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Chapter 23 : Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell

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Abstract:

This chapter concentrates on the repair mechanism in , but the lessons learned in this organism should also apply to analogous systems in other organisms. Although there are several distinct DNA mismatch repair systems, in this chapter the term is used to denote the MutSLH system. DNA polymerase III, the replicative enzyme, catalyzes resynthesis of nucleotides and ligation followed by Dam methylation to complete the process. An alternative to the futile cycling model based on double-strand DNA breaks (DSBs) recombinational repair is described in the chapter to explain how mismatch repair sensitizes mutants (and human cells) to methylating agents and cisplatin. In mutants there is constant repair of DSBs, and the recombinational capacity of the cell is probably near its maximum. This conclusion is based on the higher basal level of transcription of certain SOS genes in dam cells, suggesting that one or more of the RecA or RuvA or RuvB proteins is limiting. The hypothesis that dam bacteria are sensitive to these agents because of inability to repair all DSBs is quite plausible. An important common theme is the requirement for replication forks to stall or collapse at lesions. The hyperrecombination phenotype is explained by the increased number of DSBs leading to increased initiation of recombination. Together with the roles for Dam methylation in controlling transcription initiation and its role in regulating initiation of chromosome replication and its synchronization, almost all the phenotypic properties can now be explained.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23

Key Concept Ranking

DNA Synthesis
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DNA Polymerase III
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DNA Polymerase I
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Figures

Image of Figure 1.
Figure 1.

MutSLH DNA repair in . One arm of a replication fork is shown at the top of the figure with methylated and unmethylated GATC () sequences and a replication mistake (M) generating a base-base or deletion/insertion mismatch. The mismatch is bound by MutS, and, in an ATP-dependent reaction, a ternary complex is formed with MutS, MutL, and MutH proteins. Incision by activated MutH occurs in the newly synthesized strand at an unmethylated GATC sequence. The nick is extended into a gap by excision in either the 3′ to 5′ or the 5′ to 3′ direction. Only the 5′ to 3′direction is depicted in the figure. The gap is formed by the action of exonucleases, including exonuclease I (ExoI), ExoVII, ExoX, and RecJ, and the direction of excision is determined by the UvrD helicase. Resynthesis is accomplished by DNA polymerase III holoenzyme, and the nick is sealed by DNA ligase. Subsequent methylation by Dam completes the process.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Image of Figure 2.
Figure 2.

Daughter-strand gap (DSG) and double-strand break (DSB) repair of platinated DNA. (A) DSG pathway. Step 1: persistent cisplatin DNA adducts are encountered by the replication complex. Stalled replication results in the formation of a DSG opposite the adduct. Step 2: interactions between the proteins of the RecFOR pathway and the replication fork initiate RecA nucleation and strand exchange. Step 3: the ensuing RecA-catalyzed strand exchange (with the aid of the RecFOR accessory proteins) results in the formation of a Holliday junction. Step 4: branch migration of the Holliday junction catalyzed by the RuvAB or RecG proteins results in the repair of the DSG and restoration of the replication fork. Step 5: resolution of the Holliday junction by RuvC restores two double-stranded DNA molecules. This could be a mechanism of damage tolerance, as the cisplatin adduct is bypassed by recombinational repair and persists in the DNA for subsequent removal by nucleotide excision repair. (B) DSB pathway. Step 6: the replication complex encounters an unrepaired DSG or a nick opposite the adduct. Collapse of the replication fork forms a DSB and a DSG; the DSG portion of the collapsed replication fork is processed by the DSG pathway using a complementary strand from a homologous chromosome. Step 7: the RecBCD complex (sectored circle) binds the free end of the DSB and generates single-stranded DNA that is a substrate for RecA nucleation. Step 8: RecA nucleoprotein filaments catalyze the invasion of the RecBCD-generated single-strand tail into the homologous duplex. Step 9: RecA-catalyzed strand exchange and branch migration result in the formation of a Holliday junction and restoration of the replication fork. Step 10: resolution of the Holliday junction by RuvC yields two intact duplexes (only one molecule is shown). Reprinted from ( ) with permission of the publisher.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Image of Figure 3.
Figure 3.

Generation of DSBs in a mutant. (A) DSBs produced by MutH nicking at the same GATC on complementary strands produces a substrate for DSB repair. (B) Replication through DNA with a nick or gap leads to replication fork collapse, effectively producing a DSB of one fork arm, which becomes a substrate for RecBCD action in DSB repair. Ligation of the nick by DNA ligase produces an intact duplex on the complementary strand.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Image of Figure 4.
Figure 4.

