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991.
Evolutionary control of leaf element composition in plants 总被引:5,自引:1,他引:4
Watanabe T Broadley MR Jansen S White PJ Takada J Satake K Takamatsu T Tuah SJ Osaki M 《The New phytologist》2007,174(3):516-523
Leaf nitrogen (N) and phosphorus (P) concentrations are correlated in plants. Higher-level phylogenetic effects can influence leaf N and P. By contrast, little is known about the phylogenetic variation in the leaf accumulation of most other elements in plant tissues, including elements with quantitatively lesser roles in metabolism than N, and elements that are nonessential for plant growth. Here the leaf composition of 42 elements is reported from a statistically unstructured data set comprising over 2000 leaf samples, representing 670 species and 138 families of terrestrial plants. Over 25% of the total variation in leaf element composition could be assigned to the family level and above for 21 of these elements. The remaining variation corresponded to differences between species within families, to differences between sites which were likely to be caused by soil and climatic factors, and to variation caused by sampling techniques. While the majority of variation in leaf mineral composition is undoubtedly associated with nonevolutionary factors, identifying higher-level phylogenetic variation in leaf elemental composition increases our understanding of terrestrial nutrient cycles and the transfer of toxic elements from soils to living organisms. Identifying mechanisms by which different plant families control their leaf elemental concentration remains a challenge. 相似文献
992.
The unicellular green alga Chlamydomonas reinhardtii can acclimate to a broad range of environmental CO(2) concentrations. We observed that the cells synthesized a specific 43 kDa protein, H43, in the periplasmic space under photoautotrophic high-CO(2) conditions. Under low-CO(2) conditions, H43 disappeared. However, H43 mRNA expression was observed even under heterotrophic low-CO(2) conditions when the cells were grown with 17.4 mM acetate in darkness. When the cells were treated with 4,4'-dithiocyanatostilbene-2,2'-disulfonate (DIDS) and mersalyl to modify cell surface proteins, H43 mRNA expression was strongly affected under both heterotrophic and photoautotrophic conditions. The H43 induction pattern in a mitochondrial respiration-deficient mutant dum-1 that lacks cytochrome c oxidase was the same, but the level was much lower than that in the wild type. Even under illumination, the dissolved CO(2) concentration in the culture rapidly increased slightly following the addition of acetate and dramatically increased even further by the inhibition of photosynthesis with DCMU. Radiotracer experiments with [U-(14)C]acetate revealed that (14)CO(2) release from cells was greater in darkness than in the light due to the great stimulation of internal CO(2) evolution, resulting in an increase in external CO(2) concentration. Strong light inhibited H43 induction and DCMU promoted the induction under photoheterotrophic low-CO(2) conditions. The results demonstrate that H43 is strictly regulated by a concentration of CO(2) resulting from respiration and photosynthesis. Our results suggest that Chlamydomonas induces high-CO(2)-responsive protein H43 by sensing the concentration of ambient CO(2) with the contribution of cell surface protein. 相似文献
993.
Rhizome transition to storage organ is under phytochrome control in lotus <Emphasis Type="Italic">(Nelumbo nucifera)</Emphasis> 总被引:1,自引:0,他引:1
We examined photoperiodic response of lotus (Nelumbo
nucifera) rhizome morphogenesis (its transition to a storage organ) by using seed-derived plants. Rhizome enlargement (increase in
girth) was brought about under 8, 10 and 12 h photoperiods, whereas the rhizomes elongated under 13 and 14 h photoperiods.
Rhizomes elongated under 14 h light regimes supplied as 8 h of natural light plus 6 h supplemental hours of white, yellow
or red light, but similar treatments with supplemental blue, green or far red light, caused enlargement in girth of the rhizomes.
A 2 h interruption of the night with white, yellow or red light, in plants entrained to 8 h photoperiod brought rhizome elongation,
whereas 2 h-blue, green or far red light night breaks still resulted in rhizome increase in girth. The inhibitory effect of
a red (R) light night break on rhizome increase in girth was reversed by a far-red (FR) light given immediately afterwards.
