HOSOKAWA, Masahito



Faculty of Science and Engineering, Graduate School of Advanced Science and Engineering

Job title

Associate Professor(non-tenure-track)

Education 【 display / non-display

  • 2008.04

    Tokyo University of Agriculture and Technology  

Degree 【 display / non-display

  • 東京農工大学   博士(工学)

Research Experience 【 display / non-display

  • 2021.04

    Waseda University

  • 2018.11

    bitBiome, Inc.   Director, CSO

  • 2018.09

    Waseda University   Research Institute for Science and Engineering

  • 2015.10

    科学技術振興機構   さきがけ研究者

  • 2014.04

    Waseda University   Institute for Nanoscience and Nanotechnology

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Research Areas 【 display / non-display

  • Applied biochemistry

Papers 【 display / non-display

  • Recovery of strain-resolved genomes from human microbiome through an integration framework of single-cell genomics and metagenomics.

    Koji Arikawa, Keigo Ide, Masato Kogawa, Tatsuya Saeki, Takuya Yoda, Taruho Endoh, Ayumi Matsuhashi, Haruko Takeyama, Masahito Hosokawa

    Microbiome   9 ( 1 ) 202 - 202  2021.10  [Refereed]  [International journal]

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    BACKGROUND: Obtaining high-quality (HQ) reference genomes from microbial communities is crucial for understanding the phylogeny and function of uncultured microbes in complex microbial ecosystems. Despite improvements in bioinformatic approaches to generate curated metagenome-assembled genomes (MAGs), existing metagenome binners obtain population consensus genomes but they are nowhere comparable to genomes sequenced from isolates in terms of strain level resolution. Here, we present a framework for the integration of single-cell genomics and metagenomics, referred to as single-cell (sc) metagenomics, to reconstruct strain-resolved genomes from microbial communities at once. RESULTS: Our sc-metagenomics integration framework, termed SMAGLinker, uses single-cell amplified genomes (SAGs) generated using microfluidic technology as binning guides and integrates them with metagenome-assembled genomes (MAGs) to recover improved draft genomes. We compared sc-metagenomics with the metagenomics-alone approach using conventional metagenome binners. The sc-metagenomics approach showed precise contig binning and higher recovery rates (>97%) of rRNA and plasmids than conventional metagenomics in genome reconstruction from the cell mock community. In human microbiota samples, sc-metagenomics recovered the largest number of genomes with a total of 103 gut microbial genomes (21 HQ, with 65 showing >90% completeness) and 45 skin microbial genomes (10 HQ, with 40 showing >90% completeness), respectively. Conventional metagenomics recovered one Staphylococcus hominis genome, whereas sc-metagenomics recovered two S. hominis genomes from identical skin microbiota sample. Single-cell sequencing revealed that these S. hominis genomes were derived from two distinct strains harboring specifically different plasmids. We found that all conventional S. hominis MAGs had a substantial lack or excess of genome sequences and contamination from other Staphylococcus species (S. epidermidis). CONCLUSIONS: SMAGLinker enabled us to obtain strain-resolved genomes in the mock community and human microbiota samples by assigning metagenomic sequences correctly and covering both highly conserved genes such as rRNA genes and unique extrachromosomal elements, including plasmids. SMAGLinker will provide HQ genomes that are difficult to obtain using metagenomics alone and will facilitate the understanding of microbial ecosystems by elucidating detailed metabolic pathways and horizontal gene transfer networks. SMAGLinker is available at https://github.com/kojiari/smaglinker . Video abstract.

    DOI PubMed

  • Cortical transcriptome analysis after spinal cord injury reveals the regenerative mechanism of central nervous system in CRMP2 knock-in mice.

    Ayaka Sugeno, Wenhui Piao, Miki Yamazaki, Kiyofumi Takahashi, Koji Arikawa, Hiroko Matsunaga, Masahito Hosokawa, Daisuke Tominaga, Yoshio Goshima, Haruko Takeyama, Toshio Ohshima

    Neural regeneration research   16 ( 7 ) 1258 - 1265  2021.07  [Refereed]  [International journal]

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    Recent studies have shown that mutation at Ser522 causes inhibition of collapsin response mediator protein 2 (CRMP2) phosphorylation and induces axon elongation and partial recovery of the lost sensorimotor function after spinal cord injury (SCI). We aimed to reveal the intracellular mechanism in axotomized neurons in the CRMP2 knock-in (CRMP2KI) mouse model by performing transcriptome analysis in mouse sensorimotor cortex using micro-dissection punching system. Prior to that, we analyzed the structural pathophysiology in axotomized or neighboring neurons after SCI and found that somatic atrophy and dendritic spine reduction in sensorimotor cortex were suppressed in CRMP2KI mice. Further analysis of the transcriptome has aided in the identification of four hemoglobin genes Hba-a1, Hba-a2, Hbb-bs, and Hbb-bt that are significantly upregulated in wild-type mice with concomitant upregulation of genes involved in the oxidative phosphorylation and ribosomal pathways after SCI. However, we observed substantial upregulation in channel activity genes and downregulation of genes regulating vesicles, synaptic function, glial cell differentiation in CRMP2KI mice. Moreover, the transcriptome profile of CRMP2KI mice has been discussed wherein energy metabolism and neuronal pathways were found to be differentially regulated. Our results showed that CRMP2KI mice displayed improved SCI pathophysiology not only via microtubule stabilization in neurons, but also possibly via the whole metabolic system in the central nervous system, response changes in glial cells, and synapses. Taken together, we reveal new insights on SCI pathophysiology and the regenerative mechanism of central nervous system by the inhibition of CRMP2 phosphorylation at Ser522. All these experiments were performed in accordance with the guidelines of the Institutional Animal Care and Use Committee at Waseda University, Japan (2017-A027 approved on March 21, 2017; 2018-A003 approved on March 25, 2018; 2019-A026 approved on March 25, 2019).

