Ryu Ueda

Keio University, Tokyo, Tokyo-to, Japan

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Publications (77)376.2 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Notch signaling is an evolutionarily conserved mechanism that controls many cell-fate specifications through local cell-cell interactions. The core mechanisms of Notch activation and its subsequent intracellular signaling are well understood. Various cellular functions are required for the activation and regulation of Notch signaling. Among them, the endocytosis of Notch and its ligands is important for the activation and suppression of Notch signaling. The endosomal sorting complex required for transport (ESCRT) proteins are required to sort ubiquitinated membrane proteins, such as Notch, into early endosomes. A loss-of-function allele of vacuolar protein sorting 2 (vps2), which encodes a component of ESCRT-III, has been reported. However, this vps2 mutant still produces the N-terminal half of the protein, and its phenotypes were studied in only a few organs. Here, we generated the first null mutant allele of Drosophila vps2, designated vps2(2), to better understand the function of this gene. In Drosophila wing imaginal discs homozygous for the vps2(2) allele, early endosomes and multivesicular bodies (MVBs) were enlarged, and Notch and Delta accumulated inside them. As reported for the previous vps2 mutant, the epithelium grew excessively under this condition. We further studied the roles of vps2 by RNA interference-knockdown. These experiments revealed that a partial reduction of vps2 attenuated Notch signaling; in contrast, the loss-of-function vps2 mutant is reported to up-regulate the Notch signaling in eye imaginal disc cells. These results suggest that Notch signaling can be up- or down-regulated, depending on the level of vps2 expression. Finally, we found that vps2 overexpression also resulted in early-endosome enlargement and the accumulation of Notch and Delta. In these cells, a portion of the Vps2 protein was detected in MVBs and colocalized with Notch. These data indicate that the expression of vps2 must be precisely regulated to maintain the normal structure of early endosomes.
    Genes & Genetic Systems 01/2013; 88(1):45-57. · 1.13 Impact Factor
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    ABSTRACT: The Golgi apparatus is an intracellular organelle playing central roles in post-translational modification and in the secretion of membrane and secretory proteins. These proteins are synthesized in the endoplasmic reticulum (ER) and transported to the cis-, medial-and trans-cisternae of the Golgi. While trafficking through the Golgi, proteins are sequentially modified with glycan moieties by different glycosyltransferases. Therefore, it is important to analyze the glycosylation function of the Golgi at the level of cisternae. Markers widely used for cis-, medial- and trans-cisternae/trans Golgi network (TGN) in Drosophila are GM130, 120 kDa and Syntaxin16 (Syx16); however the anti-120 kDa antibody is no longer available. In the present study, Drosophila Golgi complex-localized glycoprotein-1 (dGLG1) was identified as an antigen recognized by the anti-120 kDa antibody. A monoclonal anti-dGLG1 antibody suitable for immunohistochemistry was raised in rat. Using these markers, the localization of glycosyltransferases and nucleotide-sugar transporters (NSTs) was studied at the cisternal level. Results showed that glycosyltransferases and NSTs involved in the same sugar modification are localized to the same cisternae. Furthermore, valuable functional information was obtained on the localization of novel NSTs with as yet incompletely characterized biochemical properties.
    Cell Structure and Function 01/2012; 37(1):55-63. · 2.35 Impact Factor
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    ABSTRACT: Glycosylation plays crucial regulatory roles in various biological processes such as development, immunity, and neural functions. For example, α1,3-fucosylation, the addition of a fucose moiety abundant in Drosophila neural cells, is essential for neural development, function, and behavior. However, it remains largely unknown how neural-specific α1,3-fucosylation is regulated. In the present study, we searched for genes involved in the glycosylation of a neural-specific protein using a Drosophila RNAi library. We obtained 109 genes affecting glycosylation that clustered into nine functional groups. Among them, members of the RNA regulation group were enriched by a secondary screen that identified genes specifically regulating α1,3-fucosylation. Further analyses revealed that an RNA-binding protein, second mitotic wave missing (Swm), upregulates expression of the neural-specific glycosyltransferase FucTA and facilitates its mRNA export from the nucleus. This first large-scale genetic screen for glycosylation-related genes has revealed novel regulation of fucTA mRNA in neural cells.
