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Biomedical subjects

J Kuć

Publications and source records attributed to J Kuć.

10 recordsLinked to original sources
PubMed2001

Ca2+-dependent and Ca2+-independent excretion modes of salicylic acid in tobacco cell suspension culture.

14C-salicylic acid (SA) was used to monitor SA metabolism and its regulation in tobacco cell suspension culture. Two SA concentrations (20 microM and 200 microM) were used for comparison. SA was quickly taken up in both treatments, and the 200 microM-treated cells absorbed approximately 15 times that of 20 microM-treated cells within 5 min. More than 85% and 50% of the absorbed SA were excreted in free form to the culture medium within 5 h from cells treated with 200 microM and 20 microM SA, respectively. SA excretion was significantly inhibited by EGTA and the inhibition could be reversed by the addition of exogenous Ca2+ to the culture medium in the 200 microM SA treatment. However, EGTA had little or no effect on SA excretion in the 20 microM SA treatment. The data suggest that tobacco suspension-cultured cells may contain both Ca2+-dependent and Ca2+-independent pathways for SA excretion. Reduced glutathione (an active oxygen species scavenger), staurosporine (a protein kinase inhibitor), and cycloheximide (an inhibitor of de novo protein synthesis) also blocked intracellular SA excretion to the culture medium in the 200 microM but not in the 20 microM SA treatment. These data support the existence of alternative SA excretion pathways in tobacco suspension-cultured cells. Tobacco cells may use both Ca2+-dependent and Ca2+-independent excretion pathways to cope with different intracellular SA status, and the pathway influenced by EGTA, reduced glutathione, staurosporine, and cycloheximide is activated by SA at 200 microM, but not at 20 microM.

Autoradiography↗
PubMed1990

Compounds from plants that regulate or participate in disease resistance.

Disease resistance is multifactorial. The response phase includes: synthesis of phytoalexins, i.e. low molecular weight antimicrobial compounds which accumulate at sites of infection; systemically produced enzymes which degrade pathogens, e.g. chitinases, beta-1,3-glucanases and proteases; systemically produced enzymes which generate antimicrobial compounds and protective biopolymers, e.g. peroxidases and phenoloxidases; biopolymers which restrict the spread of pathogens, e.g. hydroxyproline-rich glycoproteins, lignin, callose; and compounds which regulate the induction and/or activity of the defence compounds, e.g. elicitors of plant and microbial origin, immunity signals from immunized plants and compounds which release immunity signals. Disease resistance in plants is not determined by the presence or absence of genes for resistance mechanisms, it is determined by the speed and degree of gene expression and the activity of the gene products. It is likely, therefore, that all plants have the genetic potential for resistance. This potential can be expressed systemically (immunization) after restricted inoculation with pathogens, attenuated pathogens or selected non-pathogens, or treatment with chemical substances that are produced by immunized plants or chemicals which release such signals. Immunization is effective against diseases caused by fungi, bacteria and viruses, and it has been successfully tested in the laboratory and field. Advances in science have provided information and technology to enhance resistance to plant pests. Pesticides are part of this technology, but they also contribute to a complex world problem which threatens our environment and hence our survival. The future will see the restriction of pesticide use and a greater reliance on resistant plants generated using immunization and other biological control technologies, genetic engineering and classical plant breeding. However, as with past and current technology, we will have created unique problems. The survival of our planet depends upon anticipating these problems and meeting the challenge of their solution.

Breeding↗
PubMed1989

Direct detection of beta-1,3-glucanase isozymes on polyacrylamide electrophoresis and isoelectrofocusing gels.

A procedure to assay isozymes of beta-1,3-glucanase directly on polyacrylamide gel electrophoresis (PAGE) and isoelectrofocusing (IEF) gels by using 2,3,5-triphenyltetrazolium chloride is described. The reagent reacts with reducing sugars released by beta-1,3-glucanases from the substrate laminarin. Acidic and neutral isozymes of beta-1,3-glucanase were detected and quantified on 17.5% native PAGE gels run with an anodic buffer system. A significant linear relationship (alpha = less than 0.01, R = 0.991) was observed between amounts of beta-1,3-glucanase loaded and intensity of bands stained with the reagent on native PAGE gels. A full isozyme pattern was obtained on 7.5% IEF gels with a pH range of 3.5-9.5. The IEF gels were heated in a microwave oven during the staining process to minimize diffusion.

Electrophoresis, Polyacrylamide Gel↗
PubMed1985

Phytoalexins.

