記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：MDPI AG  

Plastid ribosome biogenesis is important for plant growth and development. REGULATOR OF FATTY ACID COMPOSITION3 (RFC3) is a member of the bacterial ribosomal protein S6 family and is important for lateral root development. rfc3-2 dramatically reduces the plastid rRNA level and produces lateral roots that lack stem cells. In this study, we isolated a suppressor of rfc three2 (sprt2) mutant that enabled recovery of most rfc3 mutant phenotypes, including abnormal primary and lateral root development and reduced plastid rRNA level. Northern blotting showed that immature and mature plastid rRNA levels were reduced, with the exception of an early 23S rRNA intermediate, in rfc3-2 mutants. These changes were recovered in rfc3-2 sprt2-1 mutants, but a second defect in the processing of 16S rRNA appeared in this line. The results suggest that rfc3 mutants may be defective in at least two steps of plastid rRNA processing, one of which is specifically affected by the sprt2-1 mutation. sprt2-1 mutants had a mutation in CRM FAMILY MEMBER 3b (CFM3b), which encodes a plastid-localized splicing factor. A bimolecular fluorescence complementation (BiFC) assay suggested that RFC3 and SPRT2/CFM3b interact with each other in plastids. These results suggest that RFC3 suppresses the nonspecific action of SPRT2/CFM3b and improves the accuracy of plastid rRNA processing.

DOI： 10.3390/plants9030328

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

The tRNA modification at the wobble position of Lys, Glu and Gln (wobbleU* modification) is responsible for the fine-tuning of protein translation efficiency and translation rate. This modification influences organism function in accordance with growth and environmental changes. However, the effects of wobbleU* modification at the cellular, tissue, or individual level have not yet been elucidated. In this study, we show that sulfur modification of wobbleU* of the tRNAs affects leaf development in Arabidopsis thaliana. The sulfur modification was impaired in the two wobbleU*-modification mutants: the URM1-like protein-defective mutant and the Elongator complex-defective mutants. Analyses of the mutant phenotypes revealed that the deficiency in the wobbleU* modification increased the airspaces in the leaves and the leaf size without affecting the number and the area of palisade mesophyll cells. On the other hand, both mutants exhibited increased number of leaf epidermal pavement cells but with reduced cell size. The deficiency in the wobbleU* modification also delayed the initiation of the endoreduplication processes of mesophyll cells. The phenotype of ASYMMETRIC LEAVES2-defective mutant was enhanced in the Elongator-defective mutants, while it was unchanged in the URM1-like protein-defective mutant. Collectively, the findings of this study suggest that the tRNA wobbleU* modification plays an important role in leaf morphogenesis by balancing the development between epidermal and mesophyll tissues.

DOI： 10.1093/pcp/pcz064

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1242/bio.028175

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Organ size regulation is dependent on the precise spatial and temporal regulation of cell proliferation and cell expansion. A number of transcription factors have been identified that play a key role in the determination of aerial lateral organ size, but their functional relationship to various chromatin modifiers has not been well understood. To understand how leaf size is regulated, we previously isolated the oligocellula1 (oli1) mutant of Arabidopsis thaliana that develops smaller first leaves than the wild type (WT) mainly due to a reduction in the cell number. In this study, we further characterized oli1 leaf phenotypes and identified the OLI1 gene as well as interaction partners of OLI1. Detailed characterizations of leaf development suggested that the cell proliferation rate in oli1 leaf primordia is lower than that in the WT. In addition, oli1 was associated with a slight delay of the progression from the juvenile to adult phases of leaf traits. A classical map-based approach demonstrated that OLI1 is identical to HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENES15 (HOS15). HOS15/OLI1 encodes a homolog of human transducin β-like protein1 (TBL1). TBL1 forms a transcriptional repression complex with the histone deacetylase (HDAC) HDAC3 and either nuclear receptor co-repressor (N-CoR) or silencing mediator for retinoic acid and thyroid receptor (SMRT). We found that mutations in HISTONE DEACETYLASE9 (HDA9) and a switching-defective protein 3, adaptor 2, N-CoR, and transcription factor IIIB-domain protein gene, POWERDRESS (PWR), showed a small-leaf phenotype similar to oli1. In addition, hda9 and pwr did not further enhance the oli1 small-leaf phenotype, suggesting that these three genes act in the same pathway. Yeast two-hybrid assays suggested physical interactions, wherein PWR probably bridges HOS15/OLI1 and HDA9. Earlier studies suggested the roles of HOS15, HDA9, and PWR in transcriptional repression. Consistently, transcriptome analyses showed several genes commonly upregulated in the three mutants. From these findings, we propose a possibility that HOS15/OLI1, PWR, and HDA9 form an evolutionary conserved transcription repression complex that plays a positive role in the regulation of final leaf size.

DOI： 10.3389/fpls.2018.00580

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：AMER SOC PLANT BIOLOGISTS  

Ribosome-related mutants in Arabidopsis thaliana share several notable characteristics regarding growth and development, which implies the existence of a common pathway that responds to disorders in ribosome biogenesis. As a first step to explore this pathway genetically, we screened a mutagenized population of root initiation defective2 (rid2), a temperature-sensitive mutant that is impaired in pre-rRNA processing, and isolated suppressor of root initiation defective two1 (sriw1), a suppressor mutant in which the defects of cell proliferation observed in rid2 at the restrictive temperature was markedly rescued. sriw1 was identified as a missense mutation of the NAC transcription factor gene ANAC082 The sriw1 mutation greatly alleviated the developmental abnormalities of rid2 and four other tested ribosome-related mutants, including rid3 However, the impaired pre-rRNA processing in rid2 and rid3 was not relieved by sriw1 Expression of ANAC082 was localized to regions where phenotypic effects of ribosome-related mutations are readily evident and was elevated in rid2 and rid3 compared with the wild type. These findings suggest that ANAC082 acts downstream of perturbation of biogenesis of the ribosome and may mediate a set of stress responses leading to developmental alterations and cell proliferation defects.

DOI： 10.1105/tpc.17.00255

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：CELL PRESS  

The spatial gradient of signaling molecules is pivotal for establishing developmental patterns of multicellular organisms. It has long been proposed that these gradients could arise from the pure diffusion process of signaling molecules between cells, but whether this simplest mechanism establishes the formation of the tissue-scale gradient remains unclear. Plasmodesmata are unique channel structures in plants that connect neighboring cells for molecular transport. In this study, we measured cellular- and tissue-scale kinetics of molecular transport through plasmodesmata in Arabidopsis thaliana developing leaf primordia by fluorescence recovery assays. These trans-scale measurements revealed biophysical properties of diffusive molecular transport through plasmodesmata and revealed that the tissue-scale diffusivity, but not the cellular-scale diffusivity, is spatially different along the leaf proximal-to-distal axis. We found that the gradient in cell size along the developmental axis underlies this spatially different tissue-scale diffusivity. We then asked how this diffusion-based framework functions in establishing a signaling gradient of endogenous molecules. ANGUSTIFOLIA3 (AN3) is a transcriptional co-activator, and as we have shown here, it forms a long-range signaling gradient along the leaf proximal-to-distal axis to determine a cell-proliferation domain. By genetically engineering AN3 mobility, we assessed each contribution of cell-to-cell movement and tissue growth to the distribution of the AN3 gradient. We constructed a diffusion-based theoretical model using these quantitative data to analyze the AN3 gradient formation and demonstrated that it could be achieved solely by the diffusive molecular transport in a growing tissue. Our results indicate that the spatially different tissue-scale diffusivity is a core mechanism for AN3 gradient formation. This provides evidence that the pure diffusion process establishes the formation of the long-range signaling gradient in leaf development.

