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)
In order to supply the tetrazolium salt procedure to flow cytometry we have synthesized monotetrazolium salts which are converted into fluorescent formazans on reduction. In this preliminary study we investigated the "oxygen sensitivity" of four of our compounds and compared them to the commercially available nitrotetrazole blue (NBT). The amount of formazan produced by Ehrlich ascites tumour cells via the
succinic dehydrogenase
reaction during oxic and anoxic incubations was determined by elution technique. Under oxic conditions no NBT formazan but much cyano-di-chlorophenyl formazan (==CCPC) was generated. The yields of this formazan differed only slightly between oxic and anoxic incubations. Twice as much of the amount of the other three formazans cyano-ditolyl- (==CTC, Stellmach 1984), cyanodiphenyl- (==CPC), and cyano-dianisyl tetrazolium chloride (==CAC), were produced in nitrogen atmosphere as in oxygen. The amount of all formazans investigated increased both in oxic and in anoxic conditions if cyanide was present. All cyano-aryl formazans have the maximum of absorbance between 430 and 470 nm and fluoresce in the spectral range above 580 nm with
CTC
formazan being the brightest. The tetrazolium salts, i.e. in unreduced state, did not fluoresce in the visible part of the spectrum. The formazans could be applied to flow cytometry. After staining the nuclear DNA with the fluorochrome DAPI, we obtained detailed two-parametric distributions correlating the amount of formazan per cell with the DNA content. The results are a step to establish a method for automated identification of malignant cells.
...
PMID:[Fluorescent formazans in flow cytometry. Studies of their oxygen sensitivity]. 250 18
Sclerotinia homoeocarpa isolates were collected from golf courses in Japan and the United States (2016-2017). Japan isolates were collected during a monitoring study and the U.S. isolates were collected due to field failure. Five
succinate dehydrogenase
inhibitor (SDHI) active ingredients (boscalid, fluopyram, fluxapyroxad, isofetamid, and penthiopyrad) were examined using in vitro sensitivity assays to determine cross-resistance. Sequence analysis revealed a point mutation leading to an amino acid substitution (H267Y) and a silent mutation (CTT to
CTC
) at codon 181 in the SdhB subunit gene. Isolates with the B-H267Y (n = 10) mutation were resistant to boscalid and penthiopyrad and had increased sensitivity to fluopyram. SdhB silent mutation 181C>T isolates (n = 2) were resistant to boscalid, isofetamid, and penthiopyrad. Sequence analysis revealed 3 mutations leading to an amino acid substitution (G91R, n = 5; G150R, n = 1; G159W, n = 1) in the SdhC subunit gene. Isolates harboring the SdhC (G91R or G150R) mutations were resistant to boscalid, fluxapyroxad, isofetamid, and penthiopyrad. A genetic transformation system was used to generate mutants from a SDHI sensitive isolate to confirm the B-H267Y and C-G91R mutations were direct determinants of SDHI resistance and associated with in vitro sensitivity assay results.
...
PMID:Resistance of Sclerotinia homoeocarpa Field Isolates to Succinate Dehydrogenase Inhibitor Fungicides. 3030 34
Dollar spot, caused by the ascomycete fungus Clarireedia (formerly, Sclerotinia) is one of the most resource-demanding diseases on amenity turfgrasses in North America. Differential resistance to the
succinate dehydrogenase
inhibitor (SDHI) fungicide class, conferred by singular point mutations on the SdhB, SdhC, and SdhD subunits of SDH, has been recently reported in dollar spot as well as many other plant-pathogenic fungal diseases. Four unique mutations were previously reported from field isolates of Clarireedia collected from two different cool-season golf courses in Japan and Rhode Island, USA: an amino acid substitution H267Y and a silent mutation (CTT to
CTC
) at codon 181 on the SdhB subunit gene, and amino acid substitutions G91R and G150R on the SdhC subunit gene. To properly diagnose and monitor SDHI resistance in the field, a rapid detection system for known mutations is crucial. As part of this study, additional SDHI-resistant Clarireedia isolates were collected from Rutgers University research plots and in vitro sensitivity to four SDHI active ingredients was assessed. SdhB, -C and -D subunits of these isolates were sequenced to reveal an additional mutation on the SdhB subunit gene, H267R. Cleaved amplified polymorphic sequence (CAPS) and derived CAPS (dCAPS) molecular markers were developed to detect five mutations conferring SDHI resistance in Clarireedia isolates and validated using samples from two additional golf courses, in Connecticut and Wisconsin, experiencing SDHI field failure. This PCR-based molecular detection system will be useful for continued monitoring, assessment, and prevention of SDHI resistance in the field.
...
PMID:A rapid molecular detection system for SdhB and SdhC point mutations conferring differential SDHI resistance in populations of Clarireedia. 3275 32