Answer:
Explanation:
Opium, mepedrone, cannabis, or weeds, I've heard these only
Stop being addict or your life's purpose is wasted, if not you, at least think of your family
Griffith's experiment worked with two types of pneumococcal bacteria (a rough type and a smooth type) and identified that a "transforming principle" could transform them from one type to another.
At first, bacteriologists suspected the transforming factor was a protein. The "transforming principle" could be precipitated with alcohol, which showed that it was not a carbohydrate. But Avery and McCarty observed that proteases (enzymes that degrade proteins) did not destroy the transforming principle. Neither did lipases (enzymes that digest lipids). Later they found that the transforming substance was made of nucleic acids but ribonuclease (which digests RNA) did not inactivate the substance. By this method, they were able to obtain small amounts of highly purified transforming principle, which they could then analyze through other tests to determine its identity, which corresponded to DNA.
Answer:
most forms of cancer are caused by somatic mutations
Explanation:
I think its acid fermentation, but I could be wrong. My class studied this a while ago.
Ti plasmid encoded octopine and nopaline catabolism in Agrobac terium Ti plasmid-encoded genes required by the micro organism for opine catabolism.
The occ and noc areas in octopine and nopaline Ti plasmids, respectively, are accountable for the catabolism of octopine and nopaline in Agrobacterium. The functions are activated within the presence of the opines with the aid of OccR and NocR, related regulatory proteins, and the promoters incorporate commonplace collection motifs.
we have investigated Ti plasmid in heterologous interactions among the regulators and the promoters. previous experiments the usage of all possible heterologous combos of opines, regulators, and promoters in vivo had demonstrated that handiest the aggregate of nopalme, NocR, and the occ promoter led to restricted promoter activation. We now display that OccR and NocR bind to the heterologous promoters in vitro and in vivo.
The weak or non-existent promoter activation truly located can be explained by the idea that OccR and NocR use distinct activation mechanisms; we investigated protein-brought about DNA bending due to reports that the two regulators vary in this respect.
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