DOI： 10.1016/j.bpj.2017.06.072

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

The model plant Arabidopsis thaliana has five double-stranded RNA-binding proteins (DRB1-DRB5), two of which, DRB1 and DRB4, are well characterized. In contrast, the functions of DRB2, DRB3 and DRB5 have yet to be elucidated. In this study, we tried to uncover their functions using drb mutants and DRB-over-expressed lines. In over-expressed lines of all five DRB genes, the over-expression of DRB2 or DRB3 (DRB2ox or DRB3ox) conferred a downward-curled leaf phenotype, but the expression profiles of ten small RNAs were similar to that of the wild-type (WT) plant. Phenotypes were examined in response to abiotic stresses. Both DRB2ox and DRB3ox plants exhibited salt-tolerance. When these plants were exposed to cold stress, drb2 and drb3 over-accumulated anthocyanin but DRB2ox and DRB3ox did not. Therefore, the over-expression of DRB2 or DRB3 had pleiotropic effects on host plants. Microarray and deep-sequencing analyses indicated that several genes encoding key enzymes for anthocyanin biosynthesis, including chalcone synthase (CHS), dihydroflavonol reductase (DFR) and anthocyanidin synthase (ANS), were down-regulated in DRB3ox plants. When DRB3ox was crossed with the pap1-D line, which is an activation-tagged transgenic line that over-expresses the key transcription factor PAP1 (Production of anthocyanin pigmentation1) for anthocyanin biosynthesis, over-expression of DRB3 suppressed the expression of PAP1, CHS, DFR and ANS genes. DRB3 negatively regulates anthocyanin biosynthesis by modulating the level of PAP1 transcript. Since two different small RNAs regulate PAP1 gene expression, a possible function of DRB3 for small RNA biogenesis is discussed.

DOI： 10.1007/s10265-016-0886-0

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Frontiers Media S.A.  

Leaf abaxial-adaxial patterning is dependent on the mutual repression of leaf polarity genes expressed either adaxially or abaxially. In Arabidopsis thaliana, this process is strongly affected by mutations in ribosomal protein genes and in ribosome biogenesis genes in a sensitized genetic background, such as asymmetric leaves2 (as2). Most ribosome-related mutants by themselves do not show leaf abaxialization, and one of their typical phenotypes is the formation of pointed rather than rounded leaves. In this study, we characterized two ribosome-related mutants to understand how ribosome biogenesis is linked to several aspects of leaf development. Previously, we isolated oligocellula2 (oli2) which exhibits the pointed-leaf phenotype and has a cell proliferation defect. OLI2 encodes a homolog of Nop2 in Saccharomyces cerevisiae, a ribosome biogenesis factor involved in pre-60S subunit maturation. In this study, we found another pointed-leaf mutant that carries a mutation in a gene encoding an uncharacterized protein with a G-patch domain. Similar to oli2, this mutant, named g-patch domain protein1 (gdp1), has a reduced number of leaf cells. In addition, gdp1 oli2 double mutants showed a strong genetic interaction such that they synergistically impaired cell proliferation in leaves and produced markedly larger cells. On the other hand, they showed additive phenotypes when combined with several known ribosomal protein mutants. Furthermore, these mutants have a defect in pre-rRNA processing. GDP1 and OLI2 are strongly expressed in tissues with high cell proliferation activity, and GDP1-GFP and GFP-OLI2 are localized in the nucleolus. These results suggest that OLI2 and GDP1 are involved in ribosome biogenesis. We then examined the effects of gdp1 and oli2 on adaxial-abaxial patterning by crossing them with as2. Interestingly, neither gdp1 nor oli2 strongly enhanced the leaf polarity defect of as2. Similar results were obtained with as2 gdp1 oli2 triple mutants although they showed severe growth defects. These results suggest that the leaf abaxialization phenotype induced by ribosome-related mutations is not merely the result of a general growth defect and that there may be a sensitive process in the ribosome biogenesis pathway that affects adaxial-abaxial patterning when compromised by a mutation.

DOI： 10.3389/fpls.2017.02240

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：WILEY-BLACKWELL  

To gain more insight into the physiological function of nitrogen dioxide (NO2), we investigated the effects of exogenous NO2 on growth in Arabidopsis thaliana.
Plants were grown in air without NO2 for 1 wk after sowing and then grown for 1-4 wk in air with (designated treated plants) or without (control plants) NO2. Plants were irrigated semiweekly with a nutrient solution containing 19.7 mM nitrate and 10.3 mM ammonium.
Five-week-old plants treated with 50 ppb NO2 showed a <= 2.8-fold increase in biomass relative to controls. Treated plants also showed early flowering. The magnitude of the effects of NO2 on leaf expansion, cell proliferation and enlargement was greater in developing than in maturing leaves. Leaf areas were 1.3-8.4 times larger on treated plants than corresponding leaves on control plants. The NO2-induced increase in leaf size was largely attributable to cell proliferation in developing leaves, but was attributable to both cell proliferation and enlargement in maturing leaves. The expression of different sets of genes for cell proliferation and/or enlargement was induced by NO2, but depended on the leaf developmental stage.
Collectively, these results indicated that NO2 regulates organ growth by controlling cell proliferation and enlargement.

DOI： 10.1111/nph.12609

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

• To gain more insight into the physiological function of nitrogen dioxide (NO₂), we investigated the effects of exogenous NO₂ on growth in Arabidopsis thaliana. • Plants were grown in air without NO₂ for 1 wk after sowing and then grown for 1-4 wk in air with (designated treated plants) or without (control plants) NO₂. Plants were irrigated semiweekly with a nutrient solution containing 19.7 mM nitrate and 10.3 mM ammonium. • Five-week-old plants treated with 50 ppb NO₂ showed a ≤ 2.8-fold increase in biomass relative to controls. Treated plants also showed early flowering. The magnitude of the effects of NO₂ on leaf expansion, cell proliferation and enlargement was greater in developing than in maturing leaves. Leaf areas were 1.3-8.4 times larger on treated plants than corresponding leaves on control plants. The NO₂-induced increase in leaf size was largely attributable to cell proliferation in developing leaves, but was attributable to both cell proliferation and enlargement in maturing leaves. The expression of different sets of genes for cell proliferation and/or enlargement was induced by NO₂, but depended on the leaf developmental stage. • Collectively, these results indicated that NO₂ regulates organ growth by controlling cell proliferation and enlargement.

