Anomeric 2′-Deoxycytidines and Silver Ions: Hybrid Base Pairs with Greatly Enhanced Stability and Efficient DNA Mismatch Detection with α-dC

2017 ◽  
Vol 23 (49) ◽  
pp. 11776-11779 ◽  
Author(s):  
Xiurong Guo ◽  
Frank Seela
2005 ◽  
pp. 2509 ◽  
Author(s):  
Kazushige Yamana ◽  
Yudai Fukunaga ◽  
Yusuke Ohtani ◽  
Sayaka Sato ◽  
Mitsunobu Nakamura ◽  
...  

ChemPhysChem ◽  
2017 ◽  
Vol 18 (21) ◽  
pp. 2977-2980 ◽  
Author(s):  
Qing Liu ◽  
Guocheng Liu ◽  
Ting Wang ◽  
Jing Fu ◽  
Rujiao Li ◽  
...  

Genetics ◽  
1992 ◽  
Vol 132 (2) ◽  
pp. 567-574
Author(s):  
W Stephan ◽  
C H Langley

Abstract Double strand breaks (DSBs) are often repaired via homologous recombination. Recombinational repair processes are expected to be influenced by nucleotide heterozygosity through mismatch detection systems. Unrepaired DSBs have severe biological consequences and are often lethal. We show that natural selection due to inhibition of recombinational repair associated with polymorphisms could influence their molecular evolution. The main conclusions from this analysis are that, for increasing population size, mismatch detection leads to a limit on average heterozygosity of otherwise selectively neutral polymorphism, an excess of rare variants, and a slowing down of the rate of neutral molecular evolution. The first two results suggest that mismatch detection may account for the surprisingly narrow range of observed average heterozygosities, given the great variation in population size between species.


Genetics ◽  
1987 ◽  
Vol 116 (3) ◽  
pp. 343-347
Author(s):  
Margaretha Carraway ◽  
Philip Youderian ◽  
M G Marinus

ABSTRACT The mismatch repair system of Escherichia coli K12 removes mispaired bases from DNA. Mismatch repair can occur on either strand of DNA if it lacks N6-methyladenines within 5′-GATC-3′ sequences. In hemimethylated heteroduplexes, repair occurs preferentially on the unmethylated strand. If both strands are fully methylated, repair is inhibited. Mutant (dam  -) strains of E. coli defective in the adenine methylase that recognizes 5′-GATC-3′ sequences (Dam), and therefore defective in mismatch repair, show increased spontaneous mutation rates compared to otherwise isogenic dam  + hosts. We have isolated and characterized 91 independent mutations that arise as a consequence of the Dam- defect in a plasmid-borne phage P22 repressor gene, mnt. The majority of these mutations are A:T→G:C transitions that occur within six base pairs of the two 5′-GATC-3′ sequences in the mnt gene. In contrast, the spectrum of mnt  - mutations in a dam  + host is comprised of a majority of insertions of IS elements and deletions that do not cluster near Dam recognition sites. These results show that Dam-directed post-replicative mismatch repair plays a significant role in the rectification of potential transition mutations in vivo, and suggest that sequences associated with Dam recognition sites are particularly prone to replication or repair errors.


2019 ◽  
Vol 31 (11) ◽  
pp. 2232-2237
Author(s):  
Nivedita Basu ◽  
Thu Huong Ho ◽  
François‐Xavier Guillon ◽  
Yuanyuan Zhang ◽  
Pascal Bigey ◽  
...  

2015 ◽  
Vol 112 (35) ◽  
pp. 10914-10919 ◽  
Author(s):  
Ruoyi Qiu ◽  
Miho Sakato ◽  
Elizabeth J. Sacho ◽  
Hunter Wilkins ◽  
Xingdong Zhang ◽  
...  

DNA mismatch repair (MMR) identifies and corrects errors made during replication. In all organisms except those expressing MutH, interactions between a DNA mismatch, MutS, MutL, and the replication processivity factor (β-clamp or PCNA) activate the latent MutL endonuclease to nick the error-containing daughter strand. This nick provides an entry point for downstream repair proteins. Despite the well-established significance of strand-specific nicking in MMR, the mechanism(s) by which MutS and MutL assemble on mismatch DNA to allow the subsequent activation of MutL’s endonuclease activity by β-clamp/PCNA remains elusive. In both prokaryotes and eukaryotes, MutS homologs undergo conformational changes to a mobile clamp state that can move away from the mismatch. However, the function of this MutS mobile clamp is unknown. Furthermore, whether the interaction with MutL leads to a mobile MutS–MutL complex or a mismatch-localized complex is hotly debated. We used single molecule FRET to determine that Thermus aquaticus MutL traps MutS at a DNA mismatch after recognition but before its conversion to a sliding clamp. Rather than a clamp, a conformationally dynamic protein assembly typically containing more MutL than MutS is formed at the mismatch. This complex provides a local marker where interaction with β-clamp/PCNA could distinguish parent/daughter strand identity. Our finding that MutL fundamentally changes MutS actions following mismatch detection reframes current thinking on MMR signaling processes critical for genomic stability.


2005 ◽  
Vol 44 (12) ◽  
pp. 4112-4114 ◽  
Author(s):  
Elena V. Bichenkova ◽  
Xuan Yu ◽  
Pranab Bhadra ◽  
Helena Heissigerova ◽  
Simon J. A. Pope ◽  
...  

10.1038/80186 ◽  
2000 ◽  
Vol 18 (10) ◽  
pp. 1027-1027 ◽  
Author(s):  
Natalie DeWitt

Sign in / Sign up

Export Citation Format

Share Document