Cell Biochemistry and Biophysics

, Volume 50, Issue 3, pp 133–141

MRGing Chromatin Dynamics and Cellular Senescence

Review Paper

DOI: 10.1007/s12013-008-9006-7

Cite this article as:
Garcia, S.N. & Pereira-Smith, O. Cell Biochem Biophys (2008) 50: 133. doi:10.1007/s12013-008-9006-7


Normal primary cells have a finite ability to divide in culture and after a number of population doublings enter a state of irreversible cell cycle arrest known as replicative senescence. Several cellular stresses have been shown to induce a senescence-like growth arrest including shortened telomeres, DNA-damaging stresses, and drastic changes in chromatin structure, for example, through histone deacetylase (HDAC) induction. Histones are core components of chromatin which are subject to a number of chemical modifications that influence the dynamic state of chromatin structure. Proper chromatin structure formation is crucial for most DNA-dependent processes including transcription, replication, and repair which have a profound impact on cellular proliferation and senescence. Several genes important for chromatin remodeling such as the tumor suppressors p53 and retinoblastoma (Rb) affect cellular senescence by mediating changes in chromatin structure and gene expression. The Morf4-Related Gene (MRG) family of transcription factors forms stable interactions with chromatin-modifying complexes including histone acetyltransferase (HAT) and HDAC complexes and interact with Rb. Further, the MRG family was founded by a gene, Mortality Factor on Chromosome 4, capable of inducing senescence in immortalized cell lines. In this paper, we review the role of the MRG family of proteins in chromatin dynamics and cellular senescence.


NuA4Sin3-HDAC1Eaf3DNA repairAging

Copyright information

© Humana Press Inc. 2008

Authors and Affiliations

  1. 1.Department of Cellular and Structural Biology, STCBM 3.100The University of Texas Health Sciences Center at San AntonioSan AntonioUSA