Regulator Trafficking on Bacterial Transcription Units In Vivo

被引:191
作者
Mooney, Rachel A. [1 ]
Davis, Sarah E. [1 ]
Peters, Jason M. [1 ,2 ]
Rowland, Jennifer L. [1 ]
Ansari, Aseem Z. [1 ,3 ]
Landick, Robert [1 ,4 ]
机构
[1] Univ Wisconsin, Dept Biochem, Madison, WI 53706 USA
[2] Univ Wisconsin, Dept Genet, Madison, WI 53706 USA
[3] Univ Wisconsin, Genome Ctr, Madison, WI 53706 USA
[4] Univ Wisconsin, Dept Bacteriol, Madison, WI 53706 USA
关键词
COLI RNA-POLYMERASE; TERMINATION FACTOR-RHO; PROTEIN-DNA INTERACTIONS; NUSA GENE PROTEIN; ESCHERICHIA-COLI; ALPHA-SUBUNIT; CHROMATIN IMMUNOPRECIPITATION; DEPENDENT TERMINATION; ELONGATION COMPLEXES; FACTOR SIGMA(70);
D O I
10.1016/j.molcel.2008.12.021
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
The trafficking patterns of the bacterial regulators of transcript elongation sigma(70), rho, NusA, and NusG on genes in vivo and the explanation for promoter-proximal peaks of RNA polymerase (RNAP) are unknown. Genome-wide, E coli ChIP-chip revealed distinct association patterns of regulators as RNAP transcribes away from promoters (rho first, then NusA, then NusG). However, the interactions of elongating complexes with these regulators did not differ significantly among most transcription units. A modest variation of NusG signal among genes reflected increased NusG interaction as transcription progresses, rather than functional specialization of elongating complexes. Promoter-proximal RNAP peaks were offset from sigma(70) peaks in the direction of transcription and co-occurred with NusA and p peaks, suggesting that the RNAP peaks reflected elongating, rather than initiating, complexes. However, inhibition of rho did not increase RNAP levels within genes downstream from the RNAP peaks, suggesting the peaks are caused by a mechanism other than rho-dependent attenuation.
引用
收藏
页码:97 / 108
页数:12
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