論文 - 山崎　秀雄

Leaf-goldenning induced by high-light in Ficus microcarpa L.f., a tropical fig

Yamasaki H, Heshiki R, Ikehara N

JOURNAL OF PLANT RESEARCH   108   171 - 180   1995年06月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

　概要を見る

A novel yellow-leaved cultivar of tropical tree was characterized with morphological, histochemical and biochemical analysis. #IFicus microcarpa#IR L. f. cv. Golden Leaf shows characteristic golden (yellow) leaves as well as normal green leaves under the subtropical field condition. Except the appearance of the yellow leaves, morphological characteristics of Golden Leaf agreed to those of wild-type. The yellow leaves of Golden Leaf contained low amount of chlorophyll (8%) and carotenoid (26%), whereas flavonoid level was 5-fold higher than that of wild-type. TLC of hydrolysate of the methanol-extract showed the increase of two flavonols in the yellow leaves. Fluorescence from leaf transverse section indicated that those changes in pigment contents took place in mesophyll cells. Despite low content of photosynthetic pigments the yellow leaves involved the comparable amount of Rubisco subunits to wild-type. The reduced chlorophyll content of the yellow leaves was restored by shading them from high-light but the UV shading did not alter the pigment content. Those characteristics of the yellow leaves were not observed in the green leaves of Golden Leaf. Results suggest that Golden Leaf is attributed to a chloroplast mutant of #IF. microcarpa#IR that is sensitive to continuous high-light irradiation. The mechanism of the leaf-goldenning (yellowing) is discussed in relation to high-light stress and to leaf-senescence.

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熱帯植物ガジュマルFicus microcarpa L. f. の生葉中スーパーオキシドジスムターゼ（SOD）

平敷りか, 池原規勝, 山崎秀雄

沖縄生物学会誌   33   49 - 54   1995年03月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

　概要を見る

Superoxide dismutase (SOD) activity of leaf-extract was investigated in the tropical fig tree #IFicus microcarpa#IR L. f. The leaf-extract contained a large amount of components that showed SOD-like activity on polyacrylamide gel after electrophoresis. Characteristics of their absorption spectrum agreed with those of flavonoids. Improving the sample preparation with polyvinyl polypyrrolidone treatment and gel filtration chromatography, we determined the total SOD activity of the leaf-extract to be 364 units/mg protein and identified the major SOD isozymes to be Fe-SOD and Cu/Zn-SOD. Significance of SODs involved in leaves was discussed in relation to environmental stress on tropical plants.

ヤドリフカノキSchefflera arboricola Hayata の生葉中フラボノール

崎浜靖子, 池原規勝, 山崎秀雄

沖縄生物学会誌   33   43 - 48   1995年03月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

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Two flavonol gylcosides were isolated from the fresh leaves of the tropical tree #ISchefflera arboricola#IR Hayata. The major flavonol glycosides of #IS. arboricola#IR were identified to be quercetin and kaempferol glycosides on the basis of thin layer chromatogram and absorption spectral data. The absorption coefficients of these glycosides were estimated to be 14.7 mM#U-1#URcm#U-1#UR at A#D358#DR (the quercetin glycoside) and 16.0 mM#U-1#URcm#U-1#UR at A#D346#DR (the kaempferol glycoside).

Characteristic Changes in Relaxation Times of Water Protons in Vigna radiata Seedlings Exposed to Temperature Stress

Iwaya-Inoue M, Yoshimura K, Yamasaki H, Kaku S

Plant & Cell Physiology   34   705 - 711   1993年07月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

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Water protons in hypocotyl tissues from etiolated seedlings of #IVigna radiata#IR that were exposed to temperature stress showed characteristic relaxation behaviors for #U1#URH#D-#DRNMR. Cold stress treatment (0°C) caused gradual prolongation of NMR relaxation times (T#D1#DR). After exposure of tissues to cold stress for 24 h, T#D1#DR returned to the initial value as a result of subsequent incubation at normal temperature (20°C). By contrast, heat stress treatment (40°C) induced a time-dependent decrease in T#D1#DR, which did not return completely to the initial value upon subsequent incubation at 20°C after exposure to heat stress for 4 h. We examined changes in various physical factors that influence the response of T#D1#DR to temperature stress, namely, water content and the concentrations of protein, diamagnetic (K#U+#UR, Na#U+#UR, Ca#D2#DR#U+#UR and Mg#D2#DR#U+#UR) and paramagnetic (Mn#D2#DR+#U #URand Fe#D2#DR#U+#UR) ions in the tissues. From the relationships between T#D1#DR and these factors in vitro, we could not interpret the responses of T1 to the temperature stress only in terms of a change in water content. A synergistic effect of an Mn#D2#DR#U+#UR -protein complex and pH might be essential for the mechanism of changes in T#D1#DR that are due to cold stress. The influence of heat stress on structural water in tissues is discussed in terms of water-protein interactions.

