Sauer F, Wassarman D A, Rubin G M, Tjian R
Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley 94720-3204, USA.
Cell. 1996 Dec 27;87(7):1271-84. doi: 10.1016/s0092-8674(00)81822-x.
Mutations in the genes for two highly conserved TAFs, TAF(II)60 and TAF(II)110, reduce transcription of Bicoid-dependent target genes in vivo. By means of several distinct genetic test systems, specific activator-TAF interactions are shown to support both simple and synergistic enhancement of transcription in the embryo. These studies provide in vivo evidence that TAFs can serve as coactivators to receive gene-specific transcriptional activation signals. This genetic system also presents the opportunity to study the function of basal transcription components in regulating development of complex organisms.
两个高度保守的TAF基因TAF(II)60和TAF(II)110发生突变,会在体内降低双尾依赖型靶基因的转录。通过几种不同的遗传测试系统,特定的激活因子-TAF相互作用被证明可支持胚胎中简单和协同的转录增强。这些研究提供了体内证据,表明TAF可作为共激活因子来接收基因特异性转录激活信号。这个遗传系统也为研究基础转录成分在调节复杂生物体发育中的功能提供了机会。