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Interconnection between PHA and Stress Robustness of Bacteria
Published in Martin Koller, The Handbook of Polyhydroxyalkanoates, 2020
Stanislav Obruca, Petr Sedlacek, Iva Pernicova, Adriana Kovalcik, Ivana Novackova, Eva Slaninova, Ivana Marova
Generally, microorganisms surviving in extreme conditions are called extremophiles. In the literature, the term for ultraviolet radiation-resistant (UVR) microorganisms which are known for the production of various metabolites such as pigments, mycosporine-like amino acids, melanin, pannarin and sphaerophorin, can be found [75,76]. Another group of UVR microorganisms possesses the capability to repair already-changed DNA due to their specific enzymes, e.g. photolyases, which directly break covalent bonding between pyrimidine dimers to form original pyrimidine monomers. This process is known as photoreactivation and it requires light in the near U/blue light (300–500 nm) region as an energy source [72,77]. Another enzymatic DNA repair pathway includes the DNA glycosylase base excision repair (BER) where the glycosyl bond between damaged base and deoxyribose is hydrolyzed. Next, DNA repair mode is based on the repair enzyme called UV-damage endonuclease (UVDE) which can recognize the photoproducts and cut them out immediately. The last of the most frequently used DNA repair pathways which was identified is the nucleotide excision repair (NER) which belongs to the main defensive strategies against UV radiation. This strategy consists of the removal of a damaged oligonucleotide [72,77,78].
Spectral Self-Interference Fluorescence Microscopy to Study Conformation of Biomolecules with Nanometer Accuracy
Published in Sarhan M. Musa, Nanoscale Spectroscopy with Applications, 2018
Xirui Zhang, Philipp S. Spuhler, David S. Freedman, M. Selim Ünlü
The versatility of the presented platform makes the system an advanced tool to study more complex DNA–protein interactions. For example, in DNA base excision repair (BER) [164–167], a damaged base is specifically recognized and removed by DNA glycosylate to generate an abasic site. Depending on the initial events, the repair patches may be single nucleotide (short patch) or 2–10 nucleotides (long patch). For the short patch repair, the phosphodi-ester bond at 3’ of the abasic site is cleaved by glycosylate, and the 5’ bond is incised by APE1 endonuclease, which then recruits DNA polymerase to fill the gap that is ligated by a DNA–ligase complex. During the process of BER, the conformation and flexibility of DNA changes with the binding of different enzymes, which kinks the DNA to different angles [168–175]. Through careful design of experiments, the SSFM platform can potentially detect DNA BER through direct detection of DNA conformational changes and protein-binding events. Monitoring DNA repair is an example of applying the SSFM platform to study more challenging DNA–protein interaction processes. The application of polymer-functionalized surfaces and micro-array sensor formats adds the capacity of parallel detection of thousands of sequences. SSFM provides critical information required to move DNA interfacial applications forward. What’s more, the quantification of DNA conformations and conformational changes, through integration with new surface functionalization techniques and label-free detection, provides critical information to understand DNA–protein interactions in their native environment, allowing the SSFM platform to play a unique and productive role in emerging biotechnological fields.
DNA damage in mononuclear cells following maximal exercise in sedentary and physically active lean and obese men
Published in European Journal of Sport Science, 2021
Alessandra Peres, Igor M. Da Silva, Maeli Santos, Ângela Beretta, Vanessa Moraes Andrade, Pedro R. T. RomãO, Gilson P. Dorneles
In the case of over-accumulation of such DNA damage and insufficient DNA repair mechanisms, it is suggested that dividing cells may promote a mutational profile leading to disease (Sancar, Lindsey-Boltz, Ünsal-Kaçmaz, & Linn, 2004). DNA damage can be subdivided into two main types: (a) endogenous damage such as attack by ROS produced from metabolic products or due to replication errors, including processes such as oxidation of bases and generation of DNA strand interruptions, alkylation or hydrolysis of bases, and mismatch of bases; (b) exogenous damage caused by external agents, such as ultraviolet radiation, hydrolysis or thermal disruption, plant toxins, mutagenic chemicals, and viruses (Chatterjee & Walker, 2017; Friedberg, 2003). Once DNA is damaged, it is usually repaired by mechanisms such as base excision repair (BER), nucleotide excision repair (NER), or other homologous and nonhomologous mechanisms (Chatterjee & Walker, 2017).