorescein assay, it was found that benzothiadiazole,
salicylic acid
and the complex I inhibitor rotenone, increased reactive oxygen species production within cells in a concentration-dependent manner. The results indicate that both benzothiadiazole and
salicylic acid
affect the mitochondria of treated plant cells and result in increased production of reactive oxygen species. The biochemical basis of this response could be related to the inhibition of the NADH:ubiquinone oxidoreductase activity of complex I that results in channelling of electrons via
complex II
, with concomitant higher levels of superoxide production.
...
PMID:Benzothiadiazole inhibits mitochondrial NADH:ubiquinone oxidoreductase in tobacco. 1677 35
This study was designed to investigate the mechanisms that are associated with manganese (Mn) toxicity. In addition, the association between Mn toxicity and 3, 4, 5 amino
salicylic acid
(ASA), anti-oxidants, including N-acetyl cysteine (NAC), was examined by dopaminergic cell line, SK-M-NC. Our studies showed that Mn influenced the mitochondria dysfunction and endoplasmic reticulum stress (ER stress). It reduced the mitochondria complex I activity but did not affect the
complex II
, III, or IV activities. The presence of 3, 4, 5 ASA protected against Mn-induced-apoptosis, as did NAC. However, the salicylate analogues and the antioxidants did not mediate ER stress in this model. The salicylate analogues reduced reactive oxygen species (ROS) and reversed the deficient mitochondrial membrane potential that was induced by Mn. Taken together, the 3, 4, 5 ASA worked in a similar way, regulating the Mn-induced mitochondrial dysfunction and protecting cells.
...
PMID:The effects of 3, 4 or 5 amino salicylic acids on manganese-induced neuronal death: ER stress and mitochondrial complexes. 2147 46
Mitochondria are both a source of ATP and a site of reactive oxygen species (ROS) production. However, there is little information on the sites of mitochondrial ROS (mROS) production or the biological role of such mROS in plants. We provide genetic proof that mitochondrial
complex II
(Complex II) of the electron transport chain contributes to localized mROS that regulates plant stress and defense responses. We identify an Arabidopsis mutant in the Complex II subunit, SDH1-1, through a screen for mutants lacking GSTF8 gene expression in response to
salicylic acid
(SA). GSTF8 is an early stress-responsive gene whose transcription is induced by biotic and abiotic stresses, and its expression is commonly used as a marker of early stress and defense responses. Transcriptional analysis of this mutant, disrupted in stress responses 1 (dsr1), showed that it had altered SA-mediated gene expression for specific downstream stress and defense genes, and it exhibited increased susceptibility to specific fungal and bacterial pathogens. The dsr1 mutant also showed significantly reduced
succinate dehydrogenase
activity. Using in vivo fluorescence assays, we demonstrated that root cell ROS production occurred primarily from mitochondria and was lower in the mutant in response to SA. In addition, leaf ROS production was lower in the mutant after avirulent bacterial infection. This mutation, in a conserved region of SDH1-1, is a unique plant mitochondrial mutant that exhibits phenotypes associated with lowered mROS production. It provides critical insights into Complex II function with implications for understanding Complex II's role in mitochondrial diseases across eukaryotes.
...
PMID:Mitochondrial complex II has a key role in mitochondrial-derived reactive oxygen species influence on plant stress gene regulation and defense. 2167 Mar 6
Mitochondria are known for their role in ATP production and generation of reactive oxygen species, but little is known about the mechanism of their early involvement in plant stress signaling. The role of mitochondrial
succinate dehydrogenase
(
SDH
) in
salicylic acid
(SA) signaling was analyzed using two mutants:
disrupted in stress response1
(
dsr1
), which is a point mutation in SDH1 identified in a loss of SA signaling screen, and a knockdown mutant (
sdhaf2
) for
SDH
assembly factor 2 that is required for FAD insertion into SDH1. Both mutants showed strongly decreased SA-inducible stress promoter responses and low
SDH
maximum capacity compared to wild type, while
dsr1
also showed low succinate affinity, low catalytic efficiency, and increased resistance to
SDH
competitive inhibitors. The SA-induced promoter responses could be partially rescued in
sdhaf2
, but not in
dsr1
, by supplementing the plant growth media with succinate. Kinetic characterization showed that low concentrations of either SA or ubiquinone binding site inhibitors increased
SDH
activity and induced mitochondrial H
2
O
2
production. Both
dsr1
and
sdhaf2
showed lower rates of SA-dependent H
2
O
2
production in vitro in line with their low SA-dependent stress signaling responses in vivo. This provides quantitative and kinetic evidence that SA acts at or near the ubiquinone binding site of
SDH
to stimulate activity and contributes to plant stress signaling by increased rates of mitochondrial H
2
O
2
production, leading to part of the SA-dependent transcriptional response in plant cells.
...
