Faculty Profiles - MUNEMASA Shintaro

Papers - MUNEMASA Shintaro

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The Myrosinases TGG1 and TGG2 Function Redundantly in Reactive Carbonyl Species Signaling in Arabidopsis Guard Cells Reviewed International coauthorship International journal

Mohammad Saidur Rhaman, Toshiyuki Nakamura, Yoshimasa Nakamura, Shintaro Munemasa, Yoshiyuki Murata

Plant and Cell Physiology 61 ( 5 ) 967 - 977 2020.5

Language：English Publishing type：Research paper (scientific journal) Publisher：Oxford University Press (OUP)

<title>Abstract</title>
Myrosinase (β-thioglucoside glucohydrolase, enzyme nomenclature, EC 3.2.1.147, TGG) is a highly abundant protein in Arabidopsis guard cells, of which TGG1 and TGG2 function redundantly in abscisic acid (ABA)- and methyl jasmonate-induced stomatal closure. Reactive carbonyl species (RCS) are α,β-unsaturated aldehydes and ketones, which function downstream of reactive oxygen species (ROS) production in the ABA signalling pathway in guard cells. Among the RCS, acrolein is the most highly reactive, which is significantly produced in ABA-treated guard cells. To clarify the ABA signal pathway downstream of ROS production, we investigated the responses of tgg mutants (tgg1-3, tgg2-1 and tgg1-3 tgg2-1) to acrolein. Acrolein induced stomatal closure and triggered cytosolic alkalization in wild type (WT), tgg1-3 single mutants and in tgg2-1 single mutants, but not in tgg1-3 tgg2-1 double mutants. Exogenous Ca2+ induced stomatal closure and cytosolic alkalization not only in WT but also in all of the mutants. Acrolein- and Ca2+-induced stomatal closures were inhibited by an intracellular acidifying agent, butyrate, a Ca2+ chelator, ethylene glycol tetraacetic acid (EGTA) and a Ca2+ channel blocker, LaCl3. Acrolein induced cytosolic free calcium concentration ([Ca2+]cyt) elevation in guard cells of WT plants but not in the tgg1-3 tgg2-1 double mutants. Exogenous Ca2+ elicited [Ca2+]cyt elevation in guard cells of WT and tgg1-3 tgg2-1. Our results suggest that TGG1 and TGG2 function redundantly, not between ROS production and RCS production, but downstream of RCS production in the ABA signal pathway in Arabidopsis guard cells.

DOI： 10.1093/pcp/pcaa024

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Other Link： http://academic.oup.com/pcp/article-pdf/61/5/967/33207245/pcaa024.pdf

Yeast screening system reveals the inhibitory mechanism of cancer cell proliferation by benzyl isothiocyanate through down-regulation of Mis12 Reviewed International journal

Naomi Abe-Kanoh, Narumi Kunisue, Takumi Myojin, Ayako Chino, Shintaro Munemasa, Yoshiyuki Murata, Ayano Satoh, Hisao Moriya, Yoshimasa Nakamura

Scientific Reports 9 ( 1 ) 8866 - 8866 2019.12

Language：English Publishing type：Research paper (scientific journal) Publisher：Springer Science and Business Media LLC

Benzyl isothiocyanate (BITC) is a naturally-occurring isothiocyanate derived from cruciferous vegetables. BITC has been reported to inhibit the proliferation of various cancer cells, which is believed to be important for the inhibition of tumorigenesis. However, the detailed mechanisms of action remain unclear. In this study, we employed a budding yeast Saccharomyces cerevisiae as a model organism for screening. Twelve genes including MTW1 were identified as the overexpression suppressors for the antiproliferative effect of BITC using the genome-wide multi-copy plasmid collection for S. cerevisiae. Overexpression of the kinetochore protein Mtw1 counteracts the antiproliferative effect of BITC in yeast. The inhibitory effect of BITC on the proliferation of human colon cancer HCT-116 cells was consistently suppressed by the overexpression of Mis12, a human orthologue of Mtw1, and enhanced by the knockdown of Mis12. We also found that BITC increased the phosphorylated and ubiquitinated Mis12 level with consequent reduction of Mis12, suggesting that BITC degrades Mis12 through an ubiquitin-proteasome system. Furthermore, cell cycle analysis showed that the change in the Mis12 level affected the cell cycle distribution and the sensitivity to the BITC-induced apoptosis. These results provide evidence that BITC suppresses cell proliferation through the post-transcriptional regulation of the kinetochore protein Mis12.