Plants respond to infection by accumulating low-molecular-weight antimicrobial stress metabolites called phytoalexins. The phytoalexins are generally lipophilic substances that are products of a plant's secondary metabolism, and they often accumulate at infection sites to concentrations which are inhibitory to the development of fungi and bacteria. Resistance and susceptibility in plants are not determined by the presence or absence of genetic information for resistance mechanisms, including biosynthetic pathways for phytoalexin synthesis, but, rather, by the speed with which the information is expressed, the activity of the gene products, and the magnitude of the resistance response. Unlike the antibody-antigen component of the immune system in animals, low specificity is the general rule for the induction of phytoalexin accumulation and their activity against microorganisms. Annual plants can be systemically immunized against diseases caused by fungi, bacteria, and viruses by restricted infection with the pathogens, avirulent forms of pathogens, or compounds formed in immunized plants. Immunization induces plants to respond rapidly to infection with a multicomponent resistant response. The biosynthesis and accumulation of phytoalexins is one component of this resistant response. Resistance may be elicited by components in the walls and cell surfaces of fungi and bacteria and by compounds liberated from cells, their walls, or surfaces. Resistance can be enhanced or suppressed by products produced by the pathogen, the host, or by their interaction. The successful pathogen avoids recognition by the plant as nonself, suppresses the resistance response, or detoxifies its products. The actors in this play for survival on the metabolic level include the shikimate, acetate-malonate, and acetate-mevalonate pathways; glucans; oligogalacturonates; glycoproteins; lipopolysaccharides; and poly-unsaturated fatty acids. The play is directed by the genetic information of host and pathogen, and this direction is at the level of recognition and not by the presence or absence of mechanisms to contain the development of infectious agents.

Bacteria↗
PubMed1984

Phytoalexins and disease resistance mechanisms from a perspective of evolution and adaptation.

Plants respond to cellular injury and infection by accumulating low molecular weight antimicrobial stress metabolites called phytoalexins. The accumulation of phytoalexins, together with lignification, suberization, callose formation and the production of agglutinins and inhibitors of extracellular microbial hydrolases, appears to be part of a multi-component response mechanism associated with disease resistance and wound repair. Compared to the antibody-antigen response in animals, the phytoalexin response in plants has low specificity for induction and activity of the phytoalexins. Plants also contain preformed antimicrobial chemical and physical barriers to infection in their external tissues. The successful pathogen has evolved to cope with preformed inhibitors and barriers and either avoids eliciting the response mechanism, or suppresses the mechanism, or detoxifies its antimicrobial components. Annual plants can be systemically immunized against diseases caused by viruses, bacteria and fungi by limited infection with any one of the respective organisms. As with animals, disease resistance in plants depends on the rate and magnitude of response rather than on the ability to respond. The genetic information for disease resistance is found in all organisms, and disease resistance is the rule in nature. The interactions of plants with microorganisms in their environment are nature's example of diplomacy--compromise, adjustment to change and avoidance of deadly conflict.

Adaptation, Biological↗
PubMed1974

Effect of Ethrel and Ceratocystis fimbriata on the Synthesis of Fatty Acids and 6-Methoxy Mellein in Carrot Root.

The rate of incorporation of (14)C from acetate-1-(14)C into fatty acids by carrot root discs, 18 hours after inoculation with Ceratocystis fimbriata, was 9-fold greater than that in freshly cut discs. The rate in discs treated with water or Ethrel was 3-fold greater. The rate of incorporation of (14)C from glucose-U-(13)C into fatty acids was 3-fold greater 18 hours after any of the above treatments. The rate of (14)C incorporation from malonate-2-(14)C into fatty acids 24 hours after inoculation with C. fimbriata or treatment with water was 25 and 60%, respectively, of that in freshly cut discs. Linoleic acid was the principal fatty acid in carrot root, but incorporation of (14)C from acetate-1-(14)C into the acid was low until 18 hours after inoculation with C. fimbriata or treatment with Ethrel. Turnover rates of the fatty acids appeared low and were similar for all treatments.There was little or no incorporation of (14)C from acetate or malonate into 3-methyl-6-methoxy-8-hydroxy-3,4-dihydroisocoumarin (6-methoxy mellein) in fresh carrot discs or in discs treated with water, but label was incorporated rapidly in discs inoculated with C. fimbriata or treated with Ethrel. The rate of incorporation of label from acetate into fatty acids was severalfold higher than into 6-methoxy mellein, but the rate of incorporation of label from malonate was approximately equal into fatty acids and 6-methoxy mellein 24 hours after inoculation. The rate of fatty acid synthesis does not appear directly related to the accumulation of 6-methoxy mellein.

Journal Article↗