You are scientist working for the USDA(United States Department of Agriculture)

Question

You are scientist working for the USDA(United States Department of Agriculture) and are studying Aflatoxin B_1, a potent substance produced by Aspergillus on stored grain products. You hypothesize that the toxin damages DNA, so you incubate a sample of DNA with Aflatoxin B_1. What do you expect to be the result of this experiment? The genetic code links nucleic acid and protein information in living organisms. Three nucleotides encode an amino acid, and it is now known that the nucleotide code is read in sequence and is nonoverlapping It is also known that there are 64 different possible nucleotide sequences, but only 20 common amino acids, allowing for redundancy in the genetic code What evolutionary advantage is there in such redundancy?

Explanation / Answer

Aflatoxin and DNA damage

Aflatoxin B(1) (AFB(1))- N(7)- guanine is the overwhelming adduct framed upon the response of AFB(1)- 8,9-exo-epoxide with guanine buildups in DNA. AFB(1)- N(7)- guanine can change over to the ring-opened formamidopyrimidine, or the adducted strand can experience depurination. Aflaxton B1 quickly represses RNA combination

Aflatoxins are sustenance borne optional dangerous parasitic metabolites delivered amid the development of Aspergillus flavus and A. parasiticus. Aflatoxins are outstanding hepatotoxic, hepatocarcinogenic and mutagenic specialists. These impacts are for the most part because of adduct development with DNA, RNA and protein. What's more, it likewise causes lipid peroxidation and additionally oxidative harm to DNA. AFB1 have genotoxic potential in an assortment of test frameworks. Other aflatoxin has not been so widely examined, but rather in an assortment of studies B2, G1, G2 and M1 have all demonstrated proof of genotoxicity..

Hence , cell will not grow on incubation with Aflatoxin B(1).

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WHAT EVOLUTIONARY ADVANTAGE IS THER EIN SUCH REDUENCY

Genetic redundancy:

It alludes to the basic marvel that erasing or changing a gene from a genome has negligible or no effect on the phenotype or wellness of the life form as a result of utilitarian pay presented by at least one different genes. Here I compress investigations of practical redundancies between copy genes and those among metabolic responses that separately speak to hereditary redundancies at the individual gene level and at the frameworks level. examine the predominance of hereditary redundancies in a genome, transformative starting points of these redundancies, and instruments in charge of their steady upkeep. I demonstrate that hereditary redundancies are exceedingly inexhaustible. While some of them might be developmentally transient, many are steady. Most of the steady redundancies are probably going to have been specifically kept, not as a result of their potential advantages concerning future pernicious changes, but since of their real advantages at present or in the later past. The rest are most likely protected by choice on nonredundant pleiotropic capacities. The studies condensed here show the utility of frameworks investigation for comprehension developmental wonders and the significance of transformative thinking in revealing the capacities and roots of systemic properties.

It is a term regularly used to depict circumstances where a given biochemical capacity is repetitively encoded by at least two genes. From a developmental angle, genes with covering capacities suggests insignificant, assuming any, particular weights following up on these genes. One along these lines expects that the genes taking an interest in such buffering of transformations will be liable to serious mutational float veering their capacities or potentially expression designs with significantly high rates. To be sure it has been demonstrated that the practical uniqueness of paralogous matches in both yeast and human is an amazingly quick process. Considering these thoughts, the very presence of hereditary buffering, and the useful redundancies required for it, shows a Catch 22 in light of the developmental ideas. On one hand, for hereditary buffering to occur there is a need for redundancies of gene capacity, then again such redundancies are unmistakably flimsy in face of characteristic choice and are accordingly probably not going to be found in advanced genomes.

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