p53 transcription has been previously associated with oxidative stress-induced genotoxicity, and mediates several cellular stress responses including arrest in the cell cycle, preventing mutation propagation, initiation of DNA repair mechanisms and initiation of apoptosis when DNA damage is extensive [ 47, 50, 51].
All vectors containing the ccdB gene were propagated in the E. coli strain DB3.1, which contains the gyrA462 mutation that enables propagation of Gateway vectors encoding the ccdB gene [35].
E. coli DB3.1 contains the gyrA462 mutation that enables propagation of Gateway vectors encoding the ccdB gene [ 21]. A. tumefaciens GV3101 pMP900 [ 43] was used to assess the functionality of plant transformation vectors.
To shed light on the experimental conversion of a rigidly invariant code to a mutating code, the present study examined code mutations determining the propagation of Bacillus subtilis on Trp and 4-, 5- and 6-fluoro-tryptophans.
A proper modeling of the SOS response is an essential component of developing a quantitative theory of mutation-propagation in cellular organisms, which is important for understanding phenomena such as the emergence of antibiotic drug resistance in bacteria, and cancer in multicellular organisms [2] [4].
Because the SOS response is a genetic repair pathway that works in conjuction with other cellular repair pathways, a proper understanding of the SOS response is important for developing a coherent theory of mutation-propagation that will be useful for understanding the emergence of antibiotic drug resistance in bacteria, and cancer in multicellular organisms [2] [4].
We may also imagine that the correlations can be caused by the "contagious" propagation of mutations across the genes in the biological pathways responsible for the function.
Mitotic catastrophe, also known as reproductive death, occurs because cells enter mitosis in the presence of residual or misrepaired DNA DSBs, leading to the propagation of mutations and chromosomal aberrations which ultimately results in cell death [54].
The successful propagation of mutations from small founder populations implies that cells have mechanisms to buffer the impact of single gene mutations on their interaction partners.
Genotoxic insults that induce DNA breaks must be repaired in order to prevent the propagation of mutations that can contribute to malignant transformation.
