Sandaltzopoulos R, Becker P B
Gene Expression Programme, European Molecular Biology Laboratory, Heidelberg, Germany.
Mol Cell Biol. 1998 Jan;18(1):361-7. doi: 10.1128/MCB.18.1.361.
Transcription by RNA polymerase II is highly regulated at the level of initiation and elongation. Well-documented transcription activation mechanisms, such as the recruitment of TFIID and TFIIB, control the early phases of preinitiation complex formation. The heat shock genes provide an example for transcriptional regulation at a later step: in nuclei TFIID can be detected at the TATA box prior to heat induction. Using cell-free systems for chromatin reconstitution and transcription, we have analyzed the mechanisms by which heat shock factor (HSF) increases transcription of heat shock genes in chromatin. HSF affected transcription of naked DNA templates in multiple ways: (i) by speeding up the rate of preinitiation complex formation, (ii) by increasing the number of productive templates, and (iii) by increasing the reinitiation rate. Under the more physiological conditions of potentiated chromatin templates, HSF affected only the reinitiation rate. Activator-dependent reinitiation of transcription, obviating the slow assembly of the TFIID-TFIIA complex on a promoter, may be especially crucial for genes requiring a fast response to inducers.
RNA聚合酶II的转录在起始和延伸水平上受到高度调控。有充分文献记载的转录激活机制，如TFIID和TFIIB的募集，控制着起始前复合物形成的早期阶段。热休克基因提供了后期转录调控的一个例子：在细胞核中，热诱导前可在TATA框处检测到TFIID。利用无细胞系统进行染色质重构和转录，我们分析了热休克因子（HSF）增加染色质中热休克基因转录的机制。HSF以多种方式影响裸露DNA模板的转录：（i）通过加快起始前复合物的形成速率，（ii）通过增加有活性模板的数量，以及（iii）通过增加重新起始速率。在染色质模板增强的更生理条件下，HSF仅影响重新起始速率。转录的激活剂依赖性重新起始，避免了TFIID-TFIIA复合物在启动子上缓慢组装，对于需要对诱导剂快速响应的基因可能尤为关键。
