Hikari Yohitane | Ph.D., The University of Tokyo
Competition Sponsor: Japan Agency for Medical Research and Development
Awardee Year: 2020
The circadian clock generates transcriptional rhythms with a cycle of about 24 hours, and makes genes function only at the required time. Therefore, deficiency of the clock gene causes not only sleep disorders but also many aging-like symptoms such as hypertension, cardiac diseases, immune depression, and cataract, and significantly reduces the lifespan. Here I define the age-related circadian clock abnormality as “clock aging”. The working hypothesis is that part of the aging-associated symptoms is caused by disruption of the functional rhythms from the circadian clock. Recently, we showed that the expression profiles of a series of rhythmic genes were dramatically changed in aged mice, and we created a mouse model in which the transcriptional rhythm of a single rhythmic gene was genetically stopped by small deletion in the promoter region of the gene, for imitation of the aging state: A mouse model for “clock aging”. In this study, I elucidate the mechanisms of aging-associated symptoms as phenotypes in the clock aging mice, and pursue the molecular mechanisms that cause abnormality in clock output with aging.
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