SATB1 regulates beta-like globin genes through matrix related nuclear relocation of the cluster.
The nuclear location and relocation of genes play crucial regulatory roles in gene expression. SATB1, a MAR-binding protein, has been found to regulate beta-like globin genes through chromatin remodeling. In this study, we generated K562 cells over-expressing wild-type or nuclear matrix targeting sequences (NMTS)-deficient SATB1 and found that like wild-type SATB1, NMTS-deficient SATB1 induces out loop of beta-globin cluster from its chromosome territory (CT), while it is unable to associate the cluster with the nuclear matrix as wild-type SATB1 does and had no regulatory functions to the beta-globin cluster. Besides, our data showed that the transacting factor occupancies and chromatin modifications at beta-globin cluster were differentially affected by wild-type and NMTS-deficient SATB1. These results indicate that SATB1 regulates beta-like globin genes at the nuclear level interlaced with chromatin and DNA level, and emphasize the nuclear matrix binding activity of SATB1 to its regulatory function.
Gong
Huan
H
Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Dong Dan San Tiao, Beijing, PR China.
Wang
Zhao
Z
Zhao
Guo-wei
GW
Lv
Xiang
X
Wei
Gong-hong
GH
Wang
Li
L
Liu
De-pei
DP
Liang
Chih-chuan
CC