    PLoS Genetics 12/2010; 6(12):e1001254. · 8.17 Impact Factor
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    ABSTRACT: Recent studies have demonstrated protective roles for autophagy in various neurodegenerative disorders, including the polyglutamine diseases; however, the role of autophagy in retinal degeneration has remained unclear. Accumulation of activated rhodopsin in some Drosophila mutants leads to retinal degeneration, and although it is known that activated rhodopsin is degraded in endosomal pathways in normal photoreceptor cells, the contribution of autophagy to rhodopsin regulation has remained elusive. This study reveals that activated rhodopsin is degraded by autophagy in collaboration with endosomal pathways to prevent retinal degeneration. Light-dependent retinal degeneration in the Drosophila visual system is caused by the knockdown or mutation of autophagy-essential components, such as autophagy-related protein 7 and 8 (atg-7/atg-8), or genes essential for PE (phosphatidylethanolamine) biogenesis and autophagosome formation, including Phosphatidylserine decarboxylase (Psd) and CDP-ethanolamine:diacylglycerol ethanolaminephosphotransferase (Ept). The knockdown of atg-7/8 or Psd/Ept produced an increase in the amount of rhodopsin localized to Rab7-positive late endosomes. This rhodopsin accumulation, followed by retinal degeneration, was suppressed by overexpression of Rab7, which accelerated the endosomal degradation pathway. These results indicate a degree of cross talk between the autophagic and endosomal/lysosomal pathways. Importantly, a reduction in rhodopsin levels rescued Psd knockdown-induced retinal degeneration. Additionally, the Psd knockdown-induced retinal degeneration phenotype was enhanced by Ppt1 inactivation, which causes infantile neuronal ceroid lipofuscinosis, implying that autophagy plays a significant role in its pathogenesis. Collectively, the current data reveal that autophagy suppresses light-dependent retinal degeneration in collaboration with the endosomal degradation pathway and that rhodopsin is a key substrate for autophagic degradation in this context.
    Journal of Neuroscience 08/2010; 30(32):10703-19. · 6.75 Impact Factor
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    ABSTRACT: Walker-Warburg syndrome, a progressive muscular dystrophy, is a severe disease with various kinds of symptoms such as muscle weakness and occasional seizures. The genes of protein O-mannosyltransferases 1 and 2 (POMT1 and POMT2), fukutin, and fukutin-related protein are responsible for this syndrome. In our previous study, we cloned Drosophila orthologs of human POMT1 and POMT2 and identified their activity. However, the mechanism of onset of this syndrome is not well understood. Furthermore, little is known about the behavioral properties of the Drosophila POMT1 and POMT2 mutants, which are called rotated abdomen (rt) and twisted (tw), respectively. First, we performed various kinds of behavioral tests and described in detail the muscle structures by using these mutants. The mutant flies exhibited abnormalities in heavy exercises such as climbing or flight but not in light movements such as locomotion. Defective motor function in mutants appeared immediately after eclosion and was exaggerated with aging. Along with motor function, muscle ultrastructure in the tw mutant was altered, as seen in human patients. We demonstrated that expression of RNA interference (RNAi) for the rt gene and the tw mutant was almost completely lethal and semi-lethal, respectively. Flies expressing RNAi had reduced lifespans. These findings clearly demonstrate that Drosophila POMT mutants are models for human muscular dystrophy. We then observed a high density of myoblasts with an enhanced degree of apoptosis in the tw mutant, which completely lost enzymatic activity. In this paper, we propose a novel mechanism for the development of muscular dystrophy: POMT mutation causes high myoblast density and position derangement, which result in apoptosis, muscle disorganization, and muscle cell defects.
    PLoS ONE 07/2010; 5(7):e11557. · 3.53 Impact Factor
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    ABSTRACT: The class III phosphatidylinositol-3 kinase (PI3K (III)) regulates intracellular vesicular transport at multiple steps through the production of phosphatidylinositol-3-phosphate (PI(3)P). While the localization of proteins at distinct membrane domains are likely regulated in different ways, the roles of PI3K (III) and its effectors have not been extensively investigated in a polarized cell during tissue development. In this study, we examined in vivo functions of PI3K (III) and its effector candidate Rabenosyn-5 (Rbsn-5) in Drosophila wing primordial cells, which are polarized along the apical-basal axis. Knockdown of the PI3K (III) subunit Vps15 resulted in an accumulation of the apical junctional proteins DE-cadherin and Flamingo and also the basal membrane protein beta-integrin in intracellular vesicles. By contrast, knockdown of PI3K (III) increased lateral membrane-localized Fasciclin III (Fas III). Importantly, loss-of-function mutation of Rbsn-5 recapitulated the aberrant localization phenotypes of beta-integrin and Fas III, but not those of DE-cadherin and Flamingo. These results suggest that PI3K (III) differentially regulates localization of proteins at distinct membrane domains and that Rbsn-5 mediates only a part of the PI3K (III)-dependent processes.