PMID:Salicylic Acid-Dependent Plant Stress Signaling via Mitochondrial Succinate Dehydrogenase. 2820 41
The present study was performed to unravel the mechanisms of systemic acquired resistance (SAR) establishment and resistance signaling pathways against the canker-rot fungus (
Inonotus obliquus
strain IO-U1) infection in Japanese birch plantlet No.8. Modulation of protein-profile induced by
salicylic acid
(SA)-administration was analyzed, and SA-responsive proteins were identified. In total, 5 specifically expressed, 3 significantly increased, and 3 significantly decreased protein spots were identified using liquid chromatography/tandem mass spectrometry (LC/MS/MS) and the sequence tag method. These proteins were malate dehydrogenase,
succinate dehydrogenase
, phosphoglycerate kinase, diaminopimalate decarboxylase, arginase, chorismate mutase, cyclophilin, aminopeptidase, and unknown function proteins. These proteins are considered to be involved in SAR-establishment mechanisms in the Japanese birch plantlet No 8.
...
PMID:Proteomic Analysis of Responsive Proteins Induced in Japanese Birch Plantlet Treated with Salicylic Acid. 2825 Mar 84
To investigate if and how the integrity of the mitochondrial electron transport chain (mETC) influences susceptibility of
Arabidopsis
toward
Colletotrichum higginsianum
, we have selected previously characterized mutants with defects at different stages of the mETC, namely, the complex I mutant
ndufs4
, the
complex II
mutant
sdh2-1
, the complex III mutant
ucr8-1
, and a mutant of the uncoupling protein
ucp1-2
. Relative to wild type, the selected complex I, II, and III mutants showed decreased total respiration, increased alternative respiration, as well as increased redox charge of the NADP(H) pool and decreased redox charge of the NAD(H) pool in the dark. In the light, mETC mutants accumulated free amino acids, albeit to varying degrees. Glycine and serine, which are involved in carbon recycling from photorespiration, and N-rich amino acids were predominantly increased in mETC mutants compared to the wild type. Taking together the physiological phenotypes of all examined mutants, our results suggest a connection between the limitation in the re-oxidation of reducing equivalents in the mitochondrial matrix and the induction of nitrate assimilation into free amino acids in the cytosol, which seems to be engaged as an additional sink for reducing power. The
sdh2-1
mutant was less susceptible to
C. higginsianum
and did not show hampered
salicylic acid
(SA) accumulation as previously reported for
SDH1
knock-down plants. The ROS burst remained unaffected in
sdh2-1
, emonstrating that subunit SDH2 is not involved in the control of ROS production and SA signaling by
complex II
. Moreover, the
ndufs4
mutant showed only 20% of
C. higginsianum
colonization compared to wild type, with the ROS burst and the production of callose papillae being significantly increased compared to wild type. This indicates that a restriction of respiratory metabolism can positively affect pre-penetration resistance of
Arabidopsis
. Taking metabolite profiling data from all investigated mETC mutants, a strong positive correlation of resistance toward
C. higginsianum
with NADPH pool size, pyruvate contents, and other metabolites associated with redox poise and energy charge was evident, which fosters the hypothesis that limitations in the mETC can support resistance at post-penetration stages by improving the availability of metabolic power.
...
PMID:Deficiencies in the Mitochondrial Electron Transport Chain Affect Redox Poise and Resistance Toward
Colletotrichum higginsianum
. 3168 68
Rice blast (
Magnaporthe oryzae
) is a devastating disease affecting rice production globally. The development of cultivars with host resistance has been proved to be the best strategy for disease management. Several rice-resistance genes (R) have been recognized which induce resistance to blast in rice but R gene-mediated mechanisms resulting in defense response still need to be elucidated. Here, mutant lines generated through CRISPR/Cas9 based targeted mutagenesis to investigate the role of
Pi21
against blast resistance and 17 mutant plants were obtained in T
0
generation with the mutation rate of 66% including 26% bi-allelic, 22% homozygous, 12% heterozygous, and 3% chimeric and 17 T-DNA-free lines in T
1
generation. The homozygous mutant lines revealed enhanced resistance to blast without affecting the major agronomic traits. Furthermore, comparative proteome profiling was adopted to study the succeeding proteomic regulations, using iTRAQ-based proteomic analysis. We identified 372 DEPs, among them 149 up and 223 were down-regulated, respectively. GO analysis revealed that the proteins related to response to stimulus, photosynthesis, carbohydrate metabolic process, and small molecule metabolic process were up-regulated. The most of DEPs were involved in metabolic, ribosomal, secondary metabolites biosynthesis, and carbon metabolism pathways. 40S ribosomal protein S15 (P31674), 50S ribosomal protein L4, L5, L6 (Q10NM5, Q9ZST0, Q10L93), 30S ribosomal protein S5, S9 (Q6YU81, Q850W6, Q9XJ28), and
succinate dehydrogenase
(Q9S827) were hub-proteins. The expression level of genes related to defense mechanism, involved in signaling pathways of jasmonic acid (JA),
salicylic acid
(SA), and ethylene metabolisms were up-regulated in mutant line after the inoculation of the physiological races of
M. oryzae
as compared to WT. Our results revealed the fundamental value of genome editing and expand knowledge about fungal infection avoidance in rice.
...
PMID:Knockout of
Pi21
by CRISPR/Cas9 and iTRAQ-Based Proteomic Analysis of Mutants Revealed New Insights into
M. oryzae
Resistance in Elite Rice Line. 3263 Jun 95