Increase In Endogenous Concentration Research Articles

Plant Poly(ADP-Ribose) Polymerase 1 Is a Potential Mediator of Cross-Talk between the Cajal Body Protein Coilin and Salicylic Acid-Mediated Antiviral Defence.

The nucleolus and Cajal bodies (CBs) are sub-nuclear domains with well-known roles in RNA metabolism and RNA-protein assembly. However, they also participate in other important aspects of cell functioning. This study uncovers a previously unrecognised mechanism by which these bodies and their components regulate host defences against pathogen attack. We show that the CB protein coilin interacts with poly(ADP-ribose) polymerase 1 (PARP1), redistributes it to the nucleolus and modifies its function, and that these events are accompanied by substantial increases in endogenous concentrations of salicylic acid (SA), activation of SA-responsive gene expression and callose deposition leading to the restriction of tobacco rattle virus (TRV) systemic infection. Consistent with this, we also find that treatment with SA subverts the negative effect of the pharmacological PARP inhibitor 3-aminobenzamide (3AB) on plant recovery from TRV infection. Our results suggest that PARP1 could act as a key molecular actuator in the regulatory network which integrates coilin activities as a stress sensor for virus infection and SA-mediated antivirus defence.

Exogenous Spermidine Promotes Somatic Embryogenesis of Cunninghamia lanceolata by Altering the Endogenous Phytohormone Content

In order to study how exogenous hormones in C. lanceolata (gymnosperm) regulate somatic embryogenesis, we measured the endogenous phytohormones of two genotypes with different somatic embryogenesis efficiency and found that an increase in endogenous concentrations of IAA and ABA may be correlated to more efficient somatic embryogenesis. By applying exogenous spermidine, we found that exogenous hormones may affect somatic embryogenesis efficiency through affecting the endogenous phytohormone content. Based on these results, further studies can be conducted whereby the concentration of exogenous hormones or the levels of endogenous phytohormones by molecular methods are regulated to promote somatic embryogenesis. Our research may benefit the long-term economic output of the forestry industry and lays the foundation to studying the molecular mechanism that controls somatic embryogenesis efficiency.

Water-Deficit Response Is Not Affected by Glutathione Deficiency in <i>Arabidopsis thaliana pad</i>2-1 Plants

Changes in glutathione and ascorbate content, hydrogen peroxide and abscisic acid were studied in developing leaves in wild-type (Col-0) and glutathione-deficient mutant pad2-1 lines of Arabidopsis thaliana over a time period of 9 days of drought followed by re-watering. Glutathione deficient mutant (pad2-1) presents mechanisms of acclimation to water stress through the reduction of plant biomass and increase in endogenous concentrations of ascorbate and glutathione. These acclimation responses to stress appeared along with the first symptoms of stress and we suggest here that they are regulated by ABA and H2O2. Normally, wild type plants under conditions of stress require an initial response phase in which a decrease in antioxidants is observed before reaching acclimation through the increase in levels of antioxidants. pad2-1 is more sensitive to stress and reacts to it; however, it did not suffer more oxidative stress than Col-0 plants, even though pad2-1 had higher levels of endogenous H2O2 relative to wild-type. In both water stressed Col-0 and pad2-1 plants increases in ABA were observed, however, more sharply in wild-type stressed plants. Low levels of glutathione together with high levels of H2O2 may regulate endogenous ABA concentrations and could be related to the slow growth rates which were observed during the experiment. The results highlighted the double function of glutathione as an antioxidant and signal molecule and also, the different response patterns of wild-type and pad2-1 when faced with drought stress. The results bring new insights to the responses of pad2-1 under conditions of water stress.

The Mechanism of Quinclorac Selectivity in Grasses

The mechanism of selectivity of the auxin herbicide quinclorac was studied in susceptible and resistant biotypes of Echinochloa hispidula and E. crus-galli; in grass species of different susceptibility like Brachiaria platyphylla, Setaria viridis, E. colonum, and Digitaria sanguinalis; and in tolerant crop rice (Oryza sativa cv. Thaibonnet). No significant differences in uptake, translocation, or metabolism of quinclorac between resistant and sensitive grasses were found. Hence, the mechanism of selectivity is target-site-based. It has been demonstrated that cyanide, which accumulates as a coproduct during stimulation of ethylene biosynthesis, is the primary phytotoxic principle in the herbicidal mode of action of quinclorac in E. crus-galli (K. Grossmann and J. Kwiatkowski, 1995, Pestic. Biochem. Physiol. 51, 150). Following root treatment of plants at the third leaf stage with 100 M quinclorac in hydroponics, the reductions in shoot growth of plants were closely correlated with the stimulation of 1-aminocyclopropane-1-carboxylic acid (ACC) synthase activity and with subsequent increases in endogenous concentrations of ACC and cyanide. When compared quinclorac with other auxin herbicides including quinmerac, α-naphthaleneacetic acid and dicamba, lower ACC and cyanide levels and correlated lower growth effects were found after treatment of D. sanguinalis. In quinclorac-resistant grass species and biotypes, ACC synthase activity was not induced and plants exhibited no significant changes in ACC and cyanide levels. Thus, the selective induction of ACC synthase activity, which ultimately leads to cyanide accumulation in the tissues of susceptible plants, plays the primary role for the selectivity of grasses toward quinclorac. This selectivity could be at the level of quinclorac perception or subsequent signal transduction via the auxin pathway leading to regulation of gene expression or posttran scriptional de novo enzyme synthesis. In rice, tolerance to quinclorac could be additionally favored by a higher β-cyanoalanine synthase activity, the main HCN-detoxifying enzyme.