DOI： 10.1111/nph.12609

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Decreased cell numbers during leaf development often trigger increased cell size, a phenomenon called compensation. In compensation-exhibiting mutants, the unusually high cell expansion activity occurs through two different mechanisms during the post-mitotic stage of leaf development, except in the KIP-RELATED PROTEIN 2-overexpressing line (KRP2 o/e), whose cell sizes are 2-fold greater during proliferative growth. However, the molecular basis of compensated cell expansion (CCE) has not been characterized. The det3-1 mutant has a mutation in the C-subunit of the vacuolar-type H(+)-ATPase (V-ATPase) complex that causes a 50% decrease in its activity and cell size. To determine the contribution of V-ATPase activity to CCE, the cellular phenotypes of double mutants between det3-1 and compensation-exhibiting fugu5-1, an3-4, fas1-5 and KRP2 o/e were analyzed in detail. Interestingly, while decreased V-ATPase activity caused by det3-1 did not suppress CCE in fugu5-1, fas1-5 and an3-4, CCE in KRP2 o/e was totally suppressed. Furthermore, measurements revealed that the activity and quantity of the A-subunit of the V-ATPase complex were significantly increased in the shoots of KRP2 o/e plants. Importantly, the unusually increased size of actively dividing KRP2 o/e cells was restored to normal in the det3-1 background. Taken together, our data strongly suggest that CCE in KRP2 o/e, but not in other compensation-exhibiting mutants, occurs exclusively through the increase of V-ATPase activity.

DOI： 10.1093/pcp/pct138

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Compensation refers to an increase in cell size when the cell number is significantly decreased due to the mutation or gain of function of a gene that negatively affects the cell cycle. Given the importance of coordinated growth during organogenesis in both animal and plant systems, compensation is important to understand the mechanism of size regulation. In leaves, cell division precedes cell differentiation (which involves cell expansion); therefore, a decrease in cell number triggers enhanced cell expansion (compensated cell expansion; hereafter, CCE). Functional analyses of genes for which a loss or gain of function triggers compensation have increased our understanding of the molecular mechanisms underlying the decrease in cell number. Nevertheless, the mechanisms that induce enhanced cell expansion (the link between cell cycling and expansion), as well as the cellular machinery mediating CCE, have not been characterized. We recently characterized an important pathway involved in cell enlargement in KRP2-overexpressing plants. Here, we discuss the potential axial role of plant KRPs in triggering enlargement in cells with meristematic features.

DOI： 10.4161/psb.27204

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Leaves are determinate organs; hence, precise control of cell proliferation and post-mitotic cell expansion is essential for their growth. A defect in cell proliferation often triggers enhanced post-mitotic cell expansion in leaves. This phenomenon is referred to as 'compensation'. Several lines of evidence from studies on compensation have shown that cell proliferation and post-mitotic cell expansion are coordinately regulated during leaf development. Therefore, compensation has attracted much attention to the mechanisms for leaf growth. However, our understanding of compensation at the subcellular level remains limited because studies of compensation have focused mainly on cellular-level phenotypes. Proper leaf growth requires quantitative control of subcellular components in association with cellular-level changes. To gain insight into the subcellular aspect of compensation, we investigated the well-known relationship between cell area and chloroplast number per cell in compensation-exhibiting lines, and asked whether chloroplast proliferation is modulated in response to the induction of compensation. RESULTS: We first established a convenient and reliable method for observation of chloroplasts in situ. Using this method, we analyzed Arabidopsis thaliana mutants fugu5 and angustifolia3 (an3), and a transgenic line KIP-RELATED PROTEIN2 overexpressor (KRP2 OE), which are known to exhibit typical features of compensation. We here showed that chloroplast number per cell increased in the subepidermal palisade tissue of these lines. We analyzed tetraploidized wild type, fugu5, an3 and KRP2 OE, and found that cell area itself, but not nuclear ploidy, is a key parameter that determines the activity of chloroplast proliferation. In particular, in the case of an3, we uncovered that promotion of chloroplast proliferation depends on the enhanced post-mitotic cell expansion. The expression levels of chloroplast proliferation-related genes are similar to or lower than that in the wild type during this process. CONCLUSIONS: This study demonstrates that chloroplast proliferation is promoted in compensation-exhibiting lines. This promotion of chloroplast proliferation takes place in response to cell-area increase in post-mitotic phase in an3. The expression of chloroplast proliferation-related genes were not promoted in compensation-exhibiting lines including an3, arguing that an as-yet-unknown mechanism is responsible for modulation of chloroplast proliferation in these lines.

DOI： 10.1186/1471-2229-13-143

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：2  

During leaf development, a decrease in cell number often triggers an increase in cell size. This phenomenon, called compensation, suggests that some system coordinates cell proliferation and cell expansion, but how this is mediated at the molecular level is still unclear. The fugu2 mutants in Arabidopsis (Arabidopsis thaliana) exhibit typical compensation phenotypes. Here, we report that the FUGU2 gene encodes FASCIATA1 (FAS1), the p150 subunit of Chromatin Assembly Factor1. To uncover how the fas1 mutation induces compensation, we performed microarray analyses and found that many genes involved in the DNA damage response are up-regulated in fas1. Our genetic analysis further showed that activation of the DNA damage response and the accompanying decrease of cell number in fas1 depend on ATAXIA TELANGIECTASIA MUTATED (ATM) but not on ATM AND RAD3 RELATED. Kinematic analysis suggested that the delay in the cell cycle leads to a decrease in cell number in fas1 and that loss of ATM partially restores this phenotype. Consistently, both cell size phenotypes and high ploidy phenotypes of fas1 are also suppressed by atm, supporting that the ATM-dependent DNA damage response leads to these phenotypes. Altogether, these data suggest that the ATM-dependent DNA damage response acts as an upstream trigger in fas1 to delay the cell cycle and promote entry into the endocycle, resulting in compensated cell expansion.

DOI： 10.1104/pp.113.216796

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：CELL PRESS  

Coordinated proliferation between clonally distinct cells via inter-cell-layer signaling largely determines the size and shape of plant organs. Nonetheless, the signaling mechanism underlying this coordination in leaves remains elusive because of a lack of understanding of the signaling molecule (or molecules) involved. ANGUSTIFOLIA3 (AN3, also called GRF-INTERACTING FACTOR1) encodes a putative transcriptional coactivator with homology to human synovial sarcoma translocation protein. AN3 transcripts accumulate in mesophyll cells but are not detectable in leaf epidermal cells. However, we found here that in addition to mesophyll cells, epidermal cells of an3 leaves show defective proliferation. This spatial difference between the accumulation pattern of AN3 transcripts and an3 leaf phenotype is explained by AN3 protein movement across cell layers. AN3 moves into epidermal cells after being synthesized within mesophyll cells and helps control epidermal cell proliferation. Interference with AN3 movement results in abnormal leaf size and shape, indicating that AN3 signaling is indispensable for normal leaf development. AN3 movement does not require type II chaperonin activity, which is needed for movement of some mobile proteins. Taking these findings together, we present a novel model emphasizing the role of mesophyll cells as a signaling source coordinating proliferation between clonally independent leaf cells.