    PLoS ONE 10/2009; 4(10):e7306. · 3.53 Impact Factor
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    ABSTRACT: Cortactin was initially identified as a substrate for Src tyrosine kinase. It interacts with the filamentous actin in the cell cortex through the tandem repeats of 37-amino acid. In this report, we describe the identification of a Xenopus homolog of cortactin. The deduced amino acid sequence shares over 70% identity with human, mouse, and chicken cortactin. Northern and Western blot analyses revealed that Xenopus cortactin is widely expressed in Xenopus tissues. Analysis of the transcripts using polymerase chain reaction revealed two isoforms being different in the number of the tandem repeats. The major isoform has 6.5 tandem repeats but the minor one has 5.5 tandem repeats. As the sixth repeat, which is missed in the minor isoform, is encoded by a single exon flanked by introns on both sides, these two isoforms are likely to be generated by alternative splicing. We propose that cortactin regulates the construction of actin cytoskeleton by altering the number of its tandem repeats.
    ZOOLOGICAL SCIENCE 08/2009; · 0.88 Impact Factor
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    ABSTRACT: The genetically amenable organism Drosophila melanogaster has been estimated to have 14,076 protein coding genes in the genome, according to the flybase release note R5.13 (http://flybase.bio.indiana.edu/static_pages/docs/release_notes.html). Recent application of RNA interference (RNAi) to the study of developmental biology in Drosophila has enabled us to carry out a systematic investigation of genes affecting various specific phenotypes. In order to search for genes supporting cell survival, we conducted an immunohistochemical examination in which the RNAi of 2,497 genes was independently induced within the dorsal compartment of the wing imaginal disc. Under these conditions, the activities of a stress-activated protein kinase JNK (c-Jun N-terminal kinase) and apoptosis-executing factor Caspase-3 were monitored. Approximately half of the genes displayed a strong JNK or Caspase-3 activation when their RNAi was induced. Most of the JNK activation accompanied Caspase-3 activation, while the opposite did not hold true. Interestingly, the area activating Caspase-3 was more broadly seen than that activating JNK, suggesting that JNK is crucial for induction of non-autonomous apoptosis in many cases. Furthermore, the RNAi of essential factors commonly regulating transcription and translation showed a severe and cell-autonomous apoptosis but also elicited another apoptosis at an adjacent area in a non-autonomous way. We also found that the frequency of apoptosis varies depending on the tissues.
    Gene regulation and systems biology 02/2009; 3:11-20.
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    ABSTRACT: A variety of N-glycans attached to protein are known to involve in many important biological functions. Endoplasmic reticulum (ER) and Golgi localized enzymes are responsible to this template-independent glycan synthesis resulting glycoforms at each asparagine residues. The regulation mechanism such glycan synthesis remains largely unknown. In order to investigate the relationship between glycan structure and protein conformation, we analyzed a glycoprotein of Drosophila melanogaster, chaoptin (Chp), which is localized in photoreceptor cells and is bound to the cell membrane via a glycosylphosphatidylinositol anchor. Detailed analysis based on mass spectrometry revealed the presence of 13 N-glycosylation sites and the composition of the glycoform at each site. The synthetic pathway of glycans was speculated from the observed glycan structures and the composition at each N-glycosylation site, where the presence of novel routes were suggested. The distribution of glycoforms on a Chp polypeptide suggested that various processing enzymes act on the exterior of Chp in the Golgi apparatus, although virtually no enzyme can gain access to the interior of the horseshoe-shaped scaffold, hence explaining the presence of longer glycans within the interior. Furthermore, analysis of Chp from a mutant (RNAi against dolichyl-phosphate alpha-d-mannosyltransferase), which affects N-glycan synthesis in the ER, revealed that truncated glycan structures were processed. As a result, the distribution of glycoforms was affected for the high-mannose-type glycans only, whereas other types of glycans remained similar to those observed in the control and wild-type. These results indicate that glycan processing depends largely on the backbone structure of the parent polypeptide. The information we obtained can be applied to other members of the LRR family of proteins.
