Updated on 2025/07/27

写真a

 
TOMOOKA, Ryo
 
Affiliation
Faculty of Human Sciences, Advanced Research Center for Human Sciences
Job title
Research Associate
Degree
Doctor (Medicine) ( 2025.03 Keio University )

Research Experience

  • 2025.04
    -
    Now

    Waseda University   Faculty of Human Sciences   Research assistant

  • 2022.04
    -
    2025.03

    Japan Society for the Promotion of Science

  • 2021.10
    -
    2022.03

    Japan Science and Technology Agency

  • 2019.04
    -
    2021.03

    Keio University Hospital

Education Background

  • 2021.04
    -
    2025.03

    Keio University   Graduate School of Medicine  

  • 2013.04
    -
    2019.03

    Keio University   School of Medicine  

Research Areas

  • Molecular biology
 

Papers

  • Phase separated condensates of ATRX regulate neural progenitor identity.

    Ryo Tomooka, Tsukasa Sanosaka, Tamami Miyagi, Tomoko Andoh-Noda, Satoe Banno, Noriko Mizota, Kohsuke Kanekura, Hideyuki Okano, Jun Kohyama

    Nature communications   16 ( 1 ) 6489 - 6489  2025.07  [International journal]

     View Summary

    Mutations in the ATRX genes cause alpha-thalassemia X-linked intellectual disability (ATR-X) syndrome. Here, we show that ATRX influences the fate of human neural progenitor cells (hNPCs) by forming condensates through liquid-liquid phase separation (LLPS). The intrinsically disordered region (IDR) of ATRX is essential for LLPS and enables ATRX to form dynamic condensates that recruit co-activators. These condensates are necessary for ATRX localization at super-enhancers (SEs) in hNPCs, linking its compartmentalization to transcriptional regulation. Disruption of ATRX condensates alters gene expression and impairs neuronal differentiation. Our findings support a model in which ATRX phase separation regulates gene networks required for hNPC identity. These findings extend current understanding of ATRX function beyond its roles in chromatin structure and suggest that LLPS is a key regulatory mechanism by which ATRX supports neurodevelopment. This study opens avenues for further investigation into how dysregulation of ATRX and its phase-separation ability may contribute to the pathogenesis of ATR-X syndrome and related neurodevelopmental disorders.

    DOI PubMed

    Scopus

  • Mesenchymal properties of iPSC-derived neural progenitors that generate undesired grafts after transplantation.

    Miho Isoda, Tsukasa Sanosaka, Ryo Tomooka, Yo Mabuchi, Munehisa Shinozaki, Tomoko Andoh-Noda, Satoe Banno, Noriko Mizota, Ryo Yamaguchi, Hideyuki Okano, Jun Kohyama

    Communications biology   6 ( 1 ) 611 - 611  2023.06  [International journal]

     View Summary

    Although neural stem/progenitor cells derived from human induced pluripotent stem cells (hiPSC-NS/PCs) are expected to be a cell source for cell-based therapy, tumorigenesis of hiPSC-NS/PCs is a potential problem for clinical applications. Therefore, to understand the mechanisms of tumorigenicity in NS/PCs, we clarified the cell populations of NS/PCs. We established single cell-derived NS/PC clones (scNS/PCs) from hiPSC-NS/PCs that generated undesired grafts. Additionally, we performed bioassays on scNS/PCs, which classified cell types within parental hiPSC-NS/PCs. Interestingly, we found unique subsets of scNS/PCs, which exhibited the transcriptome signature of mesenchymal lineages. Furthermore, these scNS/PCs expressed both neural (PSA-NCAM) and mesenchymal (CD73 and CD105) markers, and had an osteogenic differentiation capacity. Notably, eliminating CD73+ CD105+ cells from among parental hiPSC-NS/PCs ensured the quality of hiPSC-NS/PCs. Taken together, the existence of unexpected cell populations among NS/PCs may explain their tumorigenicity leading to potential safety issues of hiPSC-NS/PCs for future regenerative medicine.

    DOI PubMed

    Scopus

    4
    Citation
    (Scopus)
  • Chromatin remodeler CHD7 targets active enhancer region to regulate cell type-specific gene expression in human neural crest cells.

    Tsukasa Sanosaka, Hironobu Okuno, Noriko Mizota, Tomoko Andoh-Noda, Miki Sato, Ryo Tomooka, Satoe Banno, Jun Kohyama, Hideyuki Okano

    Scientific reports   12 ( 1 ) 22648 - 22648  2022.12  [International journal]

     View Summary

    A mutation in the chromatin remodeler chromodomain helicase DNA-binding 7 (CHD7) gene causes the multiple congenital anomaly CHARGE syndrome. The craniofacial anomalies observed in CHARGE syndrome are caused by dysfunctions of neural crest cells (NCCs), which originate from the neural tube. However, the mechanism by which CHD7 regulates the function of human NCCs (hNCCs) remains unclear. We aimed to characterize the cis-regulatory elements governed by CHD7 in hNCCs by analyzing genome-wide ChIP-Seq data and identifying hNCC-specific CHD7-binding profiles. We compared CHD7-binding regions among cell types, including human induced pluripotent stem cells and human neuroepithelial cells, to determine the comprehensive properties of CHD7-binding in hNCCs. Importantly, analysis of the hNCC-specific CHD7-bound region revealed transcription factor AP-2α as a potential co-factor facilitating the cell type-specific transcriptional program in hNCCs. CHD7 was strongly associated with active enhancer regions, permitting the expression of hNCC-specific genes to sustain the function of hNCCs. Our findings reveal the regulatory mechanisms of CHD7 in hNCCs, thus providing additional information regarding the transcriptional programs in hNCCs.

    DOI PubMed

    Scopus

    5
    Citation
    (Scopus)

Research Projects

  • Development of drug discovery platform for neurodegenerative diseases using new 3D culture method

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research

    Project Year :

    2023.03
    -
    2025.03