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Prof. Allen Gathman has a great 10-minutes video on Youtube, explaining the reaction of adding nucleotide in the 5' to 3' direction, and why it doesn't work the other way. Briefly, the energy for the formation of the phosphodiester bond comes from the dNTP, which has to be added. dNTP is a nucleotide which has two additional phosphates attached to its 5' ...

Firstly, it's important to recognize that "plant viruses" do not exist. There are only "viruses that affect particular plant cells", or "viruses that affect a particular cell type". You'll see why in a moment. One of the structural components of many virus is its protein coat. Different types of biological molecules protrude from the surface of this ...

DNA replications needs a source of energy to proceed, this energy is gained by cleaving the 5'-triphosphate of the nucleotide that is added to the existing DNA chain. Any alternative polymerase mechanism needs to account for the source of the energy required for adding a nucleotide. The simplest way one can imagine to perform reverse 3'-5' polymerization ...

One case where human cells alter their DNA occurs in the immune system. In the early stages of the continuing production of B-cells and T-cells, the developing cell recombines (shuffles) genes in a particular DNA region which codes for what are called Variable, Diverse, and Joining gene segments. This shuffling is called somatic recombination or V(D)J ...

Further to LanceLafontaine's answer I'd just like to mention that, although as he mentioned viruses interact with DNA replication in different ways, DNA replication in itself is the same process in both plant and animal cells. For example, a human cheek cell and a potato root cell replicate their DNA in the same way (as both are eukaryotic cells - cells ...

I'm assuming you mean, physically changing the DNA polymer. The answer is yes. And how they do this depends upon which cells they are and what they are supposed to do. A partial list: In multicellular animals, cells DNA 'ages' where the telomeres, sequences at the ends of the chromosomes, will be degrade and shorten. This relates to how many times the ...

You seem to be assuming that mutation rates are somehow constant over evolutionary time. They are not. Mutation rates will change according to the stresses a species is subjected to. If you take a bacterial population and place it in a stressful environment (high/low temperatures, oxidative stress, lack of nourishment or whatever) you are likely to see an ...

From my reading on M. tuberculosis, I know that this organism has a pretty high mutation rate Huh, that's news to me. In fact, Mtb has a rather low mutation rate and rather low genetic variance. See the paper by Sherman & Gagneux in Nature genetics. The paper does state that mutation rate in latent infection is higher than expected or previously ...

Excess thymidine in a mitotic cell generates negative feedback on the production of deoxycytidine triphosphate from cytidine-5'-phosphate. Excess quantities of deoxyadenosine and deoxyguanosine also block progression through S-phase. However, as a reagent for the control of replication timing, thymidine has been found to work best as its blocking activity ...

During mitosis the genetic material in the cell is replicated to produce a copy of the genome for each resulting daughter cell. Due to the nature of the process, the ends of the chromosomes are not completely replicated, resulting in a slightly shorter copy of each chromosome after each round of replication. Telomeres are extensions to the end of ...