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tomimatsu kosuke Last modified date：2022.07.14

Assistant Professor / Medical Research Center for High Depth Omics
Medical Institute of Bioregulation




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Homepage
https://kyushu-u.pure.elsevier.com/en/persons/kosuke-tomimatsu
　Reseacher Profiling Tool　Kyushu University Pure
Phone
092-642-4534
Fax
092-642-4526
Country of degree conferring institution (Overseas)
No
Field of Specialization
cell biology
Total Priod of education and research career in the foreign country
00years00months
Research
Research Interests
  • Development of spatial multi-omics methods for single cell resolution
    keyword : Single cell analysis, Spatial omics
    2022.06～2022.06.
Academic Activities
Books
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Papers
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1. Kosuke Tomimatsu, Dóra Bihary, Ioana Olan, Aled J. Parry, Stefan Schoenfelder, Adelyne S. L. Chan, Guy St. C. Slater, Yoko Ito, Peter J. Rugg-Gunn, Kristina Kirschner, Camino Bermejo-Rodriguez, Tomomi Seko, Hiroyuki Kugoh, Ken Shiraishi, Koji Sayama, Hiroshi Kimura, Peter Fraser, Masako Narita, Shamith A. Samarajiwa, Masashi Narita, Locus-specific induction of gene expression from heterochromatin loci during cellular senescence, Nature Aging, 10.1038/s43587-021-00147-y, 2021.12, <title>Abstract</title> Cellular senescence is a fate-determined state, accompanied by reorganization of heterochromatin. While lineage-appropriate genes can be temporarily repressed through facultative heterochromatin, stable silencing of lineage-inappropriate genes often involves the constitutive heterochromatic mark, histone H3K9me3. The fate of these heterochromatic genes during the chromatin reorganization accompanying senescence is unclear. Here we show a small number of lineage-inappropriate genes are derepressed in senescent cells from H3K9me3 regions that gain open chromatin marks. DNA FISH experiments reveal that these gene loci, which are tightly condensed at the nuclear periphery in proliferative cells, are physically decompacted during senescence. Among these gene loci, <italic>NLRP3</italic> is predominantly expressed in immune cells, such as macrophages, where it resides within an open topologically associated domain (TAD). In contrast, <italic>NLRP3</italic> is derepressed in senescent fibroblasts, potentially due to the local disruption of the H3K9me3-rich TAD that contains it. The role of NLRP3 has been implicated in the amplification of inflammatory cytokine signalling in senescence and aging, underscoring the functional relevance of gene induction from ‘permissive’ H3K9me3 regions in senescent cells..


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