Molecular turnover, the H3.3 dilemma and organismal aging (hypothesis)

Aging Cell

Evelyne Saade²  Iryna Pirozhkova¹  Rakhan Aimbetov¹  Marc Lipinski¹ 

[1] Institute Gustave Roussy, University Paris SUD, Villejuif, France;Faculty of Public Health, Lebanese University LU, Beirut, Lebanon

关键词: aberrant repair;    aneuploidy;    chromatin;    epigenetic information;    Hayflick limit;    somatic stem cells;   

DOI  :  10.1111/acel.12332

来源: Wiley

【 摘 要 】

Summary

The H3.3 histone variant has been a subject of increasing interest in the field of chromatin studies due to its two distinguishing features. First, its incorporation into chromatin is replication independent unlike the replication-coupled deposition of its canonical counterparts H3.1/2. Second, H3.3 has been consistently associated with an active state of chromatin. In accordance, this histone variant should be expected to be causally involved in the regulation of gene expression, or more generally, its incorporation should have downstream consequences for the structure and function of chromatin. This, however, leads to an apparent paradox: In cells that slowly replicate in the organism, H3.3 will accumulate with time, opening the way to aberrant effects on heterochromatin. Here, we review the indications that H3.3 is expected both to be incorporated in the heterochromatin of slowly replicating cells and to retain its functional downstream effects. Implications for organismal aging are discussed.

【 授权许可】

CC BY   
© 2015 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.

Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.