IQB Handbook

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21ACHIEVEMENTPUBLICATIONIida T, Kobayashi T. RNA Polymerase I Activators Count and Adjust Ribosomal RNA Gene Copy Number. Mol Cell. 2019 Feb 21;73(4):645-654.e13. DOI:10.1016/j.molcel.2018.11.029Sasaki M, Kobayashi T. Ctf4 Prevents Genome Rearrangements by Suppressing DNA Double-Strand Break Formation and Its End Resection at Arrested Replication Forks. Mol Cell. 2017 May 18;66(4):533-545.e5. DOI:10.1016/j.mol-cel.2017.04.020Horigome C, Unozawa E, Ooki T, Kobayashi T. Ribosomal RNA gene repeats associate with the nuclear pore complex for maintenance after DNA damage. PLOS Genet. 2019 April 18;15(4):e1008103. DOI:10.1371/journal.pgen.1008103KOBAYASHITAKEHIKOPH.D. (1992) KYUSHU UNIVERSITYASSISTANT PROFESSOR (1993) NATIONAL INSTITUTE OF BASIC BIOLOGYPOSTDOCTORAL FELLOW (1994) ROCHE INSTITUTE FOR MOL BIOL POSTDOCTORAL FELLOW (1996) NATIONAL INSTITUTE OF HEALTHASSOCIATE PROFESSOR (2005)NATIONAL INSTITUTE OF BASIC BIOLOGYPROFESSOR (2006) NATIONAL INSTITUTE OF GENETICSPROFESSOR (2015) INSTITUTE OF MOLECULAR AND CELLULAR BIOSCIENCES, THE UNIVERSITY OF TOKYOPROFESSOR (2018) IQB / INSTITUTE FOR QUANTITATIVE BIOSCIENCES, THE UNIVERSITY OF TOKYO●MEMBER■ PROFESSOR :KOBAYASHI TAKEHIKO■ RESEARCH ASSOCIATE :IIDA TETSUSHI■ RESEARCH ASSOCIATE : SASAKI MARIKO■ RESEARCH ASSOCIATE : OYA ERIKO■ PROJECT RESEARCHER :HORI YUTARO■ PROJECT RESEARCHER :NISHIZAWA MASAFUMI■ TECHNICAL SPECIALIST :ASAKURA TOMOKOPUBLICATIONPUBLICATIONrganisms are using DNA as the genetic material for ~3 billion years. DNA is more useful for replication and repair than RNA due to the stable double stranded structure. Genome stability is essential to maintain cellular functions. In contrast, material DNA is sensitive to DNA damage such as UV and chemicals. Improper repair of DNA damage leads to an accumulation of mutations. Therefore, organisms have developed effective systems to ensure repair of DNA damage during the course of evolution. But the genome maintenance systems are not perfect that DNA damage and mutations gradually accumulate in the cell to cause cancer. To remove such risky cells, organisms developed cellular senescence. Actually, by senescence, the risk of cancer is dramatically reduced in mammals. The ribosomal RNA gene repeat (rDNA) is the most abundant gene in cells. In budding yeast, the rDNA is located on chromosome XII and contains ~150 rDNA copies. Due to the repetitive structure and heavy transcription, deletional intra-repeat recombination occurs to lose the copies. Then, the rDNA developed a gene amplification system in which DNA double strand break (DSB) and resulting amplification recombination are intendedly induced. Interestingly, the damage in the rDNA affects cellular senescence and deter-mines lifespan. We speculate that the rDNA emits the aging signal to induce senescence. We want to reveal the mechanisms. As the output of the research, we can contribute to develop a new type of medicine that reduces the risk of cancer using senescence of abnor-mal cells. ORejubination of cell : the budding yeast divides asymmetrically, one ages (mother cell, left) and another (daughter cell, right) rejuvinates. The similar cell division is abserved in stem and germ line cells. Green: rDNA, red: nucleopore protein.