RNA Polymerase Modulators and DNA Repair Activities Resolve Conflicts between DNA Replication and Transcription

Trautinger, Brigitte W.; Jaktaji, Razieh Pourahmad; Rusakova, E. E.; Lloyd, Robert G.

doi:10.1016/j.molcel.2005.06.004

Cited by 170 publications

(267 citation statements)

References 27 publications

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“…The lack of requirement for transcription elongation factors to minimize formation of paused but still active forks is in apparent conflict with the requirement for such factors to minimize the need for repair of stalled forks by recombination enzymes (20). However, recombination enzymes such as RuvABC act on forks that no longer possess an active replisome (24) rather than on those that are paused but still retain function.…”

Section: Discussionmentioning

confidence: 99%

“…The implication is that transcription factors are important within the context of inactive forks that require replisome reloading via recombination enzymes. Perhaps this requirement reflects the critical importance of such factors in minimizing the formation of backed-up arrays of stalled transcription complexes, formidable obstacles to replication that might not be surmountable by paused, active replisomes (20).…”

Section: Discussionmentioning

confidence: 99%

“…These data indicate that promotion of replisome movement by Rep along protein-coated DNA may be essential to avoid RecD2-directed cell death. A major source of nucleoprotein replicative barriers is transcription, with mutations within RNA polymerase subunits being able to suppress multiple defects in genome duplication (20,(32)(33)(34). One such mutation, rpoB [H1244Q], suppresses defects in genome duplication by reducing the stability of stalled transcription complexes (20) and inhibiting backtracking of RNA polymerase (35).…”

Section: Clearance Of Nucleoprotein Barriers Ahead Of Forks Protects mentioning

confidence: 99%

“…However, despite the critical importance of fork pausing for genome stability, the contributions of different types of barrier to replisome pausing remain unknown. In particular, although both transcription complexes and DNA damage present known challenges to fork movement in bacteria and eukaryotes (15,(19)(20)(21), the relative frequencies with which they affect fork progression in vivo is not known. This is in part because physical detection of fork pausing is only possible when such pausing occurs at specific locations in the genome and is sufficiently frequent and/or prolonged to facilitate detection.…”

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confidence: 99%

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Protein–DNA complexes are the primary sources of replication fork pausing in Escherichia coli

Gupta

Guy

Yeeles

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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102

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Replication fork pausing drives genome instability, because any loss of paused replisome activity creates a requirement for reloading of the replication machinery, a potentially mutagenic process. Despite this importance, the relative contributions to fork pausing of different replicative barriers remain unknown. We show here that Deinococcus radiodurans RecD2 helicase inactivates Escherichia coli replisomes that are paused but still functional in vitro, preventing continued fork movement upon barrier removal or bypass, but does not inactivate elongating forks. Using RecD2 to probe replisome pausing in vivo, we demonstrate that most pausing events do not lead to replisome inactivation, that transcription complexes are the primary sources of this pausing, and that an accessory replicative helicase is critical for minimizing the frequency and/or duration of replisome pauses. These findings reveal the hidden potential for replisome inactivation, and hence genome instability, inside cells. They also demonstrate that efficient chromosome duplication requires mechanisms that aid resumption of replication by paused replisomes, especially those halted by protein-DNA barriers such as transcription complexes.DNA repair | genome stability | Rep | RNA polymerase | recombination

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Clearance Of Nucleoprotein Barriers Ahead Of Forks Protects mentioning

confidence: 99%

mentioning

confidence: 99%

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Protein–DNA complexes are the primary sources of replication fork pausing in Escherichia coli

Gupta

Guy

Yeeles

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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102

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“…The same DNA template is used by RNA polymerase (RNAP) for transcription and by the replisome (DNA polymerase and associated proteins) for replication. Transcription complexes that are stalled, initiating, or terminating can slow or block replication (8,9). RNAP and the replisome can collide when moving toward each other (head-on), or when the replisome, which moves faster than RNAP, catches up with RNAP moving in the same direction (codirectional).…”

mentioning

confidence: 99%

Genome-wide coorientation of replication and transcription reduces adverse effects on replication in Bacillus subtilis

Wang

Berkmen

Grossman

2007

Proc. Natl. Acad. Sci. U.S.A.

