Yuki Shinzaki
Doshisha University
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Featured researches published by Yuki Shinzaki.
Plant Journal | 2008
Tomohisa Hasunuma; Shin-Ichi Miyazawa; Satomi Yoshimura; Yuki Shinzaki; Ken-ichi Tomizawa; Kazutoshi Shindo; Seon-Kang Choi; Norihiko Misawa; Chikahiro Miyake
SUMMARY The natural pigment astaxanthin has attracted much attention because of its beneficial effects on human health, despite its expensive market price. In order to produce astaxanthin, transgenic plants have so far been generated through conventional genetic engineering of Agrobacterium-mediated gene transfer. The results of trials have revealed that the method is far from practicable because of low yields, i.e. instead of astaxanthin, large quantities of the astaxanthin intermediates, including ketocarotenoids, accumulated in the transgenic plants. In the present study, we have overcome this problem, and have succeeded in producing more than 0.5% (dry weight) astaxanthin (more than 70% of total caroteniods) in tobacco leaves, which turns their green color to reddish brown, by expressing both genes encoding CrtW (beta-carotene ketolase) and CrtZ (beta-carotene hydroxylase) from a marine bacterium Brevundimonas sp., strain SD212, in the chloroplasts. Moreover, the total carotenoid content in the transplastomic tobacco plants was 2.1-fold higher than that of wild-type tobacco. The tobacco transformants also synthesized a novel carotenoid 4-ketoantheraxanthin. There was no significant difference in the size of the aerial part of the plant between the transformants and wild-type plants at the final stage of their growth. The photosynthesis rate of the transformants was also found to be similar to that of wild-type plants under ambient CO2 concentrations of 1500 micromol photons m(-2) s(-1) light intensity.
Functional Plant Biology | 2008
Shin-Ichi Miyazawa; Satomi Yoshimura; Yuki Shinzaki; Masayoshi Maeshima; Chikahiro Miyake
We compared the diffusion conductance to CO2 from the intercellular air space to the chloroplasts (internal conductance (g i)) between tobacco leaves acclimated to long-term drought (drought-acclimated (DA)) and those grown under sufficient irrigation (well-watered (WW)), and analysed the changes in g i in relation to the leaf anatomical characteristics and a possible CO2 transporter, aquaporin. The g i, which was estimated by combined analyses of CO2 gas exchange with chlorophyll fluorescence, in the DA plants was approximately half of that in the WW plants. The mesophyll and chloroplast surface areas exposing the intercellular air space, which potentially affect g i, were not significantly different between the WW and DA plants. The amounts of plasma membrane aquaporins (PIP), immunochemically determined using radish PIP antibodies, were unrelated to g i. After treatment with HgCl2, an aquaporin inhibitor, the water permeability of the leaf tissues (measured as the weight loss of fully-turgid leaf disks without the abaxial epidermis in 1 m sorbitol) in WW plants decreased with an increase in HgCl2 concentration. The g i in the WW plants decreased to similar levels to the DA plants when the detached leaflets were fed with 0.5 mm HgCl2. In contrast, both water permeability and g i were insensitive to HgCl2 treatments in DA plants. These results suggest that deactivation of aquaporins is responsible for the significant reduction in g i observed in plants growing under long-term drought.
Neurobiology of Aging | 2016
Tomohiro Miyasaka; Ce Xie; Satomi Yoshimura; Yuki Shinzaki; Sawako Yoshina; Eriko Kage-Nakadai; Shohei Mitani; Yasuo Ihara
Tau is a key protein in the pathogenesis of various neurodegenerative diseases, which are categorized as tauopathies. Because the extent of tau pathologies is closely linked to that of neuronal loss and the clinical symptoms in Alzheimers disease, anti-tau therapeutics, if any, could be beneficial to a broad spectrum of tauopathies. To learn more about tauopathy, we developed a novel transgenic nematode (Caenorhabditis elegans) model that expresses either wild-type or R406W tau in all the neurons. The wild-type tau-expressing worms exhibited uncoordinated movement (Unc) and neuritic abnormalities. Tau accumulated in abnormal neurites that lost microtubules. Similar abnormalities were found in the worms that expressed low levels of R406W-tau but were not in those expressing comparative levels of wild-type tau. Biochemical studies revealed that tau is aberrantly phosphorylated but forms no detergent-insoluble aggregates. Drug screening performed in these worms identified curcumin, a major phytochemical compound in turmeric, as a compound that reduces not only Unc but also the neuritic abnormalities in both wild-type and R406W tau-expressing worms. Our observations suggest that microtubule stabilization mediates the antitoxicity effect of curcumin. Curcumin is also effective in the worms expressing tau fragment, although it does not prevent the formation of tau-fragment dimers. These data indicate that curcumin improves the tau-induced neuronal dysfunction that is independent of insoluble aggregates of tau.
