Editorial Volume 3, Issue 10 pp 911—912

Protein acetylation and aging


Figure 1. Mixed acetylation phosphorylation cascades of intrinsic aging defense (shown in red) and DNA damage response pathways (shown in blue). With aging, NuA4 acetylation of Sip2 declines, resulting in Snf1 activation and subsequent Sch9 phosphorylation. Forced Sip2 acetylation eliminates Snf1 activation and Sch9 phosphorylation, delays the aging process and leads to life span extension. Similarly, following occurrence of double strand breaks (DSBs), MRN complex and CK2 are recruited to the DSB site, whereCK2 leads to the release of inhibition from tri-methylated H3K9 (H3K9me3) and the recruitment of Tip60/ATM complex to MRN. MRN activates Tip60 acetyltransferase activity and in turn results in the acetylation and subsequent phosphorylation and activation of ATM. Ac, acetylation; Ph, phosphorylation.