p300-mediated tax transactivation from recombinant chromatin: Histone tail deletion mimics coactivator function

被引:51
作者
Georges, SA
Kraus, WL
Luger, K
Nyborg, JK [1 ]
Laybourn, PJ
机构
[1] Colorado State Univ, Dept Biochem & Mol Biol, Ft Collins, CO 80523 USA
[2] Cornell Univ, Dept Genet & Mol Biol, Ithaca, NY 14853 USA
关键词
D O I
10.1128/MCB.22.1.127-137.2002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Efficient transcription of the human T-cell leukemia virus type 1 (HTLV-1) genome requires Tax, a virally encoded oncogenic transcription factor, in complex with the cellular transcription factor CREB and the coactivators p300/CBP. To examine Tax transactivation in vitro, we used a chromatin assembly system that included recombinant core histones. The addition of Tax, CREB, and p300 to the HTLV-1 promoter assembled into chromatin activated transcription several hundredfold. Chromatin templates selectively lacking aminoterminal histone tails demonstrated enhanced transcriptional activation by Tax and CREB, with significantly reduced dependence on p300 and acetyl coenzyme A (acetyl-CoA). Interestingly, Tax/CREB activation from the tailless chromatin templates retained a substantial requirement for acetyl-CoA, indicating a role for acetyl-CoA beyond histone acetylation. These data indicate that during Tax transcriptional activation, the aminoterminal histone tails are the major targets of p300 and that tail deletion and acetylation are functionally equivalent.
引用
收藏
页码:127 / 137
页数:11
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