Open AccessSox2 Deacetylation by S irt1 Is Involved in Mouse Somatic Reprogramming
Author(s) -
Mu WenLi,
Wang YaJun,
Xu Peng,
Hao DeLong,
Liu XiuZhen,
Wang TingTing,
Chen Feng,
Chen HouZao,
Lv Xiang,
Liu DePei
Publication year - 2015
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1002/stem.2012
Subject(s) - reprogramming , sox2 , biology , klf4 , induced pluripotent stem cell , sirtuin , somatic cell , embryonic stem cell , microbiology and biotechnology , stem cell , acetylation , sirtuin 1 , cellular differentiation , genetics , cell , downregulation and upregulation , gene
Mouse somatic cells can be reprogrammed into induced pluripotent stem cells by defined factors known to regulate pluripotency, including Oct4, Sox2, Klf4, and c‐Myc. Together with Oct4, Sox2 plays a major role as a master endogenous pluripotent genes trigger in reprogramming. It has been reported that Sirtuin 1 (Sirt1), a member of the Sirtuin family of NAD + ‐dependent protein deacetylases, is involved in embryonic stem cell antioxidation, differentiation, and individual development. However, as a deacetylation enzyme, whether Sirt1 influences reprogramming through its post‐translational modification function remains unknown. In this study, we provide evidence that deacetylation of Sox2 by Sirt1 is required for reprogramming. We found that a low level of Sox2 acetylation could significantly increase reprogramming efficiency. Furthermore, we found that Sox2 can be deacetylated by Sirt1 in an Oct4‐mediated manner. Compared with wild‐type cells, Sirt1‐null mouse embryonic fibroblasts exhibit decreased reprogramming efficiency, and overexpression of Sirt1 rescues this defect. In addition, Sirt1 functions in the regulation of reprogramming through deacetylating Sox2. Taken together, we have identified a new regulatory role of Sirt1 in reprogramming and provided a link between deacetylation events and somatic cell reprogramming. S tem C ells 2015;33:2135–2147