Journal of Neurochemistry | 2015
Ce Xie; Yoshiyuki Soeda; Yuki Shinzaki; Yasuko In; Koji Tomoo; Yasuo Ihara; Tomohiro Miyasaka
The carboxyl‐terminal sequence of tau composes the framework for its intracellular inclusions that appear in diverse neurodegenerative disorders known as tauopathies. However, microtubule‐associated protein 2 (MAP2), which contains a homologous carboxyl‐terminal sequence of tau, is undetectable in the mature tau inclusions. The mechanisms underlying this phenomenon have remained largely unknown. Here, we show that tau and MAP2 have different aggregation properties: tau aggregates to form filaments but MAP2 remains to be granules. Exchanging 221YKPV224 of tau (0N3R) near the PHF6 motif for 340TKKI343 of MAP2c profoundly changed aggregation properties, suggesting that the YKPV motif is important for filament formation, whereas the TKKI motif is for granule formation. Thus, these minimal sequences may determine the different fates of tau and MAP2 in the formation of inclusions in tauopathies.
Archive | 2008
Shin-Ichi Miyazawa; Satomi Yoshimura; Yuki Shinzaki; Masayoshi Maeshima; Chikahiro Miyake
We examined relationships between conductance to CO2 diffusion from stomatal cavities to the chloroplasts (mesophyll conductance, gm) and plasma membrane aquaporin contents in tobacco leaves acclimated to the long-term drought and those grown under enough irrigation. gm was determined from simultaneous analyses of CO2 gas exchange and chlorophyll fluorescence. Relative plasma membrane aquaporin content was immunochemically determined with an antibody of radish PIP2-type aquaporins. Leaf hydraulic conductivity was measured as a relative weight loss of leaf disks in 1 M sorbitol solution. gm in drought-acclimated plants was about two-third that in well-watered plants. On the other hand, relative aquaporin content on a leaf area basis was about 1.5 times lager in drought-acclimated than well-watered plants. When leaves were fed with 0.5 mM HgCl2, an inhibitor of aquaporins, gm and leaf hydraulic conductivity in well-watered plants were reduced by 20–30% while those in drought-acclimated plants were not significantly affected. These results suggest that a decrease in aquaporin activity leads to the reductions of gm in the long-term drought.
Frontiers in Neuroscience | 2018
Tomohiro Miyasaka; Yuki Shinzaki; Satomi Yoshimura; Sawako Yoshina; Eriko Kage-Nakadai; Shohei Mitani; Yasuo Ihara
Tauopathy is a type of dementia defined by the accumulation of filamentous tau inclusions in neural cells. Most types of dementia in the elderly, including Alzheimer’s disease, are tauopathies. Although it is believed that tau protein abnormalities and/or the loss of its functions results in neurodegeneration and dementia, the mechanism of tauopathy remains obscure. Loss of microtubules and/or tubulin is a known consequence of tau accumulating in neurons in Alzheimer’s disease. In other words, there is an excess level of tau relative to tubulin in tauopathy neurons. To test whether this imbalance of tau and tubulin expression results in the neurotoxicity of tau, we developed several transgenic C. elegans lines that express human tau at various levels in pan-neurons. These worms showed behavioral abnormalities in a tau expression-dependent manner. The knockdown of a tubulin-specific chaperon, or a subset of tubulin, led to enhanced tau toxicity even in low-expressing tau-transgenic worms that showed no abnormal behaviors. In addition, the suppression of tau expression in tubulin knockdown worms rescued neuronal dysfunction. Thus, not only the overexpression of tau but also a reduction in tubulin can trigger the neurotoxicity of tau. Tau expressed in worms was also highly phosphorylated and largely bound to tubulin dimers rather than microtubules. Relative amount of tubulin-unbound tau was increased in high-expressing tau-transgenic worms showing tau toxicity. We further demonstrated that tau aggregation was inhibited by co-incubation of purified tubulin in vitro, meaning sufficient amounts of tubulin can protect against the formation of tau inclusions. These results suggest that the expression ratio of tau to tubulin may be a determinant of the tauopathy cascade.
Plant and Cell Physiology | 2005
Chikahiro Miyake; Momoko Miyata; Yuki Shinzaki; Ken-ichi Tomizawa
Plant and Cell Physiology | 2005
Chikahiro Miyake; Sayaka Horiguchi; Amane Makino; Yuki Shinzaki; Hiroshi Yamamoto; Ken-ichi Tomizawa
Plant and Cell Physiology | 2004
Chikahiro Miyake; Yuki Shinzaki; Momoko Miyata; Ken-ichi Tomizawa
Plant and Cell Physiology | 2006
Chikahiro Miyake; Yuki Shinzaki; Minori Nishioka; Sayaka Horiguchi; Ken-ichi Tomizawa