Irradiation with R/FR/R inhibited the rhizome increase in girth. FR light irradiation following R/FR/R irradiation cancelled
the effect of the last R light irradiation. It was demonstrated that the critical photoperiod for rhizome transition to storage
organ is between 12 and 13 h photoperiod. It was also evident that the optimal light quality range for interruption of dark
period (night break) is between yellow and red light and that a R/FR reversible reaction is observed. From these results,
we propose that phytochrome plays an important role in photoperiodic response of rhizome increase in girth in lotus. This
is the first report on phytochrome-dependent morphogenesis of storage organs in rhizomous plants. 相似文献
994.
Watanabe Y Sakihara T Mukuda T Ando M 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》2007,177(8):867-873
The effects of isotocin (IT) and vasotocin (VT), which are fish analogues of mammalian oxytocin and vasopressin respectively,
were examined in the isolated upper esophageal sphincter (UES) muscle. IT relaxed and VT constricted the UES muscle in a concentration-dependent
manner. The relaxation by IT and the contraction by VT were completely blocked by H-9405 (an oxytocin receptor antagonist)
and by H-5350 (a V1-receptor antagonist), respectively, suggesting that the eel UES possesses both IT and VT receptors. Truncated fragments of
VT did not show any significant effects, indicating that all nine residues are essential for the VT and IT actions. IT may
relax the UES muscle through enhancing cAMP production, since similar relaxation was also observed after treatment with 3-isobutyl-1-methylxantine,
forskolin and 8-bromoadenosine, 3′, 5′-cyclic mono-phosphate (8BrcAMP). Although 8-bromoguanosine, 3′, 5′-cyclic monophosphate
also relaxed the UES, its effect was less than 1/3 of that 8BrcAMP, suggesting minor contribution of nitric oxide (NO) in
the relaxation of the UES muscle. Both peptides seem to act directly on the UES muscle, not through release of other substances
from the epithelial cells, since similar relaxation and contraction were observed even in the scraped UES preparations. When
IT and VT were intravenously administrated (in vivo experiments), the drinking rate of the seawater eel was enhanced by IT
and was inhibited by VT. These effects correspond to the in vitro results described above, relaxation by IT and contraction
by VT in the UES muscle. The significance of the relaxing effect by IT is discussed with respect to controlling the drinking
behavior of the eel. 相似文献
995.
Asaumi H Watanabe S Taguchi M Tashiro M Otsuki M 《American journal of physiology. Gastrointestinal and liver physiology》2007,293(5):G972-G978
Local tissue pressure is higher in chronic pancreatitis than in the normal pancreas. We reported recently that pressure application induces synthesis of extracellular matrix (ECM) and cytokines in pancreatic stellate cells (PSCs) and that epigallocatechin gallate (EGCG), a potent antioxidant, inhibits the transformation of PSCs from quiescent to activated phenotype and ethanol-induced synthesis of ECM and cytokines in PSCs. These results suggest that oxidative stress and reactive oxygen species (ROS) are important in PSC activation. The aim of this study was to clarify the effects of ROS on activation and functions of pressure-stimulated PSCs. We used freshly isolated rat PSCs and culture-activated PSCs. Pressure was applied on rat cultured PSCs by adding compressed helium gas into a pressure-loading apparatus. PSCs were cultured with or without antioxidants (EGCG and N-acetyl cysteine) under normal or elevated pressure. Externally applied high pressure (80 mmHg) resulted in a gradual decrease of superoxide dismutase activity in PSCs and increased intracellular ROS generation as early as 30 s, reaching a peak level at 1 h. Antioxidants significantly inhibited ROS generation. Pressure increased the expression levels of alpha-smooth muscle actin, alpha(1)(I)-procollagen, and TGF-beta1 in PSCs. EGCG suppressed these alterations, abolished pressure-induced phosphorylation of p38 MAPK, and suppressed pressure-induced PSC transformation to activated phenotype. Our results indicated that ROS is a key player in pressure-induced PSC activation and ECM synthesis. Antioxidants could be potentially effective against the development of pancreatic fibrosis in patients with chronic pancreatitis. 相似文献
996.
