Search

The 1, 4-linked glucans such as xyloglucan and amylose are known to form a complex with iodine/iodide ions and to also be precipitated with CaCl2 in the presence of iodine. Here, we show that iodine gas could be specifically incorporated into xyloglucan. Furthermore, we show that [125I]I2 gas is, over time, incorporated at high levels into the entire outer surface of poplar seedlings but that spraying seedlings with abscisic acid to close stomata decreases the incorporation of the gas. There was less incorporation of the gas in a transgenic poplar overexpressing xyloglucanase at the early stages when compared with a wild type. This shows that xyloglucan serves as a key absorber of iodine gas into a plant body. After individual leaves of cultured seedlings were exposed to the gas for 30 min, no radioiodine was emitted from those leaves over the following two weeks, indicating that no turnover occurs in radioiodine once it is bound to the polysaccharides in plant tissues. We conclude that forest trees could serve as one of the largest enormous capture systems for the radioiodine fallout following the nuclear power plant accident in Fukushima.

A megathrust earthquake caused the Fukushima–Daiichi nuclear power plant accident, which dispersed abundant radioiodines, causing them to be bound to xyloglucan into forest trees. Nevertheless, targeted xyloglucan was found in increased quantities in the annual rings of forest trees affected by the earthquake. We propose that trees could acclimate rapidly to shaking stress through an increase in xyloglucan deposition as a plant response under natural phenomena.

Nuclear power plant accidents have dispersed radiocesium into the atmosphere to contaminate trees with no turnover in heartwood, as occurred in Fukushima, and as has persisted for over 30 years around Chernobyl. Here we employ the ponding method, in which radiocesium can be flushed out from the cross-cut edges of Japanese cedar, Cryptomeria japonica (L.f.) D. Don., stem with water due to xyloglucan degradation in tracheids. Furthermore, lab-scale ponding experiments have shown that a non-detectable level of radiocesium has been observed not only in the pool water used for 575 days but also in the water containing recombinant xyloglucanase. This traditional technology is now a new biotechnology.

Cell-to-cell communication is tightly regulated in response to environmental stimuli in plants. We previously used a photoconvertible fluorescent protein Dendra2 as a model reporter to study this process. This experiment revealed that macromolecular trafficking between protonemal cells in Physcomitrella patens is suppressed in response to abscisic acid (ABA). However, it remains unknown which ABA signaling components contribute to this suppression and how. Here, we show that ABA signaling components SUCROSE NON-FERMENTING 1-RELATED PROTEIN KINASE 2 (PpSnRK2) and ABA INSENSITIVE 3 (PpABI3) play roles as an essential and promotive factor, respectively, in regulating ABA-induced suppression of Dendra2 diffusion between cells (ASD). Our quantitative imaging analysis revealed that disruption of PpSnRK2 resulted in defective ASD onset itself, whereas disruption of PpABI3 caused an 81-min delay in the initiation of ASD. Live-cell imaging of callose deposition using aniline blue staining showed that, despite this onset delay, callose deposition on cross walls remained constant in the PpABI3 disruptant, suggesting that PpABI3 facilitates ASD in a callose-independent manner. Given that ABA is an important phytohormone to cope with abiotic stresses, we further explored cellular physiological responses. We found that the acquisition of salt stress tolerance is promoted by PpABI3 in a quantitative manner similar to ASD. Our results suggest that PpABI3-mediated ABA signaling may effectively coordinate cell-to-cell communication during the acquisition of salt stress tolerance. This study will accelerate the quantitative study for ABA signaling mechanism and function in response to various abiotic stresses.

Cell-to-cell communication is tightly regulated in response to environmental stimuli in plants. We previously used a photoconvertible fluorescent protein Dendra2 as a model reporter to study this process. This experiment revealed that macromolecular trafficking between protonemal cells in Physcomitrella patens is suppressed in response to abscisic acid (ABA). However, it remains unknown which ABA signaling components contribute to this suppression and how. Here, we show that ABA signaling components SUCROSE NON-FERMENTING 1-RELATED PROTEIN KINASE 2 (PpSnRK2) and ABA INSENSITIVE 3 (PpABI3) play roles as an essential and promotive factor, respectively, in regulating ABA-induced suppression of Dendra2 diffusion between cells (ASD). Our quantitative imaging analysis revealed that disruption of PpSnRK2 resulted in defective ASD onset itself, whereas disruption of PpABI3 caused an 81-min delay in the initiation of ASD. Live-cell imaging of callose deposition using aniline blue staining showed that, despite this onset delay, callose deposition on cross walls remained constant in the PpABI3 disruptant, suggesting that PpABI3 facilitates ASD in a callose-independent manner. Given that ABA is an important phytohormone to cope with abiotic stresses, we further explored cellular physiological responses. We found that the acquisition of salt stress tolerance is promoted by PpABI3 in a quantitative manner similar to ASD. Our results suggest that PpABI3-mediated ABA signaling may effectively coordinate cell-to-cell communication during the acquisition of salt stress tolerance. This study will accelerate the quantitative study for ABA signaling mechanism and function in response to various abiotic stresses.

After the nuclear power plant accident in Fukushima, radionuclides were deposited over a large area of local forest. However, almost nothing is known about radionuclide infiltration into trees. Here, we used poplar seedlings as a model to show that radiocesium can enter directly into leaves and bark, moving via ray cells through the symplastic pathways to the xylem and concentrating around the meristems, cork, and vascular cambium. During induced potassium incorporation and reduced seasonal growth, the radiocesium in the meristems of stems mainly passes into abscission tissues such as leaves and heartwood. There is no turnover of radiocesium after it enters the heartwood.

