Cosmos white rot: First characterization, physiology, host range, disease resistance, and chemical control.

A new disease of Cosmos sulphureus Cav. causing external and internal stem discoloration, premature death, and wilting was observed in 27.8% of plants with an average disease severity rating of 4.4 in Gazipur, Bangladesh. Morphological, pathological, and molecular analyses identified the isolated fungus as Sclerotinia sclerotiorum (Lib) de Bary, the causative agent of white rot disease. The optimum growth and sclerotium formation of S. sclerotiorum occurred at 20°C and pH 5.0, while glucose, peptone, yeast extract, casein, and ascorbic acid were the appropriate nutrient sources. Furthermore, mycelial growth and sclerotial development were favored in media containing potassium, magnesium, calcium, and sodium. As many as 20 plant species of 10 families; Calendula officinalisi, Chrysanthemum indicum, Catharanthus roseus, Solanum tuberosum, S. lycopersicum, S. melongena, Capsicum annum, Lablab purpureus, Phaseolus vulgari, Lens culinaris, Vigna radiata, Vigna mungo, Daucus carota, Raphanus sativus, Brassica juncea, Punica granatum, Spinacia oleracea, Ipomoea batatas, Ipomoea aquatica, and Elaeocarpus serratus were identified as the new hosts of the pathogen in Bangladesh. None of the C. sulphureus and Cosmos bipinnatus germplasms screened were genetically resistant to the pathogen. Among the tested fungicides, Autostin 50 WDG (carbendazim) and Rovral (Dicarboxamide) were most inhibitory to the fungus, while Autostin 50 WDG provided an efficient control of the pathogen in vivo up to 15 days after spray. The acquired results on characterization, physiology, host range, resistance, and fungicidal control of the pathogen could be valuable for effectively managing cosmos white rot in the field.

Interaction of intracellular hydrogen peroxide accumulation with nitric oxide production in abscisic acid signaling in guard cells.

Reactive oxygen species and nitric oxide (NO•) concomitantly play essential roles in guard cell signaling. Studies using catalase mutants have revealed that the inducible and constitutive elevations of intracellular hydrogen peroxide (H2O2) have different roles: only the inducible H2O2 production transduces the abscisic acid (ABA) signal leading stomatal closure. However, the involvement of inducible or constitutive NO• productions, if exists, in this process remains unknown. We studied H2O2 and NO• mobilization in guard cells of catalase mutants. Constitutive H2O2 level was higher in the mutants than that in wild type, but constitutive NO• level was not different among lines. Induced NO• and H2O2 levels elicited by ABA showed a high correlation with each other in all lines. Furthermore, NO• levels increased by exogenous H2O2 also showed a high correlation with stomatal aperture size. Our results demonstrate that ABA-induced intracellular H2O2 accumulation triggers NO• production leading stomatal closure. ABBREVIATIONS: ABA: abscisic acid; CAT: catalase; cGMP: cyclic guanosine monophosphate; DAF-2DA: 4,5-diaminofluorescein-2 diacetate; H2DCF-DA: 2',7'-dichlorodihydrofluorescein diacetate; MeJA: methyljasmonate; NOS: nitric oxide synthetase; NR: nitrate reductase; POX: peroxidase; ROS: reactive oxygen species; SNAP: S-nitroso-N-acetyl-DL-penicillamine; SNP: sodium nitroprusside; NOX: NADP(H) oxidase.

Catalases negatively regulate methyl jasmonate signaling in guard cells.

Methyl jasmonate (MeJA)-induced stomatal closure is accompanied by the accumulation of hydrogen peroxide (H2O2) in guard cells. In this study, we investigated the roles of catalases (CATs) in MeJA-induced stomatal closure using cat mutants cat2, cat3-1 and cat1 cat3, and the CAT inhibitor, 3-aminotriazole (AT). When assessed with 2',7'-dichlorodihydrofluorescein, the reduction of catalase activity by means of mutations and the inhibitor accumulated higher basal levels of H2O2 in guard cells whereas they did not affect stomatal aperture in the absence of MeJA. In contrast, the cat mutations and the treatment with AT potentiated MeJA-induced stomatal closure and MeJA-induced H2O2 production. These results indicate that CATs negatively regulate H2O2 accumulation in guard cells and suggest that inducible H2O2 production rather than constitutive elevation modulates stomatal apertures in Arabidopsis.