RuvC-induced replication fork DSB. (A) The pentagon represents a miscoding lesion subject to mismatch repair. After replication of this substrate, the fork stalls owing to the need for mismatch repair. The stalled fork isomerizes into a cruciform and becomes a substrate for RuvC cleavage. DSB repair is required to restore the fork, and MutSL is predicted to inhibit this repair. Reprinted from the (49) with permission of the publisher. (B) The pentagon represents a DNA polymerase-blocking lesion which, when encountered by a replication fork, leads to unequal replication of template strands. The fork isomerizes and DNA synthesis extends the 3′ end to produce a flush-ended molecule that can revert to its normal conformation, yielding a replication fork in which the lesion has been bypassed. Alternatively, the cruciform becomes a substrate for RuvC cleavage that requires DSB repair.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Image of Figure 5.
Figure 5.

Survival of strains exposed to cisplatin (Pt) and MNNG. bacteria in the exponential phase of growth were exposed to cisplatin (open squares) or MNNG (open circles), and survival was measured as a function of drug dose. The survival of cells exposed to cisplatin (closed squares) or MNNG (closed circles) was measured the same way. The wild-type strain gave the same results as the strain.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Image of Figure 6.
Figure 6.

Futile cycling at the replication fork. DNA polymerase III holoenzyme has placed a C opposite an O6-methylguanine (G-Me) template residue. This base pair is recognized and acted upon by the mismatch repair system. Replacement of the C with a T again results in a mismatched base pair subject to repair. Because DNA polymerase III holoenzyme is required for repair synthesis, the replication fork stalls at the mismatch. In the absence of mismatch repair, no stalling of the fork occurs.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Image of Figure 7.
Figure 7.

Survival of and strains exposed to cisplatin. Exponential-phase cells growing in broth were exposed to various doses of cisplatin and then plated to determine survival. Reprinted from ( ) with permission of the publisher. Figure 8. Survival of wild-type and cells exposed to MNNG. Exponential-phase cells growing in broth were exposed to various doses of MNNG for 15 min and then plated to determine survival.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Image of Figure 8.
Figure 8.

Survival of wild-type and ABC cells exposed to MNNG. Exponential-phase cells growing in broth were exposed to various doses of MNNG for 15 min and then plated to determine survival.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Image of Figure 9.
Figure 9.

Drug-induced recombination: (A) cisplatin, (B) - DDP, and (C) MNNG. Wild-type cells (GM7330) containing duplicate inactive operons were spread on MacConkey agar plates, and filter paper disks containing various amounts of drug were added. After incubation, the plates were placed on a scanner, and a digitized image was obtained. Recombination was measured by the formation of Lac colonies (which appear as dark dots on the plates) on a background of Lac bacteria. Drug concentration increases in a counterclockwise manner on each plate except for the disks without drug, which are at the top of each plate.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Image of Figure 10.
Figure 10.

Survival of strains exposed to nitric oxide (NO). Exponential-phase cells growing in broth were exposed to various doses of NO gas and then plated to determine survival. Reprinted from the ( ) with permission of the publisher.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Image of Figure 11.
Figure 11.

RecA-catalyzed strand-transfer reaction. (A) The RecA protein, in the presence of ATP, catalyzes the transfer of a strand from a linear duplex to the complementary single-stranded circular substrate to form a nicked circle. The asterisks indicate end labels. MutSL proteins have no effect on this reaction. (B) The same reaction is shown, except that the circular DNA substrate is either methylated or platinated. MutSL proteins are predicted to inhibit the strand-transfer reaction. (C) Proposed reversal of RecA action by MutS. A recombination intermediate is shown resulting from the action of RecA. It is postulated that MutS might reverse this reaction.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Image of Figure 12.
Figure 12.

Binding isotherm of MutS and cisplatin-modified DNA. (A) MutS protein was titrated into binding reactions with or without ADP or ATP containing radiolabeled 162-bp probes with various levels of cisplatin adducts. (B) The fraction of bound cisplatin-7 probe as a function of MutS concentration. Reprinted from the ( ) with permission of the publisher.

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Tables

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Table 1.

Altered physiological properties in a dam mutant

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
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Table 3.

Effect of ruvAB and recA plasmids on recombination frequency in Hfr dam16::Kan Str × F Str crosses

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23
Generic image for table
Table 2.

Proteins encoded by some E. coli DNA repair and recombination genes

Citation: Marinus M. 2005. Dr. Jekyll and Mr. Hyde: How the MutSLH Repair System Kills the Cell, p 413-430. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch23

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