Genome wide interactions of wild-type and activator bypass forms of σ54.
Genome wide interactions of wild-type and activator bypass forms of σ54.
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野生型和激活因子旁路形式的基因组宽相互作用的σ54。
DOI：
10.1093/nar/gkv597
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发表时间：
2015-09-03
影响因子：
14.9
通讯作者：
Buck M
中科院分区：
文献类型：
--
作者：
Schaefer J;Engl C;Zhang N;Lawton E;Buck M
涉及启动子特异性因子σ54的增强子依赖性转录广泛分布于细菌中，通常与细胞包膜功能有关。对于转录起始，σ54-RNA聚合酶通过同源的AAA+ atp酶激活剂的重塑产生开放的启动子复合物。由于激活子可以在体外绕过，体内的旁路转录可能是沿着进化途径产生新的控制网络和转录模式的紧急基因表达的来源。在单个测试启动子中，未观察到体内旁路转录。我们现在在大肠杆菌中使用全基因组转录谱分析、全基因组诱变和基因过表达策略来(i)确定体内旁路转录的范围，（ii）鉴定可能改变体内旁路转录的基因。我们发现在体内普遍存在旁路转录的证据很少，只有一小部分σ54启动子在没有激活子的情况下起作用。研究结果还表明，在体内没有一个基因限制旁路转录，认为旁路转录是受到严格控制的。受σ54抑制的启动子序列明显，表明编码σ54的rpoN的丢失而不是产生rpoN旁路等位基因可能是新的基因表达模式的进化途径之一。最后，冷休克启动子在体内表现出不同寻常的σ54依赖性，不容易与传统的σ54结合位点相关。
Enhancer-dependent transcription involving the promoter specificity factor σ54 is widely distributed amongst bacteria and commonly associated with cell envelope function. For transcription initiation, σ54-RNA polymerase yields open promoter complexes through its remodelling by cognate AAA+ ATPase activators. Since activators can be bypassed in vitro, bypass transcription in vivo could be a source of emergent gene expression along evolutionary pathways yielding new control networks and transcription patterns. At a single test promoter in vivo bypass transcription was not observed. We now use genome-wide transcription profiling, genome-wide mutagenesis and gene over-expression strategies in Escherichia coli, to (i) scope the range of bypass transcription in vivo and (ii) identify genes which might alter bypass transcription in vivo. We find little evidence for pervasive bypass transcription in vivo with only a small subset of σ54 promoters functioning without activators. Results also suggest no one gene limits bypass transcription in vivo, arguing bypass transcription is strongly kept in check. Promoter sequences subject to repression by σ54 were evident, indicating loss of rpoN (encoding σ54) rather than creating rpoN bypass alleles would be one evolutionary route for new gene expression patterns. Finally, cold-shock promoters showed unusual σ54-dependence in vivo not readily correlated with conventional σ54 binding-sites.