Synergistic induction of antigen-specific CTL by fusions of TLR-stimulated dendritic cells and heat-stressed tumor cells 总被引:1,自引:0,他引:1
Koido S Hara E Homma S Mitsunaga M Takahara A Nagasaki E Kawahara H Watanabe M Toyama Y Yanagisawa S Kobayashi S Yanaga K Fujise K Gong J Tajiri H 《Journal of immunology (Baltimore, Md. : 1950)》2007,179(7):4874-4883
Dendritic cell (DC)/tumor cell fusion cells (FCs) can induce potent CTL responses. The therapeutic efficacy of a vaccine requires the improved immunogenicity of both DCs and tumor cells. The DCs stimulated with the TLR agonist penicillin-killed Streptococcus pyogenes (OK-432; OK-DCs) showed higher expression levels of MHC class I and II, CD80, CD86, CD83, IL-12, and heat shock proteins (HSPs) than did immature DCs. Moreover, heat-treated autologous tumor cells displayed a characteristic phenotype with increased expression of HSPs, carcinoembryonic Ag (CEA), MUC1, and MHC class I (HLA-A2 and/or A24). In this study, we have created four types of FC preparation by alternating fusion cell partners: 1) immature DCs fused with unheated tumor cells; 2) immature DCs fused with heat-treated tumor cells; 3) OK-DCs fused with unheated tumor cells; and 4) OK-DCs fused with heat-treated tumor cells. Although OK-DCs fused with unheated tumor cells efficiently enhanced CTL induction, OK-DCs fused with heat-treated tumor cells were most active, as demonstrated by: 1) up-regulation of multiple HSPs, MHC class I and II, CEA, CD80, CD86, CD83, and IL-12; 2) activation of CD4+ and CD8+ T cells able to produce IFN- gamma at higher levels; 3) efficient induction of CTL activity specific for CEA or MUC1 or both against autologous tumor; and 4) superior abilities to induce CD107+ IFN-gamma+ CD8+ T cells and CD154+ IFN-gamma+ CD4+ T cells. These results strongly suggest that synergism between OK-DCs and heat-treated tumor cells enhances the immunogenicity of FCs and provides a promising means of inducing therapeutic antitumor immunity. 相似文献
997.
Brandt DT Marion S Griffiths G Watanabe T Kaibuchi K Grosse R 《The Journal of cell biology》2007,178(2):193-200
The Diaphanous-related formin Dia1 nucleates actin polymerization, thereby regulating cell shape and motility. Mechanisms that control the cellular location of Dia1 to spatially define actin polymerization are largely unknown. In this study, we identify the cytoskeletal scaffold protein IQGAP1 as a Dia1-binding protein that is necessary for its subcellular location. IQGAP1 interacts with Dia1 through a region within the Diaphanous inhibitory domain after the RhoA-mediated release of Dia1 autoinhibition. Both proteins colocalize at the front of migrating cells but also at the actin-rich phagocytic cup in macrophages. We show that IQGAP1 interaction with Dia1 is required for phagocytosis and phagocytic cup formation. Thus, we identify IQGAP1 as a novel component involved in the regulation of phagocytosis by mediating the localization of the actin filament nucleator Dia1. 相似文献
998.