DOI： 10.1038/s41598-019-45248-2

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Other Link： http://www.nature.com/articles/s41598-019-45248-2

Ethylene Inhibits Methyl Jasmonate-Induced Stomatal Closure by Modulating Guard Cell Slow-Type Anion Channel Activity via the OPEN STOMATA 1/SnRK2.6 Kinase-Independent Pathway in Arabidopsis Reviewed International journal

Shintaro Munemasa, Yukari Hirao, Kasumi Tanami, Yoshiharu Mimata, Yoshimasa Nakamura, Yoshiyuki Murata

Plant and Cell Physiology 60 ( 10 ) 2263 - 2271 2019.10

Authorship：Lead author Language：English Publishing type：Research paper (scientific journal) Publisher：Oxford University Press (OUP)

<title>Abstract</title>
Signal crosstalk between jasmonate and ethylene is crucial for a proper maintenance of defense responses and development. Although previous studies reported that both jasmonate and ethylene also function as modulators of stomatal movements, the signal crosstalk mechanism in stomatal guard cells remains unclear. Here, we show that the ethylene signaling inhibits jasmonate signaling as well as abscisic acid (ABA) signaling in guard cells of Arabidopsis thaliana and reveal the signaling crosstalk mechanism. Both an ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC) and an ethylene-releasing compound ethephon induced transient stomatal closure, and also inhibited methyl jasmonate (MeJA)-induced stomatal closure as well as ABA-induced stomatal closure. The ethylene inhibition of MeJA-induced stomatal closure was abolished in the ethylene-insensitive mutant etr1–1, whereas MeJA-induced stomatal closure was impaired in the ethylene-overproducing mutant eto1–1. Pretreatment with ACC inhibited MeJA-induced reactive oxygen species (ROS) production as well as ABA-induced ROS production in guard cells but did not suppress ABA activation of OPEN STOMATA 1 (OST1) kinase in guard cell-enriched epidermal peels. The whole-cell patch-clamp analysis revealed that ACC attenuated MeJA and ABA activation of S-type anion channels in guard cell protoplasts. However, MeJA and ABA inhibitions of Kin channels were not affected by ACC pretreatment. These results suggest that ethylene signaling inhibits MeJA signaling and ABA signaling by targeting S-type anion channels and ROS but not OST1 kinase and K+ channels in Arabidopsis guard cells.

DOI： 10.1093/pcp/pcz121

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Other Link： http://academic.oup.com/pcp/article-pdf/60/10/2263/30151483/pcz121.pdf

Reactive Carbonyl Species Function as Signal Mediators Downstream of H2O2 Production and Regulate [Ca2+]cyt Elevation in ABA Signal Pathway in Arabidopsis Guard Cells Reviewed International coauthorship International journal

Md. Moshiul Islam, Wenxiu Ye, Daiki Matsushima, Mohammad Saidur Rhaman, Shintaro Munemasa, Eiji Okuma, Yoshimasa Nakamura, Md. Sanaullah Biswas, Jun’ichi Mano, Yoshiyuki Murata

Plant and Cell Physiology 60 ( 5 ) 1146 - 1159 2019.5

The mechanism of SO2-induced stomatal closure differs from O3 and CO2 responses and is mediated by nonapoptotic cell death in guard cells Reviewed International coauthorship International journal

Lia Ooi, Takakazu Matsuura, Shintaro Munemasa, Yoshiyuki Murata, Maki Katsuhara, Takashi Hirayama, Izumi C. Mori

Plant, Cell & Environment 42 ( 2 ) 437 - 447 2019.2

Language：English Publishing type：Research paper (scientific journal) Publisher：Wiley