DOI： 10.1016/j.cub.2013.03.044

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：SPRINGER  

Leaves develop as flat lateral organs from the indeterminate shoot apical meristem. The establishment of polarity along three-dimensional axes, proximal-distal, medial-lateral, and adaxial-abaxial axes, is crucial for the growth of normal leaves. The mutations of ASYMMETRIC LEAVES1 (AS1) and AS2 of Arabidopsis thaliana cause defects in repression of the indeterminate state and the establishment of axis formation in leaves. Although many mutations have been identified that enhance the adaxial-abaxial polarity defects of as1 and as2 mutants, the roles of the causative genes in leaf development are still unknown. In this study, we found that wild-type plants treated with berberine produced pointed leaves, which are often observed in the single mutants that enhance phenotypes of as1 and as2 mutants. The berberine-treated as1 and as2 mutants formed abaxialized filamentous leaves. Berberine, an isoquinoline alkaloid compound naturally produced in various plant sources, has a growth inhibitory effect on plants that do not produce berberine. We further showed that transcript levels of meristem-specific class 1 KNOX homeobox genes and abaxial determinant genes were increased in berberine-treated as1 and as2. Berberine treated plants carrying double mutations of AS2 and the large subunit ribosomal protein gene RPL5B showed more severe defects in polarity than did the as2 single mutant plants. We suggest that berberine inhibits (a) factor(s) that might be required for leaf adaxial cell differentiation through a pathway independent of AS1 and AS2. Multiple pathways might play important roles in the formation of flat symmetric leaves.

DOI： 10.1007/s11103-012-9929-7

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：COMPANY OF BIOLOGISTS LTD  

In seed plants, the shoot apical and root apical meristems form at the apical and basal poles of the embryonic axis, and leaves form at the flanks of the shoot apical meristem. ANGUSTIFOLIA3/GRF INTERACTING FACTOR1 (AN3/GIF1) encodes a putative transcriptional co-activator involved in various aspects of shoot development, including the maintenance of shoot apical meristems, cell proliferation and expansion in leaf primordia, and adaxial/abaxial patterning of leaves. Here, we report a novel function of AN3 involved in developmental fate establishment. We characterised an an3-like mutant that was found to be an allele of hanaba taranu (han), named han-30, and examined its genetic interactions with an3. an3 han double mutants exhibited severe defects in cotyledon development such that ectopic roots were formed at the apical region of the embryo, as confirmed by pWOX5::GFP expression. Additionally, gif2 enhanced the ectopic root phenotype of an3 han. Although the auxin accumulation pattern of the embryo was correct in an3 han-30, based on DR5rev::GFP expression at the globular stage, expression of the PLETHORA1 (PLT1), a master regulator of root development, expanded from the basal embryonic region to the apical region during the same developmental stage. Furthermore, the plt1 mutation suppressed ectopic root formation in an3 han. These data suggest that establishing cotyledon identity requires both AN3 and HAN to repress ectopic root formation by repressing PLT1 expression.

DOI： 10.1242/dev.081547

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Landes Bioscience  

The synthesis of DNA, RNA, and de novo proteins is fundamental for early development of the seedling after germination, but such processes release pyrophosphate (PPi) as a byproduct of ATP hydrolysis. The over-accumulation of the inhibitory metabolite PPi in the cytosol hinders these biosynthetic reactions. All living organisms possess ubiquitous enzymes collectively called inorganic pyrophosphatases (PPases), which catalyze the hydrolysis of PPi into two orthophosphate (Pi) molecules. Defects in PPase activity cause severe developmental defects and/or growth arrest in several organisms. In higher plants, a proton-translocating vacuolar PPase (H+-PPase) uses the energy of PPi hydrolysis to acidify the vacuole. However, the biological implications of PPi hydrolysis are vague due to the widespread belief that the major role of H+-PPase in plants is vacuolar acidification. We have shown that the Arabidopsis fugu5 mutant phenotype, caused by a defect in H+-PPase activity, is rescued by complementation with the yeast cytosolic PPase IPP1. In addition, our analyses have revealed that increased cytosolic PPi levels impair postgerminative development in fugu5 by inhibiting gluconeogenesis. This led us to the conclusion that the role of H+-PPase as a proton-pump is negligible. Here, we present further evidence of the growth-boosting effects of removing PPi in later stages of plant vegetative development, and briefly discuss the biological role of PPases and their potential applications in different disciplines and in various organisms. © 2012 Landes Bioscience.

DOI： 10.4161/psb.7.1.18573

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：WILEY-BLACKWELL  

CtBP/BARS is a unique protein family in having quite diversified cellular functions, intercellular localizations, and developmental roles. ANGUSTIFOLIA (AN) is the sole homolog of CtBP/BARS from Arabidopsis thaliana, although it has plant AN-specific motifs and a long C-terminus. Previous studies suggested that AN would function in the nucleus as a transcriptional co-repressor, as CtBPs function in animals; however, precise verification has been lacking. In this paper, we isolated a homologous gene (MAN) of AN from liverwort, Marchantia polymorpha. Transformation of the Arabidopsis an-1 mutant with 35S-driven MAN completely complemented the an-1 phenotype, although it lacks the putative nuclear localization signal (NLS) that exists in AN proteins isolated from other plant species. We constructed several plasmids for expressing modified ANs with amino acid substitutions in known motifs. The results clearly indicated that modified AN with mutations in the putative NLS-like domain could complement the an-1 phenotype. Therefore, we re-examined localization of AN using several techniques. Our results demonstrated that AN localizes on punctuate structures around the Golgi, partially overlapping with a trans-Golgi network resident, which highlighted an unexpected link between leaf development and membrane trafficking. We should reconsider the roles and evolutionary traits of AN based on these findings.

DOI： 10.1111/j.1365-313X.2011.04731.x

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：AMER SOC PLANT BIOLOGISTS  

Leaves are the most important, fundamental units of organogenesis in plants. Although the basic form of a leaf is clearly divided into the leaf blade and leaf petiole, no study has yet revealed how these are differentiated from a leaf primordium. We analyzed the spatiotemporal pattern of mitotic activity in leaf primordia of Arabidopsis (Arabidopsis thaliana) in detail using molecular markers in combination with clonal analysis. We found that the proliferative zone is established after a short interval following the occurrence of a rod-shaped early leaf primordium; it is separated spatially from the shoot apical meristem and seen at the junction region between the leaf blade and leaf petiole and produces both leaf-blade and leaf-petiole cells. This proliferative region in leaf primordia is marked by activity of the ANGUSTIFOLIA3 (AN3) promoter as a whole and seems to be differentiated into several spatial compartments: activities of the CYCLIN D4;2 promoter and SPATULA enhancer mark parts of it specifically. Detailed analyses of the an3 and blade-on-petiole mutations further support the idea that organogenesis of the leaf blade and leaf petiole is critically dependent on the correct spatial regulation of the proliferative region of leaf primordia. Thus, the proliferative zone of leaf primordia is spatially differentiated and supplies both the leaf-blade and leaf-petiole cells.

