Researchers Database

tanaka yuuya

    Senior Resident
Last Updated :2021/11/23

Researcher Information

Research funding number

  • 20921688

J-Global ID

Published Papers

  • Takao Morimune, Ayami Tano, Yuya Tanaka, Haruka Yukiue, Takefumi Yamamoto, Ikuo Tooyama, Yoshihiro Maruo, Masaki Nishimura, Masaki Mori
    PLOS ONE 16 (4) e0248517 - e0248517 2021/04 
    It is not fully understood how enzymes are regulated in the tiny reaction field of a cell. Several enzymatic proteins form cytoophidia, a cellular macrostructure to titrate enzymatic activities. Here, we show that the epileptic encephalopathy-associated protein Tbc1d24 forms cytoophidia in neuronal cells both in vitro and in vivo. The Tbc1d24 cytoophidia are distinct from previously reported cytoophidia consisting of inosine monophosphate dehydrogenase (Impdh) or cytidine-5’-triphosphate synthase (Ctps). Tbc1d24 cytoophidia is induced by loss of cellular juvenescence caused by depletion of Gm14230, a juvenility-associated lncRNA (JALNC) and zeocin treatment. Cytoophidia formation is associated with impaired enzymatic activity of Tbc1d24. Thus, our findings reveal the property of Tbc1d24 to form cytoophidia to maintain neuronal cellular juvenescence.
  • Faidruz Azura Jam, Takao Morimune, Atsushi Tsukamura, Ayami Tano, Yuya Tanaka, Yasuhiro Mori, Takefumi Yamamoto, Masaki Nishimura, Ikuo Tooyama, Masaki Mori
    Scientific Reports 10 (1) 2020/12 
    Abstract Cell competition is a cell–cell interaction mechanism which maintains tissue homeostasis through selective elimination of unfit cells. During early brain development, cells are eliminated through apoptosis. How cells are selected to undergo elimination remains unclear. Here we aimed to identify a role for cell competition in the elimination of suboptimal cells using an in vitro neuroepithelial model. Cell competition was observed when neural progenitor HypoE-N1 cells expressing RASV12 were surrounded by normal cells in the co-culture. The elimination through apoptosis was observed by cellular changes of RASV12 cells with rounding/fragmented morphology, by SYTOX blue-positivity, and by expression of apoptotic markers active caspase-3 and cleaved PARP. In this model, expression of juvenility-associated genes Srsf7 and Ezh2 were suppressed under cell-competitive conditions. Srsf7 depletion led to loss of cellular juvenescence characterized by suppression of Ezh2, cell growth impairment and enhancement of senescence-associated proteins. The cell bodies of eliminated cells were engulfed by the surrounding cells through phagocytosis. Our data indicates that neuroepithelial cell competition may have an important role for maintaining homeostasis in the neuroepithelium by eliminating suboptimal cells through loss of cellular juvenescence.
  • Yosuke Kadota, Faidruz Azura Jam, Haruka Yukiue, Ichiro Terakado, Takao Morimune, Ayami Tano, Yuya Tanaka, Sayumi Akahane, Mayu Fukumura, Ikuo Tooyama, Masaki Mori
    iScience 23 (3) 100929 - 100929 2589-0042 2020/03
  • Cyril J. Peter, Atsushi Saito, Yuto Hasegawa, Yuya Tanaka, Mohika Nagpal, Gabriel Perez, Emily Alway, Sergio Espeso-Gil, Tariq Fayyad, Chana Ratner, Aslihan Dincer, Achla Gupta, Lakshmi Devi, John G. Pappas, François M. Lalonde, John A. Butman, Joan C. Han, Schahram Akbarian, Atsushi Kamiya
    Nature Communications 10 (1) 2019/12 
    AbstractMany neuropsychiatric risk genes contribute to epigenetic regulation but little is known about specific chromatin-associated mechanisms governing the formation of neuronal connectivity. Here we show that transcallosal connectivity is critically dependent onC11orf46, a nuclear protein encoded in the chromosome 11p13 WAGR risk locus.C11orf46haploinsufficiency was associated with hypoplasia of the corpus callosum.C11orf46knockdown disrupted transcallosal projections and was rescued by wild type C11orf46 but not the C11orf46R236Hmutant associated with intellectual disability. Multiple genes encoding key regulators of axonal development, includingSema6a, were hyperexpressed inC11orf46-knockdown neurons. RNA-guided epigenetic editing ofSema6agene promoters via a dCas9-SunTag system with C11orf46 binding normalized SEMA6A expression and rescued transcallosal dysconnectivity via repressive chromatin remodeling by the SETDB1 repressor complex. Our study demonstrates that interhemispheric communication is sensitive to locus-specific remodeling of neuronal chromatin, revealing the therapeutic potential for shaping the brain’s connectome via gene-targeted designer activators and repressor proteins.

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