Plants closing stomata in the presence of harmful gases is believed to be a stress avoidance mechanism. SO2 , one of the major airborne pollutants, has long been reported to induce stomatal closure, yet the mechanism remains unknown. Little is known about the stomatal response to airborne pollutants besides O3 . SLOW ANION CHANNEL-ASSOCIATED 1 (SLAC1) and OPEN STOMATA 1 (OST1) were identified as genes mediating O3 -induced closure. SLAC1 and OST1 are also known to mediate stomatal closure in response to CO2 , together with RESPIRATORY BURST OXIDASE HOMOLOGs (RBOHs). The overlaying roles of these genes in response to O3 and CO2 suggested that plants share their molecular regulators for airborne stimuli. Here, we investigated and compared stomatal closure event induced by a wide concentration range of SO2 in Arabidopsis through molecular genetic approaches. O3 - and CO2 -insensitive stomata mutants did not show significant differences from the wild type in stomatal sensitivity, guard cell viability, and chlorophyll content revealing that SO2 -induced closure is not regulated by the same molecular mechanisms as for O3 and CO2 . Nonapoptotic cell death is shown as the reason for SO2 -induced closure, which proposed the closure as a physicochemical process resulted from SO2 distress, instead of a biological protection mechanism.

DOI： 10.1111/pce.13406

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Methyl-β-cyclodextrin potentiates the BITC-induced anti-cancer effect through modulation of the Akt phosphorylation in human colorectal cancer cells Reviewed International coauthorship International journal

Qifu Yang, Miku Miyagawa, Xiaoyang Liu, Beiwei Zhu, Shintaro Munemasa, Toshiyuki Nakamura, Yoshiyuki Murata, Yoshimasa Nakamura

Bioscience, Biotechnology, and Biochemistry 82 ( 12 ) 2158 - 2167 2018.12

Language：English Publishing type：Research paper (scientific journal) Publisher：Oxford University Press (OUP)

<title>ABSTRACT</title>
Methyl-β-cyclodextrin (MβCD) is an effective agent for the removal of plasma membrane cholesterol. In this study, we investigated the modulating effects of MβCD on the antiproliferation induced by benzyl isothiocyanate (BITC), an ITC compound mainly derived from papaya seeds. We confirmed that MβCD dose-dependently increased the cholesterol level in the medium, possibly through its removal from the plasma membrane of human colorectal cancer cells. The pretreatment with a non-toxic concentration (2.5 mM) of MβCD significantly enhanced the BITC-induced cytotoxicity and apoptosis induction, which was counteracted by the cholesterol supplementation. Although BITC activated the phosphoinositide 3-kinase (PI3K)/Akt pathway, MβCD dose-dependently inhibited the phosphorylation level of Akt. On the contrary, the treatment of MβCD enhanced the phosphorylation of mitogen activated protein kinases, but did not potentiate their BITC-induced phosphorylation. These results suggested that MβCD might potentiate the BITC-induced anti-cancer by cholesterol depletion and thus inhibition of the PI3K/Akt-dependent survival pathway.

Abbreviations: CDs: cyclodextrins; MβCD: methyl-β-cyclodextrin; ITCs: isothiocyanates; BITC: benzyl isothiocyanate; PI3K: phosphoinositide 3-kinase; PDK1: phosphoinositide-dependent kinase-1; MAPK: mitogen activated protein kinase; ERK1/2: extracellular signal-regulated kinase1/2; JNK: c-Jun N-terminal kinase; PI: propidium iodide; FBS: fatal bovine serum; TLC: thin-layer chromatography; PBS(-): phosphate-buffered saline without calcium and magnesium; MEK: MAPK/ERK kinase; PIP2: phosphatidylinositol-4,5-bisphosphate; PIP3: phosphatidylinositol-3,4,5-trisphosphate

DOI： 10.1080/09168451.2018.1514249

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Benzyl isothiocyanate ameliorates lipid accumulation in 3T3-L1 preadipocytes during adipocyte differentiation Reviewed International coauthorship International journal

Ying Liang, Ikumi Sasaki, Yuki Takeda, Beiwei Zhu, Shintaro Munemasa, Toshiyuki Nakamura, Yoshiyuki Murata, Yoshimasa Nakamura