    PLoS ONE 02/2009; 4(5):e5434. · 3.53 Impact Factor
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    ABSTRACT: T antigen (Galbeta1-3GalNAcalpha1-Ser/Thr), the well-known tumor-associated antigen, is a core 1 mucin-type O-glycan structure that is synthesized by core 1 beta1,3-galactosyltransferase (C1beta3GalT), which transfers Gal from UDP-Gal to Tn antigen (GalNAcalpha1-Ser/Thr). Three putative C1beta3GalTs have been identified in Drosophila. However, although all three are expressed in embryos, their roles during embryogenesis have not yet been clarified. In this study, we used P-element inserted mutants to show that CG9520, one of the three putative C1beta3GalTs, synthesizes T antigen expressed on the central nervous system (CNS) during embryogenesis. We also found that T antigen was expressed on a subset of the embryonic hemocytes. CG9520 mutant embryos showed the loss of T antigens on the CNS and on a subset of hemocytes. Then, the loss of T antigens was rescued by precise excision of the P-element inserted into the CG9520 gene. Our data demonstrate that T antigens expressed on the CNS and on a subset of hemocytes are synthesized by CG9520 in the Drosophila embryo. In addition, we found that the number of circulating hemocytes was reduced in third instar larvae of CG9520 mutant. We, therefore, named the CG9520 gene Drosophila core 1 beta1,3-galactosyltransferase 1 because it is responsible for the synthesis and function of T antigen in vivo.
    Glycobiology 10/2008; 18(12):1094-104. · 3.75 Impact Factor
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    ABSTRACT: Heparan sulfate proteoglycan plays an important role in developmental processes by modulating the distribution and stability of the morphogens Wingless, Hedgehog, and Decapentaplegic. Heparan and chondroitin sulfates share a common linkage tetrasaccharide structure, GlcAbeta1,3Galbeta1,3Galbeta1,4Xylbeta-O-Ser. In the present study, we identified Drosophila proteoglycan galactosyltransferase II (dbeta3GalTII), determined its substrate specificity, and performed its functional analysis by using RNA interference (RNAi) mutant flies. The enzyme transferred a galactose to Galbeta1,4Xyl-pMph, confirming that it is the Drosophila ortholog of human proteoglycan galactosyltransferase II. Real-time PCR analyses revealed that dbeta3GalTII is expressed in various tissues and throughout development. The dbeta3GalTII RNAi mutant flies showed decreased amounts of heparan sulfate proteoglycans. A genetic interaction of dbeta3GalTII with Drosophila beta1,4-galactoslyltransferase 7 (dbeta4GalT7) or with six genes that encode enzymes contributing to the synthesis of glycosaminoglycans indicated that dbeta3GalTII is involved in heparan sulfate synthesis for wing and eye development. Moreover, dbeta3GalTII knock-down caused a decrease in extracellular Wingless in the wing imaginal disc of the third instar larvae. These results demonstrated that dbeta3GalTII contributes to heparan sulfate proteoglycan synthesis in vitro and in vivo and also modulates Wingless distribution.
    Journal of Biological Chemistry 04/2008; 283(10):6076-84. · 4.60 Impact Factor
  • CGB Technical Report 12/2007; 2007(4).
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    ABSTRACT: We identified the causal genetic variation for the difference in the thoracic trident pigmentation intensity between two wild-derived strains of Drosophila melanogaster. It was found to be the difference in expression level of ebony, which codes for an enzyme in the melanin-synthesis pathway and has pleiotropic effects on vision and behavior.