DOI： 10.1104/pp.111.185066

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：AMER SOC PLANT BIOLOGISTS  

Postgerminative growth of seed plants requires specialized metabolism, such as gluconeogenesis, to support heterotrophic growth of seedlings until the functional photosynthetic apparatus is established. Here, we show that the Arabidopsis thaliana fugu5 mutant, which we show to be defective in AVP1 (vacuolar H+-pyrophosphatase), failed to support heterotrophic growth after germination. We found that exogenous supplementation of Suc or the specific removal of the cytosolic pyrophosphate (PPi) by the heterologous expression of the cytosolic inorganic pyrophosphatase1 (IPP1) gene from budding yeast (Saccharomyces cerevisiae) rescued fugu5 phenotypes. Furthermore, compared with the wild-type and AVP1(Pro):IPP1 transgenic lines, hypocotyl elongation in the fugu5 mutant was severely compromised in the dark but recovered upon exogenous supply of Suc to the growth media. Measurements revealed that the peroxisomal beta-oxidation activity, dry seed contents of storage lipids, and their mobilization were unaffected in fugu5. By contrast, fugu5 mutants contained similar to 2.5-fold higher PPi and similar to 50% less Suc than the wild type. Together, these results provide clear evidence that gluconeogenesis is inhibited due to the elevated levels of cytosolic PPi. This study demonstrates that the hydrolysis of cytosolic PPi, rather than vacuolar acidification, is the major function of AVP1/FUGU5 in planta. Plant cells optimize their metabolic function by eliminating PPi in the cytosol for efficient postembryonic heterotrophic growth.

DOI： 10.1105/tpc.111.085415

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：WILEY-BLACKWELL  

P>In Arabidopsis thaliana, mutations in genes encoding ribosomal proteins (r-proteins) perturb various developmental processes. Whether these perturbations are caused by overall ribosome insufficiency or partial dysfunction of the ribosome caused by deficiency of a particular ribosomal protein is not known. To distinguish these possibilities, a comparative study using several r-protein mutants was required. Here, we identified mutations in 11 r-protein genes from previously isolated denticulata and pointed-leaves mutants. Most of these mutations were associated with pointed leaves, with reduced growth due to a decrease in the number or size of palisade mesophyll and pavement cells. In addition, leaf abaxialization was usually observed when these r-protein mutations were combined with asymmetric leaves1 (as1) and as2 mutations. These results suggest that the establishment of leaf polarity is highly sensitive to ribosome functionality in general. However, several r-protein mutants showed a preference towards a specific developmental defect. For example, rpl4d mutations did not affect cell proliferation but caused strong abaxialization of leaves in the as1 and as2 backgrounds. On the other hand, rps28b enhanced leaf abaxialization of as2 to a weaker extent than expected on the basis of its negative effect on cell proliferation. In addition, hypomorphic rps6a alleles had the strongest effects on most of the phenotypes examined. These findings suggest that deficiencies in these three r-protein genes lead to production of dysfunctional ribosomes. Depending on their structural abnormalities, dysfunctional ribosomes may affect translation of specific transcripts involved in the regulation of some leaf developmental processes.

DOI： 10.1111/j.1365-313X.2010.04457.x

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：OXFORD UNIV PRESS  

Molecular genetics has been successful in identifying leaf-size regulators such as transcription factors, phytohormones, and signal molecules. Among them, a ROTUNDIFOLIA4-LIKE/DEVIL (RTFL/DVL) family of Arabidopsis, genes encoding peptides with no secretion-signal sequence, is unique in that their overexpressors have a reduced number of leaf cells specifically along the proximodistal axis. However, because the RTFL/DVL lack any obvious homology with functionally identified domains, and because of genetic redundancy among RTFL/DVL, their molecular and developmental roles are unclear. In this study we focused on one member in the family, ROTUNDIFOLIA4 (ROT4), and identified the core functional region within it and we found no proteolytic processing in planta. Developmental analysis of leaf primordia revealed that ROT4 overexpression reduces the meristematic zone size within the leaf blade. Moreover, induced local overexpression demonstrated that ROT4 acts as a regulator of the leaf shape via a change in positional cue along the longitudinal axis. Similarly, ROT4 overexpression results in a protrusion of the main inflorescence stem, again indicating a change in positional cue along the longitudinal axis. These results suggest that ROT4 affects the positional cue and cell proliferation along the body axis.

DOI： 10.1093/pcp/pcq138

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：OXFORD UNIV PRESS  

Leaf morphogenesis relies on adaxial/abaxial patterning and extensive growth. This study investigated the role of ANGUSTIFOLIA3 (AN3) from Arabidopsis thaliana in these processes. The an3 mutants produce narrower leaves that contain significantly fewer cells than the wild type. We examined the genetic interaction between an3 and asymmetric leaves2 (as2), which has a weak adaxial defect. The an3 as2 mutants developed trumpet-like leaves and accumulated transcripts of abaxially expressed genes at higher levels than an3 and as2. Gene expression analyses suggested that an3 altered the expression of a number of genes. Many of them were involved in metabolism, and several genes that promote adaxial identity cooperatively with as2 were down-regulated. Next, we performed detailed developmental analyses to examine the relationship between the narrow-leaf phenotype of an3 and leaf polarity. As a result, we showed that AN3 is required during a specific phase after an oblong shape is established in early leaf primordia. During this phase, the angle of the cell division plane relative to the longitudinal axis of the leaf primordium is more variable than in the earlier phase where transverse divisions were dominant in both the wild type and an3. Correlated with this dynamic change in cell division pattern, the leaf primordium became rounder. In an3, mitotic activity was reduced more rapidly than in the wild type, causing premature termination of the morphometric change. These results suggest that AN3 promotes cell proliferation during a specific developmental phase that is also required to correct abaxial/adaxial patterning in concert with AS2.

DOI： 10.1093/pcp/pcq178

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

The way in which the number and size of cells in an organ are determined poses a central challenge in our understanding of organ size control. Compensation is an unresolved phenomenon, whereby a decrease in cell proliferation below some threshold level triggers enhanced postmitotic cell expansion in leaf primordia. It suggests an interaction between these cellular processes during organogenesis and provides clues relevant to an understanding of organ size regulation. Although much attention has been given to compensation, it remains unclear how the cellular processes are coordinated. Here, we used a loss-of-function mutation in the transcriptional coactivator gene ANGUSTIFOLIA3 (AN3), which causes typical compensation in Arabidopsis thaliana. We established Cre/lox systems to generate leaves chimeric for AN3 expression and investigated whether compensation occurs in a cell-autonomous or non-cell-autonomous manner. We found that an3-dependent compensation is a non-cellautonomous process, and that an3 cells seem to generate and transmit an intercellular signal that enhances postmitotic cell expansion. The range of signalling was restricted to within one-half of a leaf partitioned by the midrib. Additionally, we also demonstrated that overexpression of the cyclin-dependent kinase inhibitor gene KIP-RELATED PROTEIN2 resulted in cellautonomous compensation. Together, our results revealed two previously unknown pathways that coordinate cell proliferation and postmitotic cell expansion for organ size control in plants.

