Rate this:. Like this: Like Loading September 30, at am. Piter Keo. You may reblog it, of course. And thank you very much for commenting and sharing! August 19, at pm. Atta Ullah. November 19, at am. December 4, at pm. December 6, at pm. January 26, at pm. January 27, at pm. AJAY Kumar. January 3, at am. January 3, at pm. The enzyme that converts ribose in deoxyribose is called ribonucleotide reductase. Thank you for your comment! Bengyella Peace.
February 3, at pm. July 12, at am. Ankita galgale. September 16, at pm. September 20, at am. Joseph Caponi. November 5, at pm. Naveeda Zaigham. November 9, at am. December 13, at am. Oscar Sapkota. Why is uracil not used as a nucleotide in DNA? Mar 23, See answer below:. Explanation: DNA uses thymine instead of uracil because thymine has greater resistance to photochemical mutation, making the genetic message more stable. Related questions How can transcription be terminated?
This base is also a pyrimidine and is very similar to thymine. Related Stories. But the pathogens that cause disease are increasingly developing resistance to the ZCCHC4 influences cell Although, other nucleic acid-like polymers are known, yet much remains unknown regarding possible RNA, or ribonucleic acid, is a molecule that plays a central role in the function of The modification is apparently attached to molecules only when cells are under stress, and is rapidly removed Based on the conservation pattern in the minor-groove intercalation loop it was suggested that SMUG1 may have evolved from an UNG-like enzyme by rapid divergence, possibly to meet special requirements for repair in multicellular animals Aravind and Koonin, These studies are based on relatively few sequences with low similarity.
This makes alignment and analysis difficult, and the interpretation of these data should be done with caution. The origin of SMUG1 therefore remains an open question. UNG is very widespread in bacteria, and has also been identified in most eukaryotes.
It has been suggested that UNG was introduced into eukaryotes by horizontal gene transfer Aravind and Koonin, , possibly from the mitochondrial genome Eisen and Hanawalt, UNG is also the only of these gene families that is found in a large number of viruses, indicating another possible mechanism for horizontal gene transfer. A Blast search Altschul et al. Sequence comparison of the different gene families within the UDG superfamily identifies several conserved sequence motifs, indicating a common 3D-fold for all UDG-type proteins.
It therefore seems realistic to assume that all UDG-type proteins share this common fold. The essential part of the proline-rich motif that is in direct contact with the DNA backbone is structurally conserved in MUG. However, the actual region seems to be well conserved in most sequences, the variation is mainly with respect to the specific residues found at each position. The motif contributes to uracil recognition by hydrogen bonding to polar atoms of the uracil ring.
In the uracil binding pocket there is also a favourable stacking interaction between uracil and a well-conserved phenylalanine residue found between the water-activating and the proline-rich motifs, in addition to the tyrosine from the water-activating motif mentioned above.
This motif is also involved in DNA interaction. In particular the glycine is well conserved, probably because a side chain at this position would interfere with the close contact between the protein and the DNA backbone. This motif shows some variation, but the histidine and the first proline are conserved in most sequences, except in SMUG1. The histidine is one of the active site residues, and forms hydrogen bond with uracil.
This architecture family is a very large one, with 70 topologies listed in CATH. The 3D structure for MBD4 is not known. However, structures are available for several other members of this superfamily, and it can be assumed that important structural features are conserved. The HhH—GPD-fold consists of a four-helix bundle domain and a six-helix barrel domain, with the active site and the HhH motif located at the interface between these domains. Whereas most DNA-binding proteins seem to use a charged surface rich in lysine and arginine residues to bind backbone phosphates, the DNA binding surface of OGG1 is nearly charge neutral.
UNG-proteins are highly selective for uracil, but remove 5-fluorouracil and certain oxidised pyrimidines with very low efficiency Krokan et al. The efficient removal of uracil from single-stranded DNA is puzzling since it leaves a non-informative lesion without the information in a complementary strand.
Single-stranded DNA is probably mainly found temporarily in transcribed genes and very close to the replication fork. Abasic sites resulting from uracil-removal in single-stranded DNA at the replication fork could be handled by at least three different mechanisms; i regression of the replication fork and repair by short patch or long patch BER, ii recombination repair using the old strand at the other side of the fork, iii translesion DNA synthesis.
Regression of a replication fork stalled at a single-strand lesion is well established in E. It may in principle apply to all types of lesions that stall the replication fork, including abasic sites Robu et al.
Recombination using information from the sister chromatid at stalled replication forks Gruss and Michel, , as well as translesion synthesis across abasic sites are well established processes in bacteria. Interestingly, repair of abasic sites in chromosomal DNA in E. Therefore, abasic sites resulting from the action of UNG at the replication fork is possibly unlikely to be dealt with by BER alone. For more comprehensive overviews, the reader should consult other recent reviews Dogliotti et al. The presumed major track is the short patch pathway.
The alternative long patch pathway largely uses replication proteins Dogliotti et al. As shown in Figure 2 , uracil in DNA may be present in different positions relative to a replication fork, and in addition the sequence context may vary. It seems likely that the type of uracil-DNA glycosylase, as well as the mechanism of repair in the subsequent steps will depend on these factors.
Uracil present in the fork prior to replication, e. Among the uracil-DNA glycosylases, only UNG2 specifically accumulates in the replication foci during S phase, and as discussed, all experimental evidence suggests that UNG2 has an important role in the removal of misincorporated uracil in replication foci. Uracil in different positions relative to the replication fork, and proposed mechanisms of repair in different positions.
One important problem is the following: How are deaminated cytosines that escape repair prior to replication repaired, if at all? However, UNG2 efficiently removes uracil from single-stranded DNA and may thus generate an abasic site that blocks replication.
The stalled replication fork may recruit proteins required for fork regression and homologous recombination, which are alternative mechanisms to short patch repair and long patch repair in the downstream steps subsequent to uracil removal. Involvement of recombination in the repair of abasic sites has been documented for E.
Furthermore, induction of deamination of cytosine by NO is strongly cytotoxic in E. The finding that recombination factors are required for processing of abasic sites in bacteria suggests that this may also be the case in mammalian cells, since this basic process is highly likely to be conserved.
We therefore propose that uracil in single-stranded DNA at the replication fork is incised by UNG2 and repaired by recombination or fork regression, which are both processes requiring recombination proteins. Aravind L, Koonin EV. Bartsch H, Nair J. Bellacosa A. Cell Physiol. USA 96 : — Brown TC, Jiricny J.
Nucleic Acids Res. NY Acad. Google Scholar. Gruss A, Michel B. USA 95 : — USA 98 : — Hendrich B, Bird A. Holm L, Sander C. In press. Electronic publication ahead of print, August 2, Lindahl T. USA 71 : — USA 91 : — Cell Biol. Neddermann P, Jiricny J.
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