102

118

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In many bacteria, there is a strong bias for genes to be encoded on the leading strand of DNA, resulting in coorientation of replication and transcription. In Bacillus subtilis, transcription of the majority of genes (75%) is cooriented with replication. By using genomewide profiling of replication with DNA microarrays, we found that this coorientation bias reduces adverse effects of transcription on replication. We found that in wild-type cells, transcription did not appear to affect the rate of replication elongation. However, in mutants with reversed transcription bias for an extended region of the chromosome, replication elongation was slower. This reduced replication rate depended on transcription and was limited to the region in which the directions of replication and transcription are opposed. These results support the hypothesis that the strong bias to coorient transcription and replication is due to selective pressure for processive, efficient, and accurate replication.DNA microarrays ͉ elongation of replication ͉ genomic organization ͉ genomic stability ͉ origin of replication M any aspects of the organization of bacterial genomes are conserved and important for cell survival. DNA rearrangements, including large chromosomal inversions, can lead to inviability, decreased fitness, and impaired development (1-4). It has been proposed that genomic organization affects replication, transcription, and segregation of genomes (5).One benefit of proper genomic organization may be the reduction of potential conflicts between replication and transcription (5-7). The same DNA template is used by RNA polymerase (RNAP) for transcription and by the replisome (DNA polymerase and associated proteins) for replication. Transcription complexes that are stalled, initiating, or terminating can slow or block replication (8, 9). RNAP and the replisome can collide when moving toward each other (head-on), or when the replisome, which moves faster than RNAP, catches up with RNAP moving in the same direction (codirectional). Head-on and codirectional collisions can occur when genes are on the lagging and leading strands, respectively.The consequences of head-on and codirectional collisions are different. In Escherichia coli, high levels of transcription can effectively slow or block progression of replication forks if transcription and replication are head-on, but not if they are codirectional (10). In French's landmark study, an inducible plasmid-derived origin of replication was positioned on either side of an rRNA operon, one of the most highly transcribed operons. Replication fork progression, monitored by EM, was much slower when running against, rather than with, the direction of transcription. Plasmid DNA replication in E. coli can also be hindered by head-on transcription from a strong inducible promoter, probably because of collisions between the replisome and RNAP (ref.

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Termination of DNA Replication in Prokaryotes

Rudolph

Corocher

Grainge

et al. 2019

Encyclopedia of Life Sciences

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Most bacteria and archaea have circular chromosomes, in which DNA replication begins at a site known as an origin of replication. Double-stranded DNA unwound at the origin creates two replication forks that are engaged by DNA polymerase complexes (replisomes) that advance each fork and proceed in 21 opposite directions away from the origin, copying the original strands. Termination of DNA replication 22 occurs when the two forks meet and fuse, creating two separate double-stranded DNA molecules. In 23 the well-studied bacteria Escherichia coli and Bacillus subtilis, this occurs in the terminus region, which is situated diametrically opposite the origin. Failure to terminate chromosome replication correctly can lead to problems with genome function and stability, including DNA over-replication. In contrast, some 26 archaea have multi-origin chromosomes and do not appear to specifically regulate the location of termination.

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RNA Polymerase Modulators and DNA Repair Activities Resolve Conflicts between DNA Replication and Transcription

Cited by 170 publications

References 27 publications

Protein–DNA complexes are the primary sources of replication fork pausing in Escherichia coli

Protein–DNA complexes are the primary sources of replication fork pausing in Escherichia coli

Genome-wide coorientation of replication and transcription reduces adverse effects on replication in Bacillus subtilis

Termination of DNA Replication in Prokaryotes

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