DOI： 10.1242/dev.057117

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：COMPANY OF BIOLOGISTS LTD  

The way in which the number and size of cells in an organ are determined poses a central challenge in our understanding of organ size control. Compensation is an unresolved phenomenon, whereby a decrease in cell proliferation below some threshold level triggers enhanced postmitotic cell expansion in leaf primordia. It suggests an interaction between these cellular processes during organogenesis and provides clues relevant to an understanding of organ size regulation. Although much attention has been given to compensation, it remains unclear how the cellular processes are coordinated. Here, we used a loss-of-function mutation in the transcriptional coactivator gene ANGUSTIFOLIA3 (AN3), which causes typical compensation in Arabidopsis thaliana. We established Cre/lox systems to generate leaves chimeric for AN3 expression and investigated whether compensation occurs in a cell-autonomous or non-cell-autonomous manner. We found that an3-dependent compensation is a non-cell-autonomous process, and that an3 cells seem to generate and transmit an intercellular signal that enhances postmitotic cell expansion. The range of signalling was restricted to within one-half of a leaf partitioned by the midrib. Additionally, we also demonstrated that overexpression of the cyclin-dependent kinase inhibitor gene KIP-RELATED PROTEIN2 resulted in cell-autonomous compensation. Together, our results revealed two previously unknown pathways that coordinate cell proliferation and postmitotic cell expansion for organ size control in plants.

DOI： 10.1242/dev.057117

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：AMER SOC PLANT BIOLOGISTS  

Plants grown under a canopy recognize changes in light quality and modify their growth patterns; this modification is known as shade avoidance syndrome. In leaves, leaf blade expansion is suppressed, whereas petiole elongation is promoted under the shade. However, the mechanisms that control these responses are largely unclear. Here, we demonstrate that both auxin and brassinosteroid (BR) are required for the normal leaf responses to shade in Arabidopsis (Arabidopsis thaliana). The microarray analysis of leaf blades and petioles treated with end-of-day far-red light (EODFR) revealed that almost half of the genes induced by the treatment in both parts were previously identified as auxin-responsive genes. Likewise, BR-responsive genes were overrepresented in the EODFR-induced genes. Hence, the auxin and BR responses were elevated by EODFR treatment in both leaf blades and petioles, although opposing growth responses were observed in these two parts. The analysis of the auxin-deficient doc1/big mutant and the BR-deficient rot3/cyp90c1 mutant further indicates that auxin and BR were equally required for the normal petiole elongation response to the shade stimulus. In addition, the spotlight irradiation experiment revealed that phytochrome in leaf blades but not that in petioles regulated petiole elongation, which was probably mediated through regulation of the auxin/BR responses in petioles. On the basis of these findings, we conclude that auxin and BR cooperatively promote petiole elongation in response to the shade stimulus under the control of phytochrome in the leaf blade.

DOI： 10.1104/pp.110.156802

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1093/pcp/pcp184

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1111/j.1365-313X.2009.03940.x

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1111/j.1365-313X.2009.03886.x

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1242/dev.028613

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DOI： 10.1007/s00427-007-0186-8

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記述言語：日本語   出版者・発行元：植物化学調節学会  

DOI： 10.18978/jscrp.41.2_122

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1111/j.1365-313X.2006.02896.x

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：OXFORD UNIV PRESS  

In higher plants, stems and roots show negative and positive gravitropism, respectively. However, current knowledge on the graviresponse of leaves is lacking. In this study, we analyzed the positioning and movement of rosette leaves of Arabidopsis thaliana under light and dark conditions. We found that the radial positioning of rosette leaves was not affected by the direction of gravity under continuous white light. In contrast, when plants were shifted to darkness, the leaves moved upwards, suggesting negative gravitropism. Analysis of the phosphoglucomutase and shoot gravitropism 2-1 mutants revealed that the sedimenting amyloplasts in the leaf petiole are important for gravity perception, as is the case in stems and roots. In addition, our detailed physiological analyses revealed a unique feature of leaf movement after the shift to darkness, i.e. movement could be divided into negative gravitropism and nastic movement. The orientation of rosette leaves is ascribed to a combination of these movements.

DOI： 10.1093/pcp/pci237

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記述言語：英語   出版者・発行元：Japanese Society of Plant Physiologists  

DOI： 10.1093/pcp/pcm002

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出版者・発行元：16  

DOI： 10.1101/gad.1331305

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：BLACKWELL PUBLISHING  

The development of the flat morphology of leaf blades is dependent on the control of cell proliferation as well as cell expansion. Each process has a polarity with respect to the longitudinal and transverse axes of the leaf blade. However, only a few regulatory components of these processes have been identified to date. We have characterized two genes from Arabidopsis thaliana: ANGUSTIFOLIA3 (AN3), which encodes a homolog of the human transcription coactivator SYT, and GROWTH-REGULATING FACTOR5 (AtGRF5), which encodes a putative transcription factor. AN3 is identical to GRF-INTERACTING FACTOR1 (AtGIF1). The an3 and atgrf5 mutants exhibit narrow-leaf phenotypes due to decreases in cell number. Conversely, cell proliferation in leaf primordia is enhanced and leaves grow larger than normal when AN3 or AtGRF5 is overexpressed. Both genes are expressed in leaf primordia, and in the yeast two-hybrid assay, the gene products were found to interact with each other through their N-terminal domains. These results suggest that AN3 and AtGRF5 act together and are required for the development of appropriate leaf size and shape through the promotion and/or maintenance of cell proliferation activity in leaf primordia.

DOI： 10.1111/j.1365-313X.2005.02429.x

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記述言語：日本語   出版者・発行元：共立出版  

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記述言語：英語   出版者・発行元：Japanese Society of Plant Physiologists  

DOI： 10.1093/pcp/pci016

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その他リンク： http://orcid.org/0000-0002-1589-6247

DOI： 10.1104/pp.104.055145

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.febslet.2004.07.063

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DOI： 10.1111/j.1365-313X.2004.02078.x

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DOI： 10.1046/j.1365-313X.2003.01651.x

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DOI： 10.1073/pnas.232590499

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掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/S0168-9452(01)00523-4

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DOI： 10.1046/j.1365-313x.2000.00925.x

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1034/j.1399-3054.1996.960217.x

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：AMER SOC PLANT PHYSIOLOGISTS  

The FAD7 gene, a gene for a chloroplast omega-3 fatty acid desaturase, is responsible for the trienoic fatty acid (TA) formation in leaf tissues. The TA content of the leaf tissue of the 25 degrees C-grown transgenic tobacco (Nicotiana tabacum cv SR1) plants, in which the FAD7 gene from Arabidopsis thaliana was overexpressed, increased uniformly by about 10%. Fatty acid unsaturation in all major leaf polar lipid species increased in the 25 degrees C-grown FAD7 transformants but was approximately the same between the control plants and the FAD7 transformants when grown at 15 degrees C. Therefore, the overexpression of the exogenous FAD? gene leads to the same consequence in the tobacco plants as the low-temperature-induced TA production that may be catalyzed by an endogenous, temperature-regulated chloroplast omega-3 fatty acid desaturase. In the 25 degrees C-grown control plants, the chilling treatment caused symptoms of leaf chlorosis and suppression of leaf growth. The 25 degrees C-grown FAD7 transgenic plants conferred alleviation of these chilling-induced symptoms. A reduction of the chilling injury similar to that of the FAD7 transformants was also observed in the 15 degrees C-preincubated control plants. These results indicate that the increased TA production during chilling acclimation is one of the prerequisites for the normal leaf development at low, nonfreezing temperatures.