Bioscience, Biotechnology, and Biochemistry 82 ( 12 ) 2130 - 2139 2018.12

Language：English Publishing type：Research paper (scientific journal) Publisher：Oxford University Press (OUP)

<title>ABSTRACT</title>
Benzyl isothiocyanate (BITC) is an organosulfur compound derived from cruciferous vegetables and papaya seeds. In this study, we investigated the effect of BITC on the lipid accumulation in 3T3-L1 preadipocytes during adipocyte differentiation. The treatment of BITC during the differentiation-inducing stage significantly ameliorated the lipid accumulation, whereas it had no inhibitory effect during the differentiation-maintaining stage. BITC also significantly suppressed the mRNA expression of the adipocyte-specific markers, such as CCAAT/enhancer-binding protein α (C/EBPα), C/EBPβ, C/EBPδ and peroxisome proliferator-activated receptor γ. BITC significantly inhibited the phosphorylation of extracellular signal-regulated kinase phosphorylation, whereas it enhanced that of AMP-activated protein kinase. Furthermore, BITC significantly suppressed the intracellular 2-deoxyglucose uptake as well as glucose transporter 4 expression. These results suggest that inhibition of the adipocyte differentiation and glucose uptake may mainly contribute to the inhibitory effect of BITC on the lipid accumulation in 3T3-L1 preadipocytes.

Abbreviations: PPARγ: peroxisome proliferator-activated receptor γ; CEBP: CCAAT/enhancer-binding protein; GLUT4: glucose transporter 4; AMPK: AMP-activated protein kinase; ERK1/2: extracellular signal-regulated kinase 1/2; MAPK: a mitogen-activated protein kinase; ITCs: isothiocyanates; BITC: benzyl isothiocyanate; FBS: fetal bovine serum; CS: calf serum; AITC: allyl ITC; IBMX: 3-isobutyl-1-methylxanthine; LDH: lactate dehydrogenase; KRH: Krebs-Ringer-Hepes-bicarbonate; 2-DG: 2-deoxy-d-glucose

DOI： 10.1080/09168451.2018.1514247

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Abscisic acid-independent stomatal CO2 signal transduction pathway and convergence of CO2 and ABA signaling downstream of OST1 kinase Reviewed International coauthorship International journal

Po-Kai Hsu, Yohei Takahashi, Shintaro Munemasa, Ebe Merilo, Kristiina Laanemets, Rainer Waadt, Dianne Pater, Hannes Kollist, Julian I. Schroeder

Proceedings of the National Academy of Sciences of the United States of America 115 ( 42 ) E9971 - E9980 2018.10

Language：English Publishing type：Research paper (scientific journal) Publisher：Proceedings of the National Academy of Sciences

Stomatal pore apertures are narrowing globally due to the continuing rise in atmospheric [CO₂]. CO₂ elevation and the plant hormone abscisic acid (ABA) both induce rapid stomatal closure. However, the underlying signal transduction mechanisms for CO₂/ABA interaction remain unclear. Two models have been considered: (<italic>i</italic>) CO₂ elevation enhances ABA concentrations and/or early ABA signaling in guard cells to induce stomatal closure and (<italic>ii</italic>) CO₂ signaling merges with ABA at OST1/SnRK2.6 protein kinase activation. Here we use genetics, ABA-reporter imaging, stomatal conductance, patch clamp, and biochemical analyses to investigate these models. The strong ABA biosynthesis mutants <italic>nced3/nced5</italic> and <italic>aba2-1</italic> remain responsive to CO₂ elevation. Rapid CO₂-triggered stomatal closure in PYR/RCAR ABA receptor quadruple and hextuple mutants is not disrupted but delayed. Time-resolved ABA concentration monitoring in guard cells using a FRET-based ABA-reporter, ABAleon2.15, and ABA reporter gene assays suggest that CO₂ elevation does not trigger [ABA] increases in guard cells, in contrast to control ABA exposures. Moreover, CO₂ activates guard cell S-type anion channels in <italic>nced3/nced5</italic> and ABA receptor hextuple mutants. Unexpectedly, in-gel protein kinase assays show that unlike ABA, elevated CO₂ does not activate OST1/SnRK2 kinases in guard cells. The present study points to a model in which rapid CO₂ signal transduction leading to stomatal closure occurs via an ABA-independent pathway downstream of OST1/SnRK2.6. Basal ABA signaling and OST1/SnRK2 activity are required to facilitate the stomatal response to elevated CO₂. These findings provide insights into the interaction between CO₂/ABA signal transduction in light of the continuing rise in atmospheric [CO₂].

