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Genome Stability - Science topic
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Questions related to Genome Stability
Guanine-rich DNA sequences can fold into four-stranded, noncanonical secondary structures called G-quadruplexes (G4s). G4s were initially considered a structural curiosity, but recent evidence suggests their involvement in key genome functions such as transcription, replication, genome stability, and epigenetic regulation, together with numerous connections to cancer biology.
The capacity for guanylic acid derivatives to self-aggregate was noted over a century ago. Some 50 years later, fibre diffraction revealed that guanylic acids form four-stranded, righthanded helices leading to a proposed model in which the strands are stabilised via Hoogsteen hydrogen-bonded guanines to form co-planar G-quartets.
However, why guanine specifically? Why not adenine, thymine, or cytosine quadruplex?
Different individuals possess different genetic and epigenetic information, so precise treatment is very difficult to realize.
Much of in silico pathogen studies involve culture of the clinical isolates, NGS sequencing followed by SNP calling . The novel polymorphisms are associated with drug resistance.
But, the genomic impact of the shift from host milieu to culture medium hardly gets attention. Would not the the change in growth conditions be causing acquisition of SNPs, indels and the chromosomal aberrations in the pathogen?
If drug stressor causes resistance development in the pathogens, the host immune pressure determines adaptation of pathogens too. In culture medium, the immune pressure and other competing microbes are lacking. Also the nutrient composition is much much different than host bio-fluid.
I will be surprised if not, for most of us are aware how mere optimization of growth medium substantially improves industrially-important microbial metabolite production.
Discussions and expert opinions are appreciated.
I want to check the clonal fidelity of a medicinal orchid propagated from the mother plant using axillary branching.Now cross verify the robustness of the protocol I want to use molecular markers to verify its stability. Our lab dont have any MASAP/SSAP or SNP infrastructure. I came through this paper which has applied the identical approach http://www.sciencedirect.com/science/article/pii/S0378111914000493
Can anybody suggest me a technique to measure genomic stability as histone modification read out. I am trying to measure the stability of cancer genome, what techniques can I use to measure the genomic instability in live cells, FFPE samples. Trying to establish an epigenetic signature for stability, what techniques could be of use here?
Since cells can capture visible light for photosynthesis, the ability to capture and store high energy fast events seems feasible in principle. One can imagine ways to capture atomic energy for biology. Obviously there may be issues with genome stability, but there are very radiation resistance cells and others that thrive in high temperatures that would seem to challenge DNA and RNA as well as protein and membrane stability. How might be develop atomic powered cells?
For repair of DNA double strand breaks (DSBs) by homologous recombination, ATP dependent DNA strand exchange takes place whereby a template strand invades base-paired strands of homologous DNA molecules. RAD51 aids the search for homology and strand pairing in this process. RAD51 paralogues are thought to act in homologous recombination for repair of DNA double strand breaks (DSBs) by stabilizing or destabilizing the RAD51 filament for recombination. Is there strong evidence for any other roles?
There is clear and compelling evidence that whole genome duplication events have occurred in animals, particularly the R1/R2 events in the history of modern vertebrates and R3 in teleosts, but I'm struggling to find a published rational for how these duplications are propagated to offspring. In plants it seems relatively straight forward: Hybridization between related species; somatic allotetraploidy creates chimera; chimeric tissue grows into germ tissue; self fertilization; voila, polyploid F2. It's gotta be way harder for an animal though, since they can't just grow sex organs willy nilly from somatic allotetraploid tissue... My expectation is that hermaphroditic animals would have an 'advantage' here, but my pubmed/google prowess is coming up short. Anyone out there have some insight on this mechanism?