    Genetics 11/2007; 177(2):1233-7. · 4.87 Impact Factor
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    ABSTRACT: The Drosophila circadian clock consists of integrated autoregulatory feedback loops, making the clock difficult to elucidate without comprehensively identifying the network components in vivo. Previous studies have adopted genome-wide screening for clock-controlled genes using high-density oligonucleotide arrays that identified hundreds of clock-controlled genes. In an attempt to identify the core clock genes among these candidates, we applied genome-wide functional screening using an RNA interference (RNAi) system in vivo. Here we report the identification of novel clock gene candidates including clockwork orange (cwo), a transcriptional repressor belonging to the basic helix-loop-helix ORANGE family. cwo is rhythmically expressed and directly regulated by CLK-CYC through canonical E-box sequences. A genome-wide search for its target genes using the Drosophila genome tiling array revealed that cwo forms its own negative feedback loop and directly suppresses the expression of other clock genes through the E-box sequence. Furthermore, this negative transcriptional feedback loop contributes to sustaining a high-amplitude circadian oscillation in vivo. Based on these results, we propose that the competition between cyclic CLK-CYC activity and the adjustable threshold imposed by CWO keeps E-box-mediated transcription within the controllable range of its activity, thereby rendering a Drosophila circadian clock capable of generating high-amplitude oscillation.
    Genes & Development 08/2007; 21(13):1687-700. · 12.64 Impact Factor
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    ABSTRACT: During tissue patterning, developing fields may be subdivided into several non-overlapping domains by region-specific expression of transcription factors. In Drosophila leg development, the most distal segments, the pretarsus and tarsal segment 5 (ta5), are precisely specified by interactions between tarsus homeobox genes (BarH1 and BarH2) and pretarsus homeobox genes (aristaless, clawless, and Lim1). Here, we demonstrate that trachealess and tango, both encoding bHLH-PAS proteins that are required for the formation of the embryonic tracheal system, are essential for forming two adjacent distal segments of the leg. trachealess is expressed in the pretarsus and ta5, and the concerted action of trachealess and tango seems to modulate the activity of homeobox gene regulatory loops by repressing Bar in the pretarsus and activating Bar in ta5.
    Developmental Biology 04/2007; 303(2):461-73. · 3.64 Impact Factor
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    ABSTRACT: The GalNAcbeta1,4GlcNAc (LacdiNAc or LDN) structure is a more common structural feature in invertebrate glycoconjugates when compared with the Galbeta1,4GlcNAc structure. Recently, beta1,4-N-acetylgalactosaminyltransferase (beta4GalNAcT) was identified in some invertebrates including Drosophila. However, the LDN structure has not been reported in Drosophila, and the biological function of LDN remains to be determined. In this study, we examined acceptor substrate specificity of Drosophila beta4GalNAcTA by using some N- and O-glycans on glycoproteins and neutral glycosphingolipids (GSLs). GalNAc was efficiently transferred toward N-glycans, O-glycans, and the arthro-series GSLs. Moreover, we showed that dbeta4GalNAcTA contributed to the synthesis of the LDN structure in vivo. The dbeta4GalNAcTA mRNA was highly expressed in the developmental and adult neuronal tissues. Thus, these results suggest that dbeta4GalNAcTA acts on the terminal GlcNAc residue of some glycans for the synthesis of LDN, and the LDN structure may play a role in the physiological or neuronal development of Drosophila.
    Biochemical and Biophysical Research Communications 04/2007; 354(2):522-7. · 2.28 Impact Factor
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    ABSTRACT: Drosophila melanogaster produces sexually dimorphic cuticular pheromones that are a key component of the courtship behavior leading to copulation. These molecules are hydrocarbons, with lengths of 23 and 25 carbons in males (mainly with one double bond) and 27 and 29 carbons in females (mainly with two double bonds). Here, we describe an elongase gene, eloF, with female-biased expression. The 771-bp ORF encodes a 257-aa protein that shows the highest sequence identity with mouse SSC1 elongase (33%). The activity of the cDNA expressed in yeast was elongation of saturated and unsaturated fatty acids up to C30. RNAi knockdown in Drosophila led to a dramatic modification of female hydrocarbons, with decreased C29 dienes and increased C25 dienes accompanied by a modification of several courtship parameters: an increase in copulation latency and a decrease in both copulation attempts and copulation. Feminization of the hydrocarbon profile in males by using targeted expression of the transformer gene resulted in high expression levels of eloF, suggesting that the gene is under the control of the sex-determination hierarchy. There is no expression of eloF in Drosophila simulans, which synthesize only C23 and C25 hydrocarbons. These results strongly support the hypothesis that eloF is a crucial enzyme for female pheromone biosynthesis and courtship behavior in D. melanogaster.
