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Mutagenic Consequences Of Chemical Reaction with DNA
Published in Philip L. Grover, Chemical Carcinogens and DNA, 2019
It now appears that in a normal repair proficient strain of E. coli, there is a most elegant coordination of repair processes which minimizes the chance of a dimer giving rise to a mutation. In the first instance, the dimer may be photoreactivated or excised, both efficient, accurate processes. If the dose of UV is high, DNA replication becomes stalled temporarily and restarts at the origin of replication.80,81 This allows additional excision repair to occur. If a dimer is replicated, a gap is formed in the newly synthesized DNA that can be filled accurately by recombination repair. If gaps in daughter strands overlap, thus preventing recombination repair, Reannealing And Post-replication Excision occurs. It is only when all these processes fail that error-prone repair will be called into operation. In a repair proficient strain, this may well not be for a residuum of repair resistant damage, but for rare cases where conventional repair goes wrong.
Introduction to Molecular Biology
Published in Martin G. Pomper, Juri G. Gelovani, Benjamin Tsui, Kathleen Gabrielson, Richard Wahl, S. Sam Gambhir, Jeff Bulte, Raymond Gibson, William C. Eckelman, Molecular Imaging in Oncology, 2008
Although knowledge of the structure of the replication machinery in eukaryotes is still limited due to its complexity, there are many similarities with the simpler prokaryotes DNA replication process. In eukaryotic cells, DNA exists in the nucleus as a very compact and condensed structure. In order to begin the replication process, this structure must be opened up, so the DNA polymerase enzyme can copy the DNA template. The replication process takes place at a specific site called origin of replication, which is rich in AT content. The first step in DNA replication begins with the binding of the origin recognition complex (ORC) to the origin of replication. ORC complex is a hexamer of related proteins that function as a replication initiation factor that promotes the unwinding or denaturation of DNA. Following the binding of the ORC complex, other proteins (Cdc6/Cdc18 and Cdt1) will bind and coordinate the recruitment of the minichromosome maintenance function (MCM) complex to the origin of replication. The MCM complex is a hexamer and is thought to be the major DNA helicase in eukaryotic organisms. Once the binding of MCM occurs, a fully licensed pre-initiation replication complex (pre-RC) now exists. This process occurs during the G1 phase of the cell cycle and therefore, cannot initiate the replication. Replication only occurs during the S phase. Thus, separating the licensing and activation is a mechanism that ensures only one replication per origin in a cell cycle.
Biology of microbes
Published in Philip A. Geis, Cosmetic Microbiology, 2006
To understand the process in detail requires far more effort. In reality, at least seven enzymes are involved in the process described in the paragraph above: initiator protein, helicase, polymerases, repair nucleases, topoisomerase, single-strand DNA-binding proteins, and DNA ligase. The initiator protein first finds the right place to begin copying and guides the helicase to the correct position (an origin of replication site) on the nucleic acid. The helicase separates the DNA by breaking the weak bonds between the nucleotides to unwind the two strands of DNA. Then the polymerases arrive to join the free nucleotides to their matching complements on the old strands using the phosphate bond energy from the nucleotide to help form the new bond to the other nucleotides as they are added to the existing chain. These polymerases work along with primases that first synthesize a short (one to five nucleotides long) RNA primer. This primer allows DNA polymerase to begin catalyzing the addition of nucleotides to a new strand complementary to the existing template upon which the new DNA synthesis is based.
When to suspect contamination rather than colonization – lessons from a putative fetal sheep microbiome
Published in Gut Microbes, 2022
Simone Bihl, Marcus de Goffau, Daniel Podlesny, Nicola Segata, Fergus Shanahan, Jens Walter, W. Florian Fricke
The isolation of RNA from microbiome samples is prone to contamination with traces of metagenomic DNA and requires extensive DNase treatment,23 Our reanalysis shows that mapped metatranscriptome reads from all fetal lamb samples, including positive and negative controls, span the entire phiX174 genome (Figure 3). This includes genome regions that have been shown to be non-transcribed, such as around the origin of replication.24 Our findings therefore indicate that at least a fraction of the metagenomic sequence data must have been derived from DNA templates, providing strong evidence for an additional source of contamination in the fetal lamb metatranscriptomes, which refutes Bi et al.’s claim of “support that the microbiome(s) present in the prenatal fetal gut are active”.
Liver-directed gene-based therapies for inborn errors of metabolism
Published in Expert Opinion on Biological Therapy, 2021
Pasquale Piccolo, Alessandro Rossi, Nicola Brunetti-Pierri
AAV is a small non-enveloped, nonpathogenic virus of the Parvoviridae family. Its single stranded DNA genome contains sequences encoding for viral replication machinery (rep) and capsid (cap) proteins flanked by palindromic inverted terminal repeats (ITR) containing the origin of replication and packaging signals. Naturally occurring AAV are replication defective and they establish latent asymptomatic infections when co-infection with a helper virus (typically adenovirus or herpes simplex virus) occurs. As a result of the infection, anti-AAV antibodies can be found in most subjects, with AAV2 showing the highest prevalence [12]. The complete lack of pathogenicity of AAV has been recently challenged by the finding of clonal integration of AAV genomes into human HCC tissues [13,14].
Determination of copy number and circularization ratio of Tn916-Tn1545 family of conjugative transposons in oral streptococci by droplet digital PCR
Published in Journal of Oral Microbiology, 2019
Tracy Munthali Lunde, Adam P. Roberts, Mohammed Al-Haroni
Four sequenced bacterial strains; B. subtilis BS34A (NZ_LN680001.1), B. subtilis BS49 (NZ_LN649259.1) E. faecium OrEc1, and E. faecium OrEc2 (unpublished data) were used to determine the accuracy of ddPCR in detecting multiple copies of Tn916-Tn1545-like elements. In B. subtilis BS49, E. faecium OrEc1, and E. faecium OrEc2, we were able to accurately detect the expected number of elements using amyE as a chromosomally located, single copy, reference gene. In B. subtilis BS34A however, the ratio between Tn916-Tn1545-like elements (represented by the intTn/xisTn genes) and the reference gene amyE was below one copy (approximately 0.75). The lower ratio may be explained by the chromosomal positioning of the two targets in relation to the origin of replication. In B. subtilis BS34A, the amyE gene (327,604–329,583 bp) is situated closer to the origin of replication in comparison to Tn916 which is in position 1,886,552–1,904,583 bp. The closer proximity of amyE to the origin of replication may result in more targets of the reference gene due to the occurrence of multiple replication forks within a cell prior to cell division, as has been previously reported in B. subtilis [34].