DOI： 10.1073/pnas.1809204115

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Other Link： https://syndication.highwire.org/content/doi/10.1073/pnas.1809204115

Eukaryotic lipid metabolic pathway is essential for functional chloroplasts and CO2 and light responses in Arabidopsis guard cells Reviewed International coauthorship International journal

Juntaro Negi, Shintaro Munemasa, Boseok Song, Ryosuke Tadakuma, Mayumi Fujita, Tamar Azoulay-Shemer, Cawas B. Engineer, Kensuke Kusumi, Ikuo Nishida, Julian I. Schroeder, Koh Iba

Proceedings of the National Academy of Sciences of the United States of America 115 ( 36 ) 9038 - 9043 2018.9

Language：English Publishing type：Research paper (scientific journal) Publisher：Proceedings of the National Academy of Sciences

Stomatal guard cells develop unique chloroplasts in land plant species. However, the developmental mechanisms and function of chloroplasts in guard cells remain unclear. In seed plants, chloroplast membrane lipids are synthesized via two pathways: the prokaryotic and eukaryotic pathways. Here we report the central contribution of endoplasmic reticulum (ER)-derived chloroplast lipids, which are synthesized through the eukaryotic lipid metabolic pathway, in the development of functional guard cell chloroplasts. We gained insight into this pathway by isolating and examining an <italic>Arabidopsis</italic> mutant, <italic>gles1</italic> (<italic>green less stomata 1</italic>), which had achlorophyllous stomatal guard cells and impaired stomatal responses to CO₂ and light. The <italic>GLES1</italic> gene encodes a small glycine-rich protein, which is a putative regulatory component of the trigalactosyldiacylglycerol (TGD) protein complex that mediates ER-to-chloroplast lipid transport via the eukaryotic pathway. Lipidomic analysis revealed that in the wild type, the prokaryotic pathway is dysfunctional, specifically in guard cells, whereas in <italic>gles1</italic> guard cells, the eukaryotic pathway is also abrogated. CO₂-induced stomatal closing and activation of guard cell S-type anion channels that drive stomatal closure were disrupted in <italic>gles1</italic> guard cells. In conclusion, the eukaryotic lipid pathway plays an essential role in the development of a sensing/signaling machinery for CO₂ and light in guard cell chloroplasts.

DOI： 10.1073/pnas.1810458115

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Guard Cell Salicylic Acid Signaling Is Integrated into Abscisic Acid Signaling via the Ca2+/CPK-Dependent Pathway Reviewed International coauthorship International journal

Md. Yeasin Prodhan, Shintaro Munemasa, Mst. Nur-E-Nazmun Nahar, Yoshimasa Nakamura, Yoshiyuki Murata

Plant Physiology 178 ( 1 ) 441 - 450 2018.9

Ion Channels Regulate Nyctinastic Leaf Opening in Samanea saman Reviewed International coauthorship International journal

Takaya Oikawa, Yasuhiro Ishimaru, Shintaro Munemasa, Yusuke Takeuchi, Kento Washiyama, Shin Hamamoto, Nobuyuki Yoshikawa, Yoshiyuki Mutara, Nobuyuki Uozumi, Minoru Ueda

Current Biology 28 ( 14 ) 2230 - 2238.e7 2018.7

Effects of calcium and EGTA on thiol homeostasis and defense-related enzymes in Cd-exposed chickpea roots Reviewed International coauthorship International journal

Lamia Sakouhi, Sondès Rahoui, Charfeddine Gharsallah, Shintaro Munemasa, Ezzeddine El Ferjani, Yoshiyuki Murata, Abdelilah Chaoui