    Proceedings of the National Academy of Sciences 04/2007; 104(11):4273-8. · 9.81 Impact Factor
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    ABSTRACT: Notch (N) and its ligands, Delta (Dl) and Serrate (Ser), are transmembrane proteins that mediate the cell-cell interactions necessary for many cell-fate decisions. In Drosophila, N is predominantly localized to the apical portion of epithelial cells, but the mechanisms and functions of this localization are unknown. Here, we found N, Dl, and Ser were mostly located in the region from the subapical complex (SAC) to the apical portion of the adherens junctions (AJs) in wing disc epithelium. N was delivered to the SAC/AJs in two phases. First, polarized exocytosis specifically delivered nascent N to the apical plasma membrane and AJs in an O-fut1-independent manner. Second, N at the plasma membrane was relocated to the SAC/AJs by Dynamin- and Rab5-dependent transcytosis; this step required the O-fut1 function. Disruption of the apical polarity by Drosophila E-cadherin (DEcad) knock down caused N and Dl localization to the SAC/AJs to fail. N, but not Dl, formed a specific complex with DEcad in vivo. Finally, our results suggest that juxtacrine signaling in epithelia generally depends on the apicobasally polarized structure of epithelial cells.
    Genes to Cells 02/2007; 12(1):89-103. · 2.86 Impact Factor
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    ABSTRACT: In Drosophila melanogaster, the Sir2 gene and four Sir2-like genes have been found to be homologous to yeast SIR2 genes. To examine whether the fly Sir2, CG5216, and two Sir2-like genes, CG5085 and CG6284, affect life span, we suppressed their expression using RNAi. Decreased expression of the Sir2 and Sir2-like genes in all cells caused lethality during development. Suppression of the Sir2 in neurons and ubiquitous silencing of the Sir2-like genes shortened life spans. The effects were severer at 28 degrees C than at 25 degrees C. These results suggest that Sir2-like genes as well as Sir2 are involved in the regulation of life span in Drosophila.
    Genes & Genetic Systems 11/2006; 81(5):341-8. · 0.87 Impact Factor
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    ABSTRACT: Despite the identification of numerous key players of the cell death machinery, little is known about their physiological role. Using RNA interference (RNAi) in vivo, we have studied the requirement of all Drosophila caspases and caspase-adaptors in different paradigms of apoptosis. Of the seven caspases, Dronc, drICE, Strica and Decay are rate limiting for apoptosis. Surprisingly, Hid-mediated apoptosis requires a broader range of caspases than apoptosis initiated by loss of the caspase inhibitor DIAP1, suggesting that Hid causes apoptosis not only by antagonizing DIAP1 but also by activating DIAP1-independent caspase cascades. While Hid killing requires Strica, Decay, Dronc/Dark and drICE, apoptosis triggered by DIAP1 depletion merely relied upon Dronc/Dark and drICE. Furthermore, we found that overexpression of DIAP2 can rescue diap1-RNAi-mediated apoptosis, suggesting that DIAP2 regulates caspases directly. Consistently, we show that DIAP2 binds active drICE. Since DIAP2 associates with Hid, we propose a model whereby Hid co-ordinately targets both DIAP1 and DIAP2 to unleash drICE.
    Cell Death and Differentiation 11/2006; 13(10):1663-74. · 8.39 Impact Factor

Publication Stats

3k Citations
376.20 Total Impact Points


  • 2012
    • Keio University
      • Department of Physiology
      Tokyo, Tokyo-to, Japan
  • 2002–2010
    • National Institute of Genetics
      • • Laboratory of Invertebrate Genetics
      • • Genetic Strains Research Center
      Mishima, Shizuoka-ken, Japan
  • 2003–2008
    • Soka University
      • • Faculty of Engineering
      • • Division of Cell Biology
      Sōka, Saitama-ken, Japan
  • 2006
    • University of Minnesota Twin Cities
      • Department of Genetics, Cell Biology and Development
      Minneapolis, MN, United States
    • Center for Molecular Genetics
      Gif, Île-de-France, France
  • 2004–2006
    • French National Centre for Scientific Research
      • Centre de génétique moléculaire
      Paris, Ile-de-France, France
    • Japan Science and Technology Agency (JST)
      Edo, Tōkyō, Japan
  • 2005
    • Kobe University
      • Department of Earth and Planetary Sciences
      Kōbe, Hyōgo, Japan
  • 1999–2004
    • The University of Tokyo
      • • Department of Biophysics and Biochemistry
      • • Faculty of Science and Graduate School of Science
      Tokyo, Tokyo-to, Japan