Disease relevance of Solicam

• Mutant strains of the cyanobacterium Synechococcus sp. PCC 7942 that are resistant to the herbicides norflurazon and fluridone were analyzed [1].
• Nucleotide sequence of the phytoene desaturase gene from Synechocystis sp. PCC 6803 and characterization of a new mutation which confers resistance to the herbicide norflurazon [2].
• Toxicity of the norflurazon to the aquatic macrophyte Vallisneria americana (Michx.) [3].
• Allergic contact dermatitis from norflurazon (Predict) [4].
• Cloning a gene coding for norflurazon resistance in cyanobacteria [5].

High impact information on Solicam

• Expression of ATH1 does not require the presence of active chloroplasts because photooxidative destruction of the chloroplast by norflurazon treatment did not influence the ATH1 mRNA level [6].
• The protein is specifically induced by blue light in mature, light-grown plants (Adamska, I., Ohad, I., and Kloppstech, K. (1992) Proc. Natl. Acad. Sci. U. S. A. 89, 2610-2613), as well as in plants developed in the light in which pigment synthesis and plastid development were inhibited by the bleaching herbicide norflurazon [7].
• By contrast, treatment with norflurazon (an inhibitor of carotenoid biosynthesis causing a similar pale cotyledon phenotype) did not result in FSM resistance [8].
• In both green- and norflurazon-treated (chlorophyll-deficient) seedlings, cryptochrome activity is fairly uniform throughout its range of maximal response (390-480 nm), with no sharply defined peak at 450 nm; however, activity at longer wavelengths was disproportionately enhanced in CRY1-overexpressing seedlings as compared with wild type [9].
• To investigate how the pea PetE gene encoding plastocyanin is regulated by plastid signals, the effects of norflurazon, lincomycin and 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU), specific inhibitors of plastid-located processes generating plastid signals, have been examined [10].

Biological context of Solicam

• Deletion of this element coincides with the loss of chloroplast-dependency of reporter gene expression, as judged by norflurazon treatment of transgenic seedlings [11].
• Inhibition of chloroplast biogenesis by bleaching in the presence of norflurazon has no influence on the expression from this P1 promoter, suggesting that the onset of transcription of nuclear gene rpI21 is independent of a plastid signal [12].
• After 1 h high light on heterotrophically grown cells in the presence of norflurazon or fluridone, photosynthesis activity in vivo and PS II activity in vitro is lost [13].
• Upon biolistic transformation using the modified phytoene desaturase gene as a reporter and selection with norflurazon, integration into the nuclear genome of H. pluvialis and phytoene desaturase gene and protein expression were demonstrated by Southern, Northern, and Western blotting, respectively, in 11 transformants [14].
• The effects of growth temperature on chloroplast responses to norflurazon and amitrole, two herbicides inhibiting carotenogenesis, at phytoene desaturation and lycopene cyclization, respectively, were studied in leaves of maize plants grown at 20 degrees C and 30 degrees C in light [15].

Anatomical context of Solicam

• In organelles of norflurazon-treated leaves neither carotenoids nor chlorophylls were detectable and the thylakoid system was dismantled [15].
• The Lhcb transcript was not detectable in cells of norflurazon-supplied leaves, having chloroplasts totally devoid of both inner membranes and pigments [16].

Associations of Solicam with other chemical compounds

• In an in vitro assay, the modified phytoene desaturase was still active in conversion of phytoene to zeta-carotene and exhibited 43-fold-higher resistance to the bleaching herbicide norflurazon [14].
• CYP2C49 rice plants showed tolerance towards 13 herbicides, including chlortoluron (100 microM), norflurazon (0.5 microM), amiprofos-methyl (2.5 microM), alachlor (0.8 microM), and isoxaben (1 microM) [17].
• The photostabilization of norflurazon obtained with TFT-clay was mainly due to energy transfer from the herbicide to the organic cation via pi-pi interactions [18].
• Here the effect of norflurazon-treatment on the expression of genes for C4 photosynthesis was investigated [19].
• In this study of Arabidopsis thaliana we demonstrate that NF-treated photobleached plants are still able to make 5-aminolevulinic acid (ALA) the first precursor of porphyrins and tetrapyrroles [20].

Gene context of Solicam

• Effect of chlorophyll reduction in Arabidopsis thaliana by methyl jasmonate or norflurazon on antioxidant systems [21].
• Treatment of soybean cotyledons with norflurazon also induced expression of Aox1 [22].
• In addition, elimination of a promotive plastid signal by Norflurazon-induced photobleaching of plastids had no effect on HEMA2 expression while being required for normal white-light induction of HEMA1 [23].
• This study examined the contribution of catalase (CAT) and superoxide dismutase (SOD) in the overall antioxidant response to norflurazon (NF)-induced oxidative stress in leaves, mesocotyls and scutella of maize (Zea mays) [24].
• We have cloned and sequenced a gene, pds, from the cyanobacterium Synechococcus PCC7942 that is responsible for resistance to the bleaching herbicide norflurazon [25].

Analytical, diagnostic and therapeutic context of Solicam

• Norflurazon was analyzed by using a HPLC method [26].
• The herbicide norflurazon was encapsulated in ethylcellulose (EC(40)) microspheres by the solvent evaporation technique to obtain controlled release formulations [27].
• The results of alkaline comet assay indicated that norflurazon in concentrations of 2 and 0.2 microM induces significant increase of primary DNA damage in planarian cells compared to the corresponding control animals [28].
• Determination of norflurazon and desmethylnorflurazon in plant tissue by high-pressure liquid chromatography [29].

References