Epigenomics and the Regulation of Aging

Abstract

It is tempting to assume that a gradual accumulation of damage ‘causes‘ an organism to age, but other biological processes present during the lifespan, whether ‘programmed‘ or ‘hijacked‘, could control the type and speed of aging. Theories of aging have classically focused on changes at the genomic level; however, individuals with similar genetic backgrounds can age very differently. Epigenetic modifications include DNA methylation, histone modifications and ncRNA. Environmental cues may be ‘remembered‘ during lifespan through changes to the epigenome that affect the rate of aging. Changes to the epigenomic landscape are now known to associate with aging, but so far causal links to longevity are only beginning to be revealed. Nevertheless, it is becoming apparent that there is significant reciprocal regulation occurring between the epigenomic levels. Future work utilizing new technologies and techniques should build a clearer picture of the link between epigenomic changes and aging.

KEYWORDS::

• aging
• DNA methylation
• histone modification
• longevity
• noncoding RNA

Acknowledgements

The authors thank H Cheng for critical reading of the manuscript.

Financial & competing interests disclosure

The authors acknowledge the support of the China Natural National Science Foundation research fund for Young International Scientists (Grant # 31150110469 to JD Boyd-Kirkup and grant #31250110212 to CD Green). G Wu is supported by grants from Shanghai Institutes of Biological Sciences (2011KIP202 to G Wu) and Chinese Ministry of Science and Technology (Grant # 2012AA020406). G Wu acknowledges the support of SA-SIBS Scholarship Program. This work was also supported by grants from the China Natural National Science Foundation (Grant #30890033, 31210103916 and 91019019), Chinese Ministry of Science and Technology (Grant #2011CB504206) and Chinese Academy of Sciences (Grant #KSCX2-EW-R-02 and KSCX2-EW-J-15) and stem cell leading project XDA01010303 to J-DJ Han. JD Boyd-Kirkup and CD Green hold Chinese Academy of Science Fellowships for Young International Scientists (#2011Y1SB05 to JD Boyd-Kirkup and #2010Y2SB06 to CD Green). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

The authors acknowledge the support of the China Natural National Science Foundation research fund for Young International Scientists (Grant # 31150110469 to JD Boyd-Kirkup and grant #31250110212 to CD Green). G Wu is supported by grants from Shanghai Institutes of Biological Sciences (2011KIP202 to G Wu) and Chinese Ministry of Science and Technology (Grant # 2012AA020406). G Wu acknowledges the support of SA-SIBS Scholarship Program. This work was also supported by grants from the China Natural National Science Foundation (Grant #30890033, 31210103916 and 91019019), Chinese Ministry of Science and Technology (Grant #2011CB504206) and Chinese Academy of Sciences (Grant #KSCX2-EW-R-02 and KSCX2-EW-J-15) and stem cell leading project XDA01010303 to J-DJ Han. JD Boyd-Kirkup and CD Green hold Chinese Academy of Science Fellowships for Young International Scientists (#2011Y1SB05 to JD Boyd-Kirkup and #2010Y2SB06 to CD Green). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.