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In RNA, uracil base-pairs with adenine and replaces thymine during DNA transcription. Methylation of uracil produces thymine. [11] In DNA, the evolutionary substitution of thymine for uracil may have increased DNA stability and improved the efficiency of DNA replication (discussed below).
After a mutation occurs, the mutagenic threat of uracil propagates through any subsequent DNA replication steps. [6] Once unzipped, mismatched guanine and uracil pairs are separated, and DNA polymerase inserts complementary bases to form a guanine-cytosine (GC) pair in one daughter strand and an adenine-uracil (AU) pair in the other. [7]
Uracil DNA glycosylase flips a uracil residue out of the duplex, shown in yellow. DNA glycosylases are responsible for initial recognition of the lesion. They flip the damaged base out of the double helix, as pictured, and cleave the N-glycosidic bond of the damaged base, leaving an AP site. There are two categories of glycosylases ...
Uracil DNA glycosylases remove uracil from DNA, which can arise either by spontaneous deamination of cytosine or by the misincorporation of dU opposite dA during DNA replication. The prototypical member of this family is E. coli UDG, which was among the first glycosylases discovered.
This also removes the need for an RNA primer to initiate RNA synthesis, as is the case in DNA replication. The non-template (sense) strand of DNA is called the coding strand, because its sequence is the same as the newly created RNA transcript (except for the substitution of uracil for thymine). This is the strand that is used by convention ...
Right: two complementary strands of DNA. Complementarity is achieved by distinct interactions between nucleobases: adenine, thymine (uracil in RNA), guanine and cytosine. Adenine and guanine are purines, while thymine, cytosine and uracil are pyrimidines. Purines are larger than pyrimidines.
5-Fluorouracil (5-FU) is a widely used in the treatment of a range of common cancers that causes DNA damage via two mechanisms. FU is thought to kill cells via the inhibition of thymidylate synthase and also deprive cells of TTP during DNA replication, which leads to the introduction of uracil in DNA causing the fragmentation of newly synthesized DNA.
5-Bromouracil (5-BrU, 5BrUra, or br5Ura [1]) is a brominated derivative of uracil that acts as an antimetabolite or base analog, substituting for thymine in DNA, and can induce DNA mutation in the same way as 2-aminopurine. [2]