Acta Physiologiae Plantarum 40 ( 1 ) 20 2018.1

Mechanism of Stomatal Closure in Plants Exposed to Drought and Cold Stress. International journal

Srinivas Agurla, Shashibhushan Gahir, Shintaro Munemasa, Yoshiyuki Murata, Agepati S Raghavendra

Advances in experimental medicine and biology 1081 215 - 232 2018

Language：English Publishing type：Research paper (scientific journal)

Drought is one of the abiotic stresses which impairs the plant growth/development and restricts the yield of many crops throughout the world. Stomatal closure is a common adaptation response of plants to the onset of drought condition. Stomata are microscopic pores on the leaf epidermis, which regulate the transpiration/CO2 uptake by leaves. Stomatal guard cells can sense various abiotic and biotic stress stimuli from the internal and external environment and respond quickly to initiate closure under unfavorable conditions. Stomata also limit the entry of pathogens into leaves, restricting their invasion. Drought is accompanied by the production and/or mobilization of the phytohormone, abscisic acid (ABA), which is well-known for its ability to induce stomatal closure. Apart from the ABA, various other factors that accumulate during drought and affect the stomatal function are plant hormones (auxins, MJ, ethylene, brassinosteroids, and cytokinins), microbial elicitors (salicylic acid, harpin, Flg 22, and chitosan), and polyamines . The role of various signaling components/secondary messengers during stomatal opening or closure has been a matter of intense investigation. Reactive oxygen species (ROS) , nitric oxide (NO) , cytosolic pH, and calcium are some of the well-documented signaling components during stomatal closure. The interrelationship and interactions of these signaling components such as ROS, NO, cytosolic pH, and free Ca2+ are quite complex and need further detailed examination.Low temperatures can have deleterious effects on plants. However, plants evolved protection mechanisms to overcome the impact of this stress. Cold temperature inhibits stomatal opening and causes stomatal closure. Cold-acclimated plants often exhibit marked changes in their lipid composition, particularly of the membranes. Cold stress often leads to the accumulation of ABA, besides osmolytes such as glycine betaine and proline. The role of signaling components such as ROS, NO, and Ca2+ during cold acclimation is yet to be established, though the effects of cold stress on plant growth and development are studied extensively. The information on the mitigation processes is quite limited. We have attempted to describe consequences of drought and cold stress in plants, emphasizing stomatal closure. Several of these factors trigger signaling components in roots, shoots, and atmosphere, all leading to stomatal closure. A scheme is presented to show the possible signaling events and their convergence and divergence of action during stomatal closure. The possible directions for future research are discussed.

DOI： 10.1007/978-981-13-1244-1_12

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Blue light and CO2 signals converge to regulate light-induced stomatal opening Reviewed International journal

Asami Hiyama, Atsushi Takemiya, Shintaro Munemasa, Eiji Okuma, Naoyuki Sugiyama, Yasuomi Tada, Yoshiyuki Murata, Ken-ichiro Shimazaki

Nature Communications 8 1284 2017.12

Inhibition of phosphatidylinositide 3-kinase impairs the benzyl isothiocyanate-induced accumulation of autophagic molecules and Nrf2 in human colon cancer cells Reviewed International coauthorship International journal

Xiaoyang Liu, Naomi Abe-Kanoh, Yujia Liu, Beiwei Zhu, Shintaro Munemasa, Toshiyuki Nakamura, Yoshiyuki Murata, Yoshimasa Nakamura

Bioscience, Biotechnology, and Biochemistry 81 ( 11 ) 2212 - 2215 2017.11

Language：English Publishing type：Research paper (scientific journal) Publisher：Oxford University Press (OUP)

<title>Abstract</title>
The regulating role of phosphatidylinositide 3-kinase (PI3K) in benzyl isothiocyanate (BITC)-induced Nrf2 activation, contributing to the inducible expression of cytoprotective genes, was investigated. BITC significantly enhanced the accumulation of Nrf2 as well as autophagic molecules in human colorectal cancer HCT-116 cells. Experiments using a PI3K-specific inhibitor suggested that PI3K plays the key role in the non-canonical Nrf2 activation by BITC.