The roles of CATALASE2 in abscisic acid signaling in Arabidopsis guard cells.

We investigated the roles of catalase (CAT) in abscisic acid (ABA)-induced stomatal closure using a cat2 mutant and an inhibitor of CAT, 3-aminotriazole (AT). Constitutive reactive oxygen species (ROS) accumulation due to the CAT2 mutation and AT treatment did not affect stomatal aperture in the absence of ABA, whereas ABA-induced stomatal closure, ROS production, and [Ca(2+)](cyt) oscillation were enhanced.

Roles of intracellular hydrogen peroxide accumulation in abscisic acid signaling in Arabidopsis guard cells.

Reactive oxygen species (ROS), including hydrogen peroxide (H(2)O(2)), are among the important second messengers in abscisic acid (ABA) signaling in guard cells. In this study, to investigate specific roles of H(2)O(2) in ABA signaling in guard cells, we examined the effects of mutations in the guard cell-expressed catalase (CAT) genes, CAT1 and CAT3, and of the CAT inhibitor 3-aminotriazole (AT) on stomatal movement. The cat3 and cat1 cat3 mutations significantly reduced CAT activities, leading to higher basal level of H(2)O(2) in guard cells, when assessed by 2',7'-dichlorodihydrofluorescein, whereas they did not affect stomatal aperture size under non-stressed condition. In addition, AT-treatment at concentrations that abolish CAT activities, showed trivial affect on stomatal aperture size, while basal H(2)O(2) level increased extensively. In contrast, cat mutations and AT-treatment potentiated ABA-induced stomatal closure. Inducible ROS production triggered by ABA was observed in these mutants and wild type as well as in AT-treated guard cells. These results suggest that ABA-inducible cytosolic H(2)O(2) elevation functions in ABA-induced stomatal closure, while constitutive increase of H(2)O(2) do not cause stomatal closure.

Cytosolic alkalization and cytosolic calcium oscillation in Arabidopsis guard cells response to ABA and MeJA.

Abscisic acid (ABA)- and methyl jasmonate (MeJA)-induced stomatal closure are accompanied by cytosolic alkalization in guard cells. However, it remains to be clarified how the alkalization functions in not only ABA signaling but also MeJA. We investigated cytosolic alkalization in guard cells during ABA-, MeJA- and Ca(2+)-induced stomatal closure of wild type, abi1-1, abi2-1, ost1-2 and coi1 using a pH-sensitive fluorescent dye, BCECF-AM. ABA induced cytosolic alkalization in guard cells of wild-type and coi1 but not in ost1-2 guard cells whereas MeJA elicited cytosolic alkalization in wild-type and ost1-2 guard cells but not in coi1. Neither ABA nor MeJA induced cytosolic alkalization in abi1-1 and abi2-1 guard cells. Exogenous Ca(2+) induced stomatal closure accompanied by cytosolic alkalization in guard cells of wild-type, abi1-1, abi2-1, ost1-2 and coi1 plants. An agent to acidify cytosol, butyrate, suppressed Ca(2+)-induced cytosolic alkalization and ABA-, MeJA- and Ca(2+)-induced cytosolic Ca(2+) oscillation in wild-type guard cells to prevent stomatal closure. These results indicate that cytosolic alkalization and cytosolic Ca(2+) oscillation coordinately function in ABA and MeJA signaling in Arabidopsis guard cells.

Proline and glycinebetaine confer cadmium tolerance on tobacco bright yellow-2 cells by increasing ascorbate-glutathione cycle enzyme activities.

Cadmium (Cd) stress significantly decreased membrane integrity and impaired the ascorbate (ASC)-glutathione (GSH) cycle in tobacco Bright Yellow-2 cells. Exogenous application of proline and glycinebetaine (betaine) significantly restored the membrane integrity and increased the activities of ASC-GSH cycle enzymes under Cd stress without maintenance of the rich ASC or GSH pools. Moreover, proline offered more efficient protection against Cd stress than betaine.