The earthquake and tsunami on 11 March 2011 led to a meltdown followed by a hydrogen explosion at the Fukushima–Daiichi nuclear power plant in Japan, causing the dispersal of abundant radionuclides into the atmosphere and ocean. The radionuclides were deposited onto trees and local residences in aerosol or gaseous forms that were partly absorbed by rain or melting snow. Here, we show that the radionuclides attached to the surfaces of trees, in which some radiocesium was incorporated into the xylem through ray cells and through symplastic pathways. The level of incorporated radiocesium varied based on tree species and age because of the ability of radiocesium to attach to the surface of the outer bark. After four years, the radiocesium level in the forest has been decreasing as it is washed out with rainwater into the sea and as it decays over time due to its half-life, but it can also be continuously recycled through leaf tissue, litter, mulch, and soil. As a result, the level of radiocesium was relatively increased in the heartwood and roots of trees at four years after the event. In private forest fields, most trees were left as afforested trees without being used for timber, although some trees were cut down. We discuss an interdisciplinary field study on the immediate effects of high radiation levels upon afforested trees in private forest fields.

Dormancy is a key process allowing land plants to adapt to changing conditions in the terrestrial habitat, allowing the cessation of growth in response to environmental or physiological cues, entrance into a temporary quiescent state, and subsequent reactivation of growth in more favorable environmental conditions [1-3]. Dormancy may be induced seasonally, sporadically (e.g., in response to drought), or developmentally (e.g., seeds and apical dominance). Asexual propagules, known as gemmae, derived via clonal reproduction in bryophytes, are often dormant until displaced from the parent plant. In the liverwort Marchantia polymorpha, gemmae are produced within specialized receptacles, gemma cups, located on the dorsal side of the vegetative thallus [4]. Mature gemmae are detached from the parent plant but may remain in the cup, with gemma growth suppressed as long as the gemmae remain in the gemma cup and the parental plant is alive [5]. Following dispersal of gemmae from gemma cups by rain, the gemmae germinate in the presence of light and moisture, producing clonal offspring [6]. In land plants, the plant hormone abscisic acid (ABA) regulates many aspects of dormancy and water balance [7]. Here, we demonstrate that ABA plays a central role in the control of gemma dormancy as transgenic M. polymorpha gemmae with reduced sensitivity to ABA fail to establish and/or maintain dormancy. Thus, the common ancestor of land plants used the ABA signaling module to regulate germination of progeny in response to environmental cues, with both gemmae and seeds being derived structures co-opting an ancestral response system.

Factor VIIIa functions as a cofactor for factor IXa in the phospholipid surface-dependent activation of factor X. Both the C2 domain of factor VIIIa and the Gla domain of factor IXa are involved in phospholipid binding and are required for the activation of factor X. In this study, we have examined the close relationship between these domains in the factor Xase complex. Enzyme-linked immunosorbent assay-based and surface plasmon resonance-based assays in the absence of phospholipid showed that Glu-Gly-Arg active site-modified factor IXa bound to immobilized recombinant C2 domain (rC2) dose-dependently (Kd = 108 nm). This binding ability was optimal under physiological conditions. A monoclonal antibody against the Gla domain of factor IXa inhibited binding by approximately 95%, and Gla domainless factor IXa failed to bind to rC2. The addition of monoclonal antibody or rC2 with factor VIIIa inhibited factor IXa-catalyzed factor X activation in the absence of phospholipid. Inhibition was not evident, however, in similar experiments in the absence of factor VIIIa, indicating that the C2 domain interacted with the Gla domain of factor IXa. A fragment designated C2-(2182-2259), derived from V8 protease-cleaved rC2, bound to Glu-Gly-Arg active site-modified factor IXa. Competitive assays, using overlapping synthetic peptides encompassing residues 2182-2259, demonstrated that peptide 2228-2240 significantly inhibited both this binding and factor Xa generation, independently of phospholipid. Our results indicated that residues 2228-2240 in the factor VIIIa C2 domain constitutes an interactive site for the Gla domain of factor IXa. The findings provide the first evidence for an essential role for this interaction in factor Xase assembly., Copyright © 2009 American Society for Biochemistry and Molecular Biology

Factor VIIIa functions as a cofactor for factor IXa in the phospholipid surface-dependent activation of factor X. Both the C2 domain of factor VIIIa and the Gla domain of factor IXa are involved in phospholipid binding and are required for the activation of factor X. In this study, we have examined the close relationship between these domains in the factor Xase complex. Enzyme-linked immunosorbent assay-based and surface plasmon resonance-based assays in the absence of phospholipid showed that Glu-Gly-Arg active site-modified factor IXa bound to immobilized recombinant C2 domain (rC2) dose-dependently (Kd = 108 nm). This binding ability was optimal under physiological conditions. A monoclonal antibody against the Gla domain of factor IXa inhibited binding by approximately 95%, and Gla domainless factor IXa failed to bind to rC2. The addition of monoclonal antibody or rC2 with factor VIIIa inhibited factor IXa-catalyzed factor X activation in the absence of phospholipid. Inhibition was not evident, however, in similar experiments in the absence of factor VIIIa, indicating that the C2 domain interacted with the Gla domain of factor IXa. A fragment designated C2-(2182-2259), derived from V8 protease-cleaved rC2, bound to Glu-Gly-Arg active site-modified factor IXa. Competitive assays, using overlapping synthetic peptides encompassing residues 2182-2259, demonstrated that peptide 2228-2240 significantly inhibited both this binding and factor Xa generation, independently of phospholipid. Our results indicated that residues 2228-2240 in the factor VIIIa C2 domain constitutes an interactive site for the Gla domain of factor IXa. The findings provide the first evidence for an essential role for this interaction in factor Xase assembly., Copyright © 2009 American Society for Biochemistry and Molecular Biology