DOI： 10.1080/09168451.2017.1374830

3,4-Dihydroxyphenylacetic acid is a potential aldehyde dehydrogenase inducer in murine hepatoma Hepa1c1c7 cells Reviewed International coauthorship International journal

Yujia Liu, Ayuki Kurita, Sayaka Nakashima, Beiwei Zhu, Shintaro Munemasa, Toshiyuki Nakamura, Yoshiyuki Murata, Yoshimasa Nakamura

Bioscience, Biotechnology, and Biochemistry 81 ( 10 ) 1978 - 1983 2017.10

Language：English Publishing type：Research paper (scientific journal) Publisher：Oxford University Press (OUP)

<title>Abstract</title>
3,4-Dihydroxyphenylacetic acid (DOPAC) is one of the major colonic microflora-produced catabolites of quercetin glycosides, such as quercetin 4′-glucoside derived from onion. Here, we investigated whether DOPAC modulates the aldehyde dehydrogenase (ALDH) activity and protects the cells from the acetaldehyde-induced cytotoxicity in vitro. DOPAC was shown to enhance not only the total ALDH activity, but also the gene expression of ALDH1A1, ALDH2 and ALDH3A1 in a concentration-dependent manner. DOPAC simultaneously stimulated the nuclear translocation of NFE2-related factor 2 and aryl hydrocarbon receptor. The pretreatment of DOPAC completely protected the cells from the acetaldehyde-induced cytotoxicity. The present study suggested that DOPAC acts as a potential ALDH inducer to prevent the alcohol-induced abnormal reaction.

DOI： 10.1080/09168451.2017.1361809

Benzyl isothiocyanate ameliorates acetaldehyde-induced cytotoxicity by enhancing aldehyde dehydrogenase activity in murine hepatoma Hepa1c1c7 cells Reviewed International coauthorship International journal

Yujia Liu, Momoko Yamanaka, Naomi Abe-Kanoh, Xiaoyang Liu, Beiwei Zhu, Shintaro Munemasa, Toshiyuki Nakamura, Yoshiyuki Murata, Yoshimasa Nakamura

Food and Chemical Toxicology 108 305 - 313 2017.10

Exogenous proline enhances the sensitivity of Tobacco BY-2 cells to arsenate Reviewed International coauthorship International journal

Mst Nur-E-Nazmun Nahar, Mohammad Muzahidul Islam, Md Anamul Hoque, Anna Yonezawa, Md Yeasin Prodhan, Toshiyuki Nakamura, Yoshimasa Nakamura, Shintaro Munemasa, Yoshiyuki Murata

Bioscience, Biotechnology, and Biochemistry 81 ( 9 ) 1726 - 1731 2017.9

Language：English Publishing type：Research paper (scientific journal) Publisher：Oxford University Press (OUP)

<title>Abstract</title>
Arsenic causes physiological and structural disorders in plants. Proline is accumulated as a compatible solute in plants under various stress conditions and mitigates stresses. Here, we investigated the effects of exogenous proline on tobacco Bright Yellow-2 (BY-2) cultured cells under stress. Arsenate did not inhibit BY-2 cell growth at 40 and 50 μM but did it at 60 μM. Proline at 0.5 to 10 mM did not affect the cell growth but delayed it at 20 mM. At 40 μM , neither 0.5 mM nor 1 mM proline affected the cell growth but 10 mM proline inhibited it. In the presence of , 10 mM proline increased the number of Evans Blue-stained (dead) cells and decreased the number of total cells. Together, our results suggest that exogenous proline does not alleviate arsenate toxicity but enhances the sensitivity of BY-2 cells to arsenate.

DOI： 10.1080/09168451.2017.1340088

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アブシジン酸誘導気孔閉口におけるカルシウムシグナル制御機構～明らかになった植物のカルシウムシグナル暗号解読システム～ Invited Reviewed

Shintaro Munemasa

Kagaku to Seibutsu 55 ( 10 ) 666 - 667 2017.9