Watanabe M Matsuyama W Shirahama Y Mitsuyama H Oonakahara K Noma S Higashimoto I Osame M Arimura K 《Journal of immunology (Baltimore, Md. : 1950)》2007,178(9):5888-5898
The chemokine receptor CXCR4, which binds the chemokine stromal cell-derived factor 1, has been reported to be involved in the chemotaxis of inflammatory cells. In addition, AMD3100, an antagonist of CXCR4, has been reported to be an attractive drug candidate for therapeutic intervention in several disorders in which CXCR4 is critically involved. However, little is known about the therapeutic value of AMD3100 in the treatment of pulmonary fibrosis. In this study, we examined the effects of AMD3100 on a murine bleomycin-induced pulmonary fibrosis model. Concurrent administration of AMD3100 and bleomycin apparently attenuated bleomycin-induced pulmonary inflammation. In this process, an inhibition of neutrophil recruitment at early stage followed by the decrease of other inflammatory cell recruitment in the lung were observed. In addition, it also inhibited the expression of cytokines, including MCP-1, MIP-2, MIP-1alpha, and TGF-beta. In contrast, when AMD3100 was administered following bleomycin treatment, the bleomycin-induced lung inflammation progressed and resulted in severe pulmonary fibrosis. In this process, an increase of inflammatory cell recruitment, an up-regulation of lung MCP-1 and TGF-beta, and a remarkable activation of p44/42 MAPK in neutrophils were observed. U0126, an inhibitor of p44/42 MAPK, significantly abolished these effects. Thus, AMD3100 has dual effect on bleomycin-induced pulmonary fibrosis. Difference of inflammatory cell recruitment and activation might be associated with the dual effect of AMD3100 on bleomycin-induced pulmonary fibrosis. 相似文献
999.
Suppression of viral replication by stress-inducible GADD34 protein via the mammalian serine/threonine protein kinase mTOR pathway 总被引:1,自引:0,他引:1
Minami K Tambe Y Watanabe R Isono T Haneda M Isobe K Kobayashi T Hino O Okabe H Chano T Inoue H 《Journal of virology》2007,81(20):11106-11115
GADD34 is a protein that is induced by a variety of stressors, including DNA damage, heat shock, nutrient deprivation, energy depletion, and endoplasmic reticulum stress. Here, we demonstrated that GADD34 induced by vesicular stomatitis virus (VSV) infection suppressed viral replication in wild-type (WT) mouse embryo fibroblasts (MEFs), whereas replication was enhanced in GADD34-deficient (GADD34-KO) MEFs. Enhanced viral replication in GADD34-KO MEFs was reduced by retroviral gene rescue of GADD34. The level of VSV protein expression in GADD34-KO MEFs was significantly higher than that in WT MEFs. Neither phosphorylation of eIF2alpha nor cellular protein synthesis was correlated with viral replication in GADD34-KO MEFs. On the other hand, phosphorylation of S6 and 4EBP1, proteins downstream of mTOR, was suppressed by VSV infection in WT MEFs but not in GADD34-KO MEFs. GADD34 was able to associate with TSC1/2 and dephosphorylate TSC2 at Thr1462. VSV replication was higher in TSC2-null cells than in TSC2-expressing cells, and constitutively active Akt enhanced VSV replication. On the other hand, rapamycin, an mTOR inhibitor, significantly suppressed VSV replication in GADD34-KO MEFs. These findings demonstrate that GADD34 induced by VSV infection suppresses viral replication via mTOR pathway inhibition, indicating that cross talk between stress-inducible GADD34 and the mTOR signaling pathway plays a critical role in antiviral defense. 相似文献
1000.
Cigarette smoke has been firmly established as an independent risk factor for atherosclerosis and other vascular diseases. The proliferation and migration of vascular smooth muscle cells (VSMC) induced by growth factors have been proposed to play an important role in the progression of atherosclerosis. In the present study, we investigated the effects of nicotine, which is one of the important constituents of cigarette smoke, on vascular endothelial growth factor (VEGF) release, in rat VSMC. The stimulation of cells with nicotine resulted in a time- and concentration-dependent release of VEGF. Hexamethonium, an antagonist of nicotinic acetylcholine receptor (nAChR), inhibited nicotine-induced VEGF release. We next investigated the mechanisms by which nicotine induces VEGF release in the cells. The nicotine-induced VEGF release was inhibited by treatment with U0126, a selective inhibitor of MEK, which attenuated the nicotine-induced ERK phosphorylation. Nicotine induced a transient phosphorylation of ERK. Furthermore, AG1478, a selective inhibitor of epidermal growth factor receptor (EGFR) kinase, inhibited nicotine-induced ERK phosphorylation and VEGF release. These data suggest that nicotine releases VEGF through nAChR in VSMC. Moreover, VEGF release induced by nicotine is mediated by an EGFR-ERK pathway in VSMC. VEGF may contribute to the risk of cardiovascular diseases in cigarette smokers. 相似文献