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その他リンク： http://orcid.org/0000-0001-9429-5396

記述言語：英語   掲載種別：研究論文（学術雑誌）  

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記述言語：英語   掲載種別：速報，短報，研究ノート等（学術雑誌）  

DOI： 10.5685/plmorphol.26.45

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記述言語：英語   出版者・発行元：日本植物学会  

DOI： 10.1007/s10265-012-0518-2

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記述言語：英語   掲載種別：書評論文，書評，文献紹介等   出版者・発行元：ELSEVIER IRELAND LTD  

Ribosomes play a basic housekeeping role in global translation. However, a number of ribosomal-protein-defective mutants show common and rare developmental phenotypes including growth defects, changes in leaf development, and auxin-related phenotypes. This suggests that translational regulation may be occurring during development. In addition, proteomic and bioinformatic analyses have demonstrated a high heterogeneity in ribosome composition. Although this might be a sign of unequal roles of individual ribosomal proteins, it does not explain every ribosomal-protein-defective phenotype. Moreover, comprehensive interpretations concerning the relationship between ribosomal-protein-defective phenotypes and molecular changes in ribosome status are lacking. In this review, we address these phenotypes based on three models, ribosome insufficiency, heterogeneity, and aberrancy, to consider how ribosomes play developmental roles. We propose that the three models are not mutually exclusive, and ribosomal-protein-defective phenotypes can be explained with one or more of these models. The three models with reference to genetic, biochemical, and bioinformatic knowledge will serve as a foundation for future studies of translational regulation. (C) 2012 Elsevier Ireland Ltd. All rights reserved.

DOI： 10.1016/j.plantsci.2012.04.008

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記述言語：英語   掲載種別：書評論文，書評，文献紹介等   出版者・発行元：FRONTIERS RESEARCH FOUNDATION  

The regulation of organ size in higher organisms is a fundamental issue in developmental biology. In flowering plants, a phenomenon called "compensation" has been observed where a cell proliferation defect in developing leaf primordia triggers excessive cell expansion. As a result, final leaf size is not significantly reduced compared to that expected from the reduction in leaf cell numbers. Recent genetic studies have revealed several key features of the compensation phenomenon. Compensation is induced either cell autonomously or non-cell autonomously depending on the trigger that impairs cell proliferation; a certain type of compensation is induced only when cell proliferation is impaired beyond a threshold level. Excessive cell expansion is achieved by either an increased cell expansion rate or a prolonged period of cell expansion via genetic pathways that are also required for normal cell expansion. These results indicate that cell proliferation and cell expansion are coordinated through multiple pathways during leaf size determination. Further classification of compensation pathways and their characterization at the molecular level will provide a deeper understanding of organ size regulation.

DOI： 10.3389/fpls.2011.00024

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記述言語：英語   掲載種別：記事・総説・解説・論説等（その他）   出版者・発行元：日本植物形態学会  

Growth within plant aerial lateral organs, such as leaves and flowers, occurs for a given period of time and stops when the organs reach their final size and shape, which are highly reproducible for genetically identical organisms grown under equivalent environments. Although leaf size is at one level simply a function of cell number and size, accumulating evidence suggests that an organ-wide integration system underlies leaf organogenesis and controls leaf size. This system, which integrates cell proliferation and expansion, has been a topic of vigorous research in recent years. In our research, we have focused on the intriguing phenomenon known as "compensation." In mutants that have a severe decrease in cell number, excessive cell enlargement is induced post-mitotically; therefore, compensation itself underscores the link between cell number and size-control systems at the level of the entire organ. In a recent large-scale histologic study of mutants of the model plant <I>Arabidopsis thaliana</I>, we identified a large number of leaf-size mutants with various combinations of cell-number and cell-size phenotypes. Five of these mutants, <I>fugu1-fugu5</I>, exhibited compensation phenotypes. Here, we highlight the recent advances in our understanding of size control and the possible mechanisms of compensated cell enlargement based on our analysis of compensation-exhibiting mutants.

DOI： 10.5685/plmorphol.22.65

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記述言語：英語   掲載種別：記事・総説・解説・論説等（学術雑誌）  

The flattened, thin lamina of leaves captures sunlight for photosynthesis and facilitates gas exchange. Therefore, the size and shape of a leaf are fundamentally important features of its integrity and function. Progress in developmental studies has suggested that long- and short-distance signaling pathways are involved in leaf formation. In this chapter, we introduce these signaling pathways, both of which can control final leaf shape and structure: a long-distance signaling pathway that governs the differentiation of leaves into sun and shade types, and a short-distance signaling pathway that appears to be involved in an organ-wide system that integrates cell proliferation and cell enlargement. Although none of the molecules involved in these two pathways have been identified, plausible mechanisms of these pathways are discussed based on present data. © 2008 Springer-Verlag Berlin Heidelberg.

DOI： 10.1007/7089_2007_148

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：記事・総説・解説・論説等（学術雑誌）   出版者・発行元：Landes Bioscience  

DOI： 10.4161/psb.2.5.4525

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：記事・総説・解説・論説等（学術雑誌）   出版者・発行元：SPRINGER TOKYO  

Size is an important parameter in the characterization of organ morphology and function. To understand the mechanisms that control leaf size, we previously isolated a number of Arabidopsis thaliana mutants with altered leaf size. Because leaf morphogenesis depends on determinate cell proliferation, the size of a mature leaf is controlled by variation in cell size and number. Therefore, leaf-size mutants should be classified according to the effects of the mutations on the cell number and/or size. A group of mutants represented by angustifolia3/grf-interacting factor1 and aintegumenta exhibits an intriguing cellular phenotype termed compensation: when the leaf cell number is decreased due to the mutation, the leaf cell size increases, leading to compensation in leaf area. Several lines of genetic evidence suggest that compensation is probably not a result of the uncoupling of cell division from cell growth. Rather, the evidence suggests an organ-wide mechanism that coordinates cell proliferation with cell expansion during leaf development. Our results provide a key, novel concept that explains how leaf size is controlled at the organ level.

DOI： 10.1007/s10265-005-0232-4

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：書評論文，書評，文献紹介等   出版者・発行元：Blackwell Publishing Ltd  

RNA silencing is a rapidly expanding research field, not only because it is a fundamental biological issue but also because its application in the control of gene expression is highly promising. Post-transcriptional gene silencing in plants is a form of RNA silencing by which target RNA is degraded in a sequence-specific manner. Findings regarding the central role that double-stranded RNA plays in triggering RNA silencing have prompted the development of many modified methods for RNA silencing. These methods, in combination with the development of genomic resources, have provided rapid and efficient means by which to investigate gene function in a wide range of plant species. This review addresses the technical aspects of RNA silencing in plants by introducing the principles of several methods of RNA silencing, as well as the advantages and disadvantages of each method. © International Society of Differentiation 2004.

