These are preliminary reports that have not been peer-reviewed. They should not be regarded as conclusive, guide clinical practice/health-related behavior, or be reported in news media as established information. For more information, please see our FAQs.
Preprints are manuscripts made publicly available before they have been submitted for formal peer review and publication. They might contain new research findings or data. Preprints can be a draft or final version of an author's research but must not have been accepted for publication at the time of submission.
submitted on 03.12.2018 and posted on 03.12.2018by xuejun guo, Dong Yang, Xiangyuan Zhang
Although the phenomenal relationship between epigenetics
and aging phenotypic changes is built up, an intrinsic connection between the
epigenetics and aging requires to be theoretically illuminated. In this study,
we propose epigenetic recording of varied cell environment and complex history could
be an origin of cellular aging. Through epigenetic modifications, the environment
and historical events can induce the chromatin template into activated or repressive
accessible structure, thereby shaping the DNA template into a spectrum of
chromatin states. The inner nature of diversity and conflicts born by cell environment
and its historical events are hence recorded into the chromatin template. This
could result in a dissipated spectrum of chromatin state and chaos of overall
gene expressions. An unavoidable degradation of epigenome entropy, similar to Shannon entropy, would be consequently
induced. The resulted disorder in epigenome, characterized by corrosion of epigenome
entropy as reflected in chromatin template, can be stably memorized and propagated
through cell divisions. Furthermore, hysteresis nature of epigenetics responding
to emerging environment could exacerbate the degradation of epigenome entropy. Besides
stochastic errors, we propose that epigenetics disorder and chaos derived from unordered
environment and complex cell experiences play an essential role in epigenetic
drift and the as-resulted cellular aging.