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Interaction of amino acid-substituted partial extension peptides of adrenodoxin precursor with artificial membranes and isolated mitochondria

Aoyagi H, Waki K, Kato T, Lee S, Yamasaki H, Furuya S

Peptide Research   5   91 - 96   1992年03月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

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The N-terminal fragment Met-Ala-Ala-Arg-Leu-Leu-Arg-Val-Ala-Ser-Ala-Ala-Leu-Gly (PA1-14) of the adrenodoxin precursor was previously found to inhibit the import of the precursor into mitochondria. In order to obtain further information on the structure-function relationship, five analogs of PA1-14 ([Leu1]PA1-14 (1), [Leu1,Ala10]PA1-14 (2), [Leu1,Ser4]PA1-14 (3), [Leu1,Arg11]PA1-14 (4) and [Leu1,Ser7,Arg10]PA1-14 (5) were synthesized. The CD study showed that PA1-14 and all analogs were random in an aqueous solution and formed an alpha-helical structure in the solution containing acidic liposomes. Peptides 1 and 2 were found to cause dye leakage from lipid vesicles more strongly than other analogs and PA1-14. All analogs completely inhibited the import of the precursor into mitochondria at a concentration of 30 microM. However, 1 and 2 destroyed the mitochondrial membrane potential. These results indicate that an increase in hydrophobicity by replacement of the Met and Ser residues by Leu and Ala, respectively, participates in the perturbation of the membranes. Furthermore, the requirement for the number and position of the Arg residue was found to be not very strict, although its presence in the extension peptide is essential for the precursor to import into mitochondria.

Inhibition of the light-induced H⁺ release from uncoupled thylakoid membranes by N-ethylmaleimide

Yamasaki H, Okayama S, Shibata M, Nishimura M

Biochemical and Biophysical Research Communications   182   1277 - 1281   1992年02月

掲載種別: 研究論文（学術雑誌）

　概要を見る

The light-induced H#U+#UR release from thylakoids, which can be observed under completely uncoupled conditions, was inhibited by the SH reagent #IN#IR-ethylmaleimide (NEM) and its analogs, while the conventional H#U+#UR uptake and electron transfer were not affected. The half-inhibiting concentration of NEM for the H#U+#UR release was 10 mM and 4 mM in thylakoids in the presence of nigericin and in CF#D1#DR-depleted thylakoids, respectively. The inhibitory effect increased with the increase in hydrophobicity of the NEM analogs: #IN#IR-methylmaleimide <#IN#IR-ethylmaleimide <#IN#IR-phenylmaleimide. It is suggested that SH groups in hydrophobic interior within the membrane are essential to the release of protons.

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Induction of the H⁺ Release from Thylakoid Membranes by Illumination in the Presence of Protonophores at High Concentrations

Hideo Yamasaki, Shigeki Furuya, Akira Kawamura, Akio Ito, Shigeki Okayama, Mitsuo Nishimura

Plant & Cell Physiology   32   925 - 934   1991年10月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

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The generally observed light-induced uptake of protons into the thylakoid lumen is diminished by adding protonophores. Instead of the H#U+#UR uptake, the release of protons was observed during illumination in the presence of various protonophores at high concentrations, namely, 1 μM nigericin, 10 μM carbonylcyanide m-chlorophenylhydrazone or 30 μM gramicidin. An uncoupler, NH#D4#DRC1 (4 mM), and a detergent, Triton X-100 (0.02%), also induced the H#U+#UR release but a K#U+#UR ionophore, valinomycin, did not. The amount of H#U+#UR released reached about 100 nmol H#U+#UR (mg Chl)−1 at pH 7.5 under continuous illumination. The rate of the H#U+#UR release was similar to that of the conventional H#U+#UR uptake but its dark relaxation was much slower than that of the H#U+#UR uptake. We compared the H#U+#UR release in protonophore-added thylakoids with the previously reported H#U+#UR release in coupling factor 1 (CF#D1#DR)-depleted thylakoids. The H#U+#UR release in thylakoids with nigericin showed similar characteristics to that in CF#D1#DR-depleted thylakoids in terms of their responses to pH, phenazine methosulfate and light intensity. Both types of H#U+#UR release were relatively insensitive to DCMU and were stimulated somewhat by DCMU at low concentrations (around 200 nM). Nigericin did not inhibit the superoxide dismutase activity of the membranes. These results indicate that the H#U+#UR release in protonophore-added thylakoids and that in CF#D1#DR depleted thylakoids involve the same mechanism and that water-derived protons from PS II that result from an impairment of the activity of superoxide dismutase, as previously proposed, are not involved. Judging from the rate of electron flow and the lumenal acidification under the illumination, we conclude that the H#U+#UR release is a light-dependent scalar process which can be observed in thylakoid membranes with high H+ permeability. The H#U+#UR release of this type was not observed in mitochondria from rat liver or in chromatophores from Rhodobacter sphaeroides.

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Non-Vectorial Light-Induced H⁺ Release from CF₁-Depleted Thylakoid Membranes. Absence of Correlation to Stoichiometric H⁺ Production and Consumption Coupled to Electron Transfer

Hideo Yamasaki, Mitsuo Nishimura

Plant & Cell Physiology   29   1081 - 1084   1988年09月 [ 査読有り ]

掲載種別: 研究論文（学術雑誌）

　概要を見る

Light-induced H#U+#UR release from CF#D1#DR-depleted thylakoid membranes was examined by monitoring the pH in the intra- and extrathylakoidal space and by analyzing the consumption and production of O#D2#DR that accompany the electron transfer. Our results indicated that the H#U+#UR release was not due to the H#U+#UR transport across the membrane or to the net H#U+#UR production in PS II as previously suggested.

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