DOI： 10.1111/j.1432-0436.2004.07202005.x

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PubMed

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：OXFORD UNIV PRESS  

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記述言語：英語   出版者・発行元：Japanese Society of Plant Physiologists  

CiNii Article

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その他リンク： https://projects.repo.nii.ac.jp/?action=repository_uri&item_id=184676

記述言語：英語   出版者・発行元：Japanese Society of Plant Physiologists  

CiNii Article

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その他リンク： https://projects.repo.nii.ac.jp/?action=repository_uri&item_id=185242

記述言語：英語   出版者・発行元：Japanese Society of Plant Physiologists  

CiNii Article

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その他リンク： https://projects.repo.nii.ac.jp/?action=repository_uri&item_id=185243

記述言語：英語   出版者・発行元：Japanese Society of Plant Physiologists  

CiNii Article

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その他リンク： https://projects.repo.nii.ac.jp/?action=repository_uri&item_id=184313

記述言語：英語   出版者・発行元：Japanese Society of Plant Physiologists  

CiNii Article

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その他リンク： https://projects.repo.nii.ac.jp/?action=repository_uri&item_id=184313

記述言語：英語  

CiNii Article

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記述言語：日本語  

CiNii Article

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記述言語：英語  

CiNii Article

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記述言語：英語   出版者・発行元：Japanese Society of Plant Physiologists  

ω-3 fatty acid desaturase is responsible for the production of α-linolenic acid, which is a major fatty acid constituent of membrane lipids in higher plants. In this study, the developmental regulation of the expression of two genes, TaFAD3 and TaFAD7, which respectively encode the microsome and plastid ω-3 fatty acid desaturases in wheat, was analyzed by in situ hybridization. The transcript of TaFAD3 was abundant in the apical meristems of both shoot and root, the leaf primordium, the leaf basal intercalary meristem, and the root vascular tissues. The level of TaFAD3 mRNA was also high in embryos developing after flowering. In mature embryos, however, it was low, whereas in germinating embryos it was once again high. These results suggest that the TaFAD3 mRNA is accumulated at a high level in cells that have an ability to proliferate. In contrast, the TaFAD7 mRNA level was very low in the shoot apical meristem, leaf primordium and leaf basal intercalary meristem, but a large accumulation of TaFAD7 mRNA was found in green tissues, suggesting that the accumulation of this mRNA is associated with chloroplast development. Although the spatial distribution patterns of TaFAD3 and TaFAD7 mRNAs clearly differed, the enhanced accumulation of the TaFAD3 and TaFAD7 mRNAs was linked with the active membrane biogenesis required for cell division and with the development of the thylakoid system in plastids, respectively.

CiNii Article

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その他リンク： http://dl.ndl.go.jp/info:ndljp/pid/10772430

記述言語：英語   出版者・発行元：Japanese Society of Plant Physiologists  

ω-3 fatty acid desaturase is responsible for the production of α-linolenic acid, which is a major fatty acid constituent of membrane lipids in higher plants. In this study, the developmental regulation of the expression of two genes, TaFAD3 and TaFAD7, which respectively encode the microsome and plastid ω-3 fatty acid desaturases in wheat, was analyzed by in situ hybridization. The transcript of TaFAD3 was abundant in the apical meristems of both shoot and root, the leaf primordium, the leaf basal intercalary meristem, and the root vascular tissues. The level of TaFAD3 mRNA was also high in embryos developing after flowering. In mature embryos, however, it was low, whereas in germinating embryos it was once again high. These results suggest that the TaFAD3 mRNA is accumulated at a high level in cells that have an ability to proliferate. In contrast, the TaFAD7 mRNA level was very low in the shoot apical meristem, leaf primordium and leaf basal intercalary meristem, but a large accumulation of TaFAD7 mRNA was found in green tissues, suggesting that the accumulation of this mRNA is associated with chloroplast development. Although the spatial distribution patterns of TaFAD3 and TaFAD7 mRNAs clearly differed, the enhanced accumulation of the TaFAD3 and TaFAD7 mRNAs was linked with the active membrane biogenesis required for cell division and with the development of the thylakoid system in plastids, respectively.

CiNii Article

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その他リンク： http://dl.ndl.go.jp/info:ndljp/pid/10772430

記述言語：日本語  

CiNii Article

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記述言語：英語  

CiNii Article

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CiNii Article

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記述言語：日本語  

CiNii Article

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記述言語：英語  

CiNii Article

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記述言語：英語  

CiNii Article

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記述言語：英語   出版者・発行元：KLUWER ACADEMIC PUBL  

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開催年月日： 2017年9月8日 - 2017年9月10日

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開催年月日： 2017年9月8日 - 2017年9月10日

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開催年月日： 2017年9月8日 - 2017年9月10日

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開催年月日： 2017年9月7日 - 2017年9月7日

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開催年月日： 2017年9月7日 - 2017年9月7日

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開催年月日： 2017年9月7日 - 2017年9月7日

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開催年月日： 2017年9月7日 - 2017年9月7日

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開催年月日： 2017年5月10日 - 2017年5月13日

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開催年月日： 2016年9月16日 - 2016年9月18日

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開催年月日： 2016年9月16日 - 2016年9月18日

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開催年月日： 2016年9月16日 - 2016年9月18日

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開催年月日： 2016年6月29日 - 2016年7月3日

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開催年月日： 2016年3月18日 - 2016年3月20日

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開催年月日： 2016年3月18日 - 2016年3月20日

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開催年月日： 2016年1月8日 - 2016年1月9日

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開催年月日： 2015年9月6日 - 2015年9月8日

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開催年月日： 2015年9月6日 - 2015年9月8日

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開催年月日： 2015年6月5日

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開催年月日： 2015年6月5日

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開催年月日： 2015年6月5日

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記述言語：英語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：ポスター発表  

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記述言語：英語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：ポスター発表  

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記述言語：英語   会議種別：ポスター発表  

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記述言語：英語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：その他  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：ポスター発表  

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記述言語：英語   会議種別：その他  

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記述言語：日本語   会議種別：その他  

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記述言語：日本語   会議種別：シンポジウム・ワークショップ パネル（公募）  

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記述言語：日本語   会議種別：その他  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：ポスター発表  

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記述言語：英語   会議種別：その他  

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記述言語：英語   会議種別：ポスター発表  

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記述言語：英語   会議種別：シンポジウム・ワークショップ パネル（公募）  

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記述言語：英語   会議種別：その他  

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記述言語：日本語   会議種別：その他  

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記述言語：日本語   会議種別：その他  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：英語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：その他  

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記述言語：日本語   会議種別：その他  

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記述言語：日本語   会議種別：その他  

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記述言語：日本語   会議種別：口頭発表（一般）  

開催地：中部大学  

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記述言語：日本語   会議種別：シンポジウム・ワークショップ パネル（指名）  

開催地：中部大学  

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記述言語：英語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：ポスター発表  

開催地：中部大学  

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記述言語：英語   会議種別：ポスター発表  

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記述言語：英語   会議種別：ポスター発表  

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記述言語：英語   会議種別：ポスター発表  

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記述言語：日本語   会議種別：口頭発表（一般）  

開催地：熊本大学  

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記述言語：日本語   会議種別：口頭発表（一般）  

開催地：熊本大学  

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記述言語：日本語   会議種別：口頭発表（一般）  

開催地：熊本大学  

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記述言語：日本語   会議種別：口頭発表（一般）  

開催地：熊本大学  

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記述言語：日本語   会議種別：ポスター発表  

開催地：熊本大学  

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記述言語：日本語   会議種別：ポスター発表  

開催地：熊本大学  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：英語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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記述言語：日本語   会議種別：口頭発表（一般）  

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