Recombinant Escherichia coli DNA polymerase IV (dinB)

1. In an SOS-constitutive mutant that expresses high levels of pol IV, few foci are observed in the absence of damage, indicating that within cells access of pol IV to DNA is dependent on the presence of damage, as opposed to concentration-driven competition for binding sites. PMID: 29351274
2. We hypothesize that damaged bases allow the switch to use of Pol IV during MBR by pausing the replicative polymerase to allow polymerase exchange in the replisome. The findings suggest that spontaneous mutation by MBR is regulated by regulation of the intracellular level of ROS PMID: 28727736
3. A mathematical model let us define the geometry (infer the structure) of the toxic intermediate as being formed when NER incises a lesion that resides in close proximity of another lesion in the complementary strand. This critical NER intermediate requires Pol IV / Pol II for repair, it is either lethal if left unrepaired or mutation-prone when repaired PMID: 28686598
4. although lagging-strand synthesis is still perturbed in holD trkA mutants, the trkA mutation allows HolD-less Pol III HE to resist increased levels of the SOS-induced bypass polymerase DinB PMID: 27280472
5. The steric gate is crucial for rNTP discrimination because of its role in specifically promoting a dNTP-induced conformational change and that rNTP discrimination occurs in a relatively closed state of the polymerases. PMID: 25684709
6. The structural dynamics of DinB changes upon substrate binding, noncognate DNA damage prevents the formation of the active conformation of DINB. PMID: 25899385
7. A DeltadinB mutation that sensitizes Escherichia coli to the lethal effects of UV- and X-radiation. PMID: 24657250
8. The study provides evidence that translesion DNA synthesis by DNA polymerase IV can directly restart replication fork stalled at a DNA lesion. PMID: 24957605
9. These findings indicate that preferential D-loop extension by Pol IV facilitates error-prone recombination and explain how Pol II reduces such errors in vivo. PMID: 23686288
10. The data shows that the Ser42 residue is present at a strategic location to stabilize mismatches in the PolIV active site, and thus facilitate the appearance of transition and transversion mutations. PMID: 23525461
11. DinB overexpression generates temporarily viable but non-reproductive cells possessing a fatally depleted chromosomal content. PMID: 23229309
12. study of this DinB derivative has revealed a key surface on DinB, which appears to modulate the strength of multiprotein complex binding, and has suggested a binding order of RecA and UmuD to DinB PMID: 23292773
13. DinB impedes replication fork progression in a way that does not activate RecA. PMID: 22820381
14. The results demonstrate that Pol IV requires the interaction with the C-terminal tail of single-stranded DNA-binding protein (SSB) to replicate DNA efficiently when the template ssDNA is covered with SSB. PMID: 22447448
15. Although it is not a source of enhanced mutagenesis in vivo, the translesion synthesis DNA polymerase IV was critical for the survival of uropathogenic Escherichia coli during urinary tract infection during an active inflammatory assault. PMID: 21597325
16. The authors demonstrate that Pol IV interacts in vitro with Rep DNA helicase and that this interaction enhances Rep's helicase activity. PMID: 21320186
17. Efficient extension of slipped DNA intermediates by DinB is required to escape primer template realignment by DnaQ. PMID: 21421753
18. By initiating or participating in double-strand break repair, SbcCD may provide DNA substrates for Pol IV polymerase activity. PMID: 21131491
19. Separate DNA Pol II- and Pol IV-dependent pathways of stress-induced mutation during double-strand-break repair in Escherichia coli are controlled by RpoS. PMID: 20639336
20. Study shows that the little finger domain of PolIV-beta interaction stabilizes the clamp-polymerase complex in vitro and is necessary for the access of PolIV to ongoing replication forks in vivo. PMID: 19843218
21. expression of a variant generated by mutation of an evolutionarily conserved tyrosine (Y79) transforms dinB into a bactericidal drug, resulting in profound toxicity even in a dinB(+) background PMID: 19948952
22. REVIEW: properties and functions of Pol IV PMID: 15588845
23. levels of Pol IV are positively affected by the heat shock-induced molecular chaperone GroE PMID: 15629916
24. Induction of dinB transcription mediated by ceftazidime produces an increase in the reversion of a +1 Lac frameshift mutation. PMID: 15687217
25. Ppk is required for the increased rate of growth-dependent mutations produced by Pol IV overexpression; results suggest Ppk is affecting the activity of Pol IV in a manner that is independent of any previously known factors that regulate this polymerase PMID: 16045619
26. preferential mutagenesis during lagging strand synthesis from overproduction of DNA polymerase IV PMID: 16166552
27. DinB and its orthologues are specialized to catalyse relatively accurate translesion synthesis over some N2-dG adducts that are ubiquitous in nature, and that lesion bypass occurs more efficiently than synthesis on undamaged DNA PMID: 16407906
28. data imply that PolIV can also promote mutation in growing cells under genome stress due to excess single-stranded DNA PMID: 16547019
29. Study shows that enhanced recombination is dependent on the factors: the RuvA Holliday junction helicase, the RecJ single-strand DNA exonuclease, the RadA/Sms RecA-paralog protein of unknown function and, surprisingly, the DinB translesion polymerase. PMID: 16904387
30. while Pol IV contributes to spontaneous mutations within the HSV-tk coding sequence, Pol IV does not play a significant role in spontaneous mutagenesis at [G/C](10), [GT/CA](10), or [TC/AG](11) microsatellite alleles PMID: 17397877
31. PolIV performs an error-free bypass of DNA damage that accumulates in the alkA tag genetic background. This result indicates that PolIV is involved in the error-free bypass of cytotoxic alkylating DNA lesions PMID: 17483416
32. Data show that an important role is described for Pol IV in producing the mutations and a high fraction of the mutations is dependent on the action of Pol IV in a (dinB) gene dosage-dependent manner. PMID: 18156258
33. Observations indicate that proteins like RecA and UmuD(2) may be responsible for managing the mutagenic potential of DinB orthologs throughout evolution. PMID: 18158902
34. Overexpression of DinB inhibits DNA replication by targeting DNA polymerase beta, and cell proliferation is also inhibited. PMID: 18761688
35. NusA, a modulator of RNA polymerase, interacts with the DNA polymerase DinB. PMID: 18996995
36. Elevated DinB expression in Delta(clpP-clpX) cells contributes to elevated mutagenesis. PMID: 19040636

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KEGG: ecj:JW0221

STRING: 316385.ECDH10B_0213