Variations in abscisic acid, indole-3-acetic acid and zeatin riboside concentrations in two Mediterranean shrubs subjected to water stress

Water stress induced an increase in endogenous concentrations of ABA in Lavandula stoechas L. plants to 13100 pmol ABA g−1 FW, which may contribute to the maintenance of water relations between the second and the third day of water stress treatment. After the third day, a sharp decrease in ABA levels was observed to 2630 pmol ABA g−1 FW, together with a decrease in water content and water potential and a loss of plant response to water stress. Water deficit did not induce an increase in endogenous ABA concentration, which remained at 514 pmol ABA g−1 FW in Rosmarinus officinalis L., which is more sclerophyllous than L. stoechas. Nevertheless, the relative water content of Rosmarinus officinalis L. after seven days of water stress decreased more than 40% and ψ reached values of −3.2 MPa. R. officinalis showed lower levels of ABA, but significantly higher levels of IAA and ZR than L. stoechas (4 times and 6 times respectively in well watered-plants). The increase in ABA levels is not a common mechanism in these two Mediterranean shrubs which survive under water stress conditions.

Promotion of hepatocellular foci in female rats by chenodeoxycholic acid

Chenodeoxycholic acid (CDC), a dihydroxylated primary bile acid, was evaluated for promotional activity in the liver of rats using a two-stage initiation-promotion model. CDC is a primary bile acid that can attain high concentrations in serum and liver during induced or naturally occurring hepatocellular disorders. Female Sprague-Dawley rats were injected once (i.p.) with diethylnitrosamine (DEN, 150 mg/kg) or sterile physiologic saline (SAL, 0.85% NaCl). Two weeks later, rats in each group were placed into one of two subgroups and fed either NIH-31 mash (Control) or NIH-31 mash containing 0.5% CDC for a 10 week period. At the end of the feeding period, blood and liver samples were collected for determination of bile acid profiles and quantitation of hepatocellular foci respectively. Serum samples were analyzed for concentrations of individual bile acids using a HPLC method that utilizes a post-column enzymatic reaction and fluorescence detection. Liver slices from the left hepatic lobe were stained for foci positive for placental glutathione S-transferase. In serum, significant increases occurred in concentrations of all forms of CDC and were accompanied by mild, insignificant increases in lithocholic acid. Decreased serum concentrations occurred in all forms of cholic and deoxycholic acids. Analysis of liver sections revealed that rats treated with DEN-CDC had significant increases in numbers and volume of foci compared to those treated with DEN-Control. For rats in groups DEN-CDC and DEN-Control, the numbers of foci per square centimeter were 32 and 12; per cubic centimeter, 2221 and 937; and the per cent volume of foci, 1.487 and 0.385 respectively. In this study, CDC was a promoter of hepatocellular foci. Because concentrations of CDC in liver and serum increase in a variety of hepatobiliary disorders, the possibility that increases in endogenous concentrations can enhance the formation of hepatocellular foci is being explored.

Neurotransmitting substances and endotoxin respone in relation to hepatic enzyme induction.

Since neurotransmission and selected enzymes of the serotonin/adrenalin pathway are altered during endotoxicosis, a variety of neurophilic drugs, some active on defined loci in the tryptophan-serotonin pathway, were evaluated for their ability to modify endotoxin lethality. Among the various putative neurotransmitters, only leucine had some sensitizing effect on endotoxin toxicity. If given prior, and not subsequent, to challenge, <i>p</i>-chlorophenyl-alanine (but not the other analogues) consistently lowered the LD<sub>50</sub> of endotoxin in mice and impaired cortisone proctection against endotoxic death. This effect could not be related to the possible increase in endogenous concentrations of tryptophan, as a result of inhibition of tryptophan hydroxylase by <i>p</i>-chlorophenylalanine (PCPA). Additionally, the endotoxin toxicity in normal mice could not be modified by the serotonin antagonists cyproheptadine and LSD-25. The inorganic mercurial HgCl<sub>2</sub> (but not its organic analoge <i>p</i>-chloromercuribenzoate), behaved like PCPA in its ability to modify the endotoxin lethality. These results are discussed in relation to hepatic enzyme induction and a common receptor-effector system possibly coordinating a variety of inter- and intra-cellular responses.