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Mutagenic Consequences Of Chemical Reaction with DNA
Published in Philip L. Grover, Chemical Carcinogens and DNA, 2019
Green et al.77 in turn have extended the Sedgwick hypothesis to argue that in excision-proficient bacteria overlapping daughter strand gaps will not be a substrate for error-prone repair, since where gaps overlap, the parental strands will reanneal and allow further excision repair to occur (Figure 3). This hypothetical Reannealing And Post-replicative Excision (RAPE) conveniently explains a number of discrepancies between mutagenesis in excision-proficient and excision-deficient strains. As evidence, Green et al.77 showed that, at a given dose of UV, the chance of daughter strand gaps (or overlapping gaps) giving rise to a mutation is very much lower in an excision-proficient than an excision-deficient strain. From this they concluded that an excision-dependent postreplication repair process must operate. On quite independent grounds (the properties of recA tsl double mutants (tsl is an allele of lexA (Table 1)), Mount et al. have reached a similar conclusion.78 Green et al. went on to suggest that RAPE can be used to explain an obscure phenomenon in E. coli and 5. typhimurium called Mutation Frequency Decline (MFD), which concerns mutation at certain tRNA suppressor loci.79
Photoexacerbated Dermatoses
Published in Henry W. Lim, Nicholas A. Soter, Clinical Photomedicine, 2018
Xeroderma pigmentosum (XP) is a genetically heterogeneous group of autosomal recessive disorders characterized by defective excision repair of DNA damaged by UVC radiation in fibroblasts in vitro (52) and by sunlight in epidermal cells in vivo (53). Cell fusion studies have been used to demonstrate the genetic heterogeneity of the defect in XP. When a fibroblast from one patient with XP is fused with the fibroblast from another patient, the defects of both cells are corrected (complemented), and the cells are said to be in different complementation groups (54). Nine complementation groups have been described, labeled A–I, although recent evidence suggests that the single members of groups H and I belong in group D and C, respectively (51). In addition, an XP variant is characterized by a defect in postreplication repair or in a later stage of excision repair. The clinical onset of the cutaneous manifestations is delayed in the XP variant.
DNA Repair During Aging
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
Surely we must discriminate between different repair processes. Thus, excision repair seems to have a good age dependency, SSB repair is probably maintained at a high level over a long period of the lifetime and reduced only in very old animals, whereas DSB repair is maintained during all of life; if one DSB is not repaired in a cell within 2 hours this cell would die.57 Those cells would not contribute to the measured repair anymore — therefore the repair capacity related to the amount of DNA would always be the same. Postreplication repair has not yet been proved in mammalian DNA, but was suggested by Park and Cleaver.241 Surely this repair has no significance in postmitotic cells or cells with a long G1-phase (most of the cells in mammals).241
Continuous tracking of startled Drosophila as an alternative to the negative geotaxis climbing assay
Published in Journal of Neurogenetics, 2019
Matthew J. Taylor, Richard I. Tuxworth
Bre1 is involved in the recruitment of Rad6 (Wood et al., 2003, p. 1), which is required for post-replication repair through ubiquitination of PCNA (Hoege, Pfander, Moldovan, Pyrowolakis, & Jentsch, 2002). Knockdown of Bre1 had no effect on the motor performance decline of our tAβ1–42 model but expression of UAS-Bre1 RNAi alone was sufficient to produce a decline in motor performance comparable to tAβ1–42-expression alone (Figure 3(b)).