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Transcriptional co‐activator activity of SYT is negatively regulated by BRM and Brg1
Author(s) -
Ishida Michiko,
Tanaka Shinya,
Ohki Misao,
Ohta Tsutomu
Publication year - 2004
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1356-9597.2004.00737.x
Subject(s) - biology , activator (genetics) , cancer research , microbiology and biotechnology , genetics , gene
The t(X;18)(p11.2;q11.2) translocation found in synovial sarcomas results in the fusion of the SYT gene on chromosome 18 to the SSX gene on chromosome X. Although the SYT‐SSX fusion proteins may trigger synovial sarcoma development, the biological functions of SYT, SSX and SYT‐SSX genes are unclear. Transfections of Gal4 DNA binding domain fusion protein constructs demonstrate that SYT protein acts as a transcriptional co‐activator at the C‐terminal domain and that the activity is repressed through the N‐terminus. The N‐terminal 70 amino acids of SYT bind not only to BRM, but also to Brg1, both of which are subunits of SWI/SNF chromatin remodelling complexes. Here, we have investigated the functions of BRM and Brg1 on the repression of SYT activity. The negative regulation of SYT transcriptional co‐activator activity is dependent on the ATP‐hydrolysis of BRM and Brg1 in the protein complexes. This indicates that the SWI/SNF protein complexes regulate SYT activity using the chromatin remodelling activity.