    DOI PubMed

  • Distinctive Regulation of Emotional Behaviors and Fear-Related Gene Expression Responses in Two Extended Amygdala Subnuclei With Similar Molecular Profiles.

    Shuhei Ueda, Masahito Hosokawa, Koji Arikawa, Kiyofumi Takahashi, Mao Fujiwara, Manami Kakita, Taro Fukada, Hiroaki Koyama, Shin-Ichiro Horigane, Keiichi Itoi, Masaki Kakeyama, Hiroko Matsunaga, Haruko Takeyama, Haruhiko Bito, Sayaka Takemoto-Kimura

    Frontiers in molecular neuroscience   14   741895 - 741895  2021  [Refereed]  [International journal]

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    The central nucleus of the amygdala (CeA) and the lateral division of the bed nucleus of the stria terminalis (BNST) are the two major nuclei of the central extended amygdala that plays essential roles in threat processing, responsible for emotional states such as fear and anxiety. While some studies suggested functional differences between these nuclei, others showed anatomical and neurochemical similarities. Despite their complex subnuclear organization, subnuclei-specific functional impact on behavior and their underlying molecular profiles remain obscure. We here constitutively inhibited neurotransmission of protein kinase C-δ-positive (PKCδ+) neurons-a major cell type of the lateral subdivision of the CeA (CeL) and the oval nucleus of the BNST (BNSTov)-and found striking subnuclei-specific effects on fear- and anxiety-related behaviors, respectively. To obtain molecular clues for this dissociation, we conducted RNA sequencing in subnuclei-targeted micropunch samples. The CeL and the BNSTov displayed similar gene expression profiles at the basal level; however, both displayed differential gene expression when animals were exposed to fear-related stimuli, with a more robust expression change in the CeL. These findings provide novel insights into the molecular makeup and differential engagement of distinct subnuclei of the extended amygdala, critical for regulation of threat processing.

    DOI PubMed

  • Draft Genome Sequence of Okeania sp. Strain KiyG1, Assembled from Single-Amplified Genomes Collected from Cape Kiyan, Okinawa, Japan.

    Muhammad Wahyudin Lewaru, Yohei Nishikawa, Keigo Ide, Masato Kogawa, Masahito Hosokawa, Ashok Zachariah Samuel, Shinpei Sumimoto, Handung Nuryadi, Shoichiro Suda, Haruko Takeyama

    Microbiology resource announcements   9 ( 46 )  2020.11  [Refereed]  [International journal]

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    The genus Okeania is a globally distributed group of microorganisms that live in shallow seabed regions. These organisms play several environmentally important roles and are also known producers of several active secondary metabolites with potential human applications. Here, we present a draft genome of Okeania sp. strain KiyG1 (92.7% completeness) that was assembled from four single-amplified genomes.

    DOI PubMed

  • Slow-Cycling Cancer Stem Cells Regulate Progression and Chemoresistance in Colon Cancer.

    Daisuke Shiokawa, Hiroaki Sakai, Hirokazu Ohata, Toshiaki Miyazaki, Yusuke Kanda, Shigeki Sekine, Daichi Narushima, Masahito Hosokawa, Mamoru Kato, Yutaka Suzuki, Haruko Takeyama, Hideki Kambara, Hitoshi Nakagama, Koji Okamoto

    Cancer research   80 ( 20 ) 4451 - 4464  2020.10  [Refereed]  [International journal]

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    Cancer chemoresistance is often attributed to the presence of cancer stem cell (CSC)-like cells, but whether they are homogeneously chemoresistant remains unclear. We previously showed that in colon tumors, a subpopulation of LGR5+ CSC-like cells driven by TCF1 (TCF7), a Wnt-responsive transcription factor, were responsible for tumorigenicity. Here we demonstrate that the tumorigenic subpopulation of mouse LGR5+ cells exists in a slow-cycling state and identify a unique 22-gene signature that characterizes these slow-cycling CSC. Seven of the signature genes are specifically expressed in slow-cycling LGR5+ cells from xenografted human colon tumors and are upregulated in colon cancer clinical specimens. Among these seven, four genes (APCDD1, NOTUM, PROX1, and SP5) are known to be direct Wnt target genes, and PROX1 was expressed in the invasive fronts of colon tumors. PROX1 was activated by TCF1 to induce CDKN1C and maintain a slow-cycling state in colon cancer organoids. Strikingly, PROX1 was required for recurrent growth after chemotherapeutic treatment, suggesting that inhibition of slow-cycling CSC by targeting the TCF1-PROX1-CDKN1C pathway is an effective strategy to combat refractory colon cancer in combination with conventional chemotherapy. SIGNIFICANCE: These findings illustrate the importance of a slow-cycling CSC subpopulation in colon cancer development and chemoresistance, with potential implications for the identified slow-cycling CSC signatures and the TCF1-PROX1-CDKN1C pathway as therapeutic targets.

    DOI PubMed

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Industrial Property Rights 【 display / non-display

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Awards 【 display / non-display

  • 第5回「バイオインダストリー奨励賞」

    2021.07   (一財)バイオインダストリー協会  

  • The Commendation for Science and Technology by the Minister of Education, Culture, Sports, Science and Technology, The Young Scientists’ Prize


    Winner: Masahito Hosokawa

  • イノベーション賞

    2019.03   科学技術振興機構さきがけ(統合1細胞領域)  

    Winner: 細川 正人

  • 第96春季年会 優秀講演賞(学術)

    2016.05   日本化学会  

    Winner: 細川 正人

Research Projects 【 display / non-display


Syllabus 【 display / non-display

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