DNA be a contender. Surprisingly, this ability is

repair is a mechanism that a cell uses to amend damaged or mismatched segments
on its sequence. Our cells are constantly exposed to insults from endogenous
and exogenous agents that can introduce damage into our DNA and generate
genomic instability. Many of these lesions cause structural damage to DNA and
can alter or eliminate fundamental cellular processes, such as DNA replication
or transcription (Dexheimer, 2013).

like any other molecule, is subject to chemical reactions. DNA damage may result
from either intrinsic or extrinsic agents. In general, the vast majority of DNA
modifications are endogenous in origin. The simplest form of endogenous DNA
damage is spontaneous hydrolysis. DNA is also susceptible to chemical
modification by reactive molecules that are created during normal cellular
metabolism. An additional type of DNA damage related to endogenous reactive
molecules is alkylation. The putative candidates of such agents include the
endogenous methyl donor, S-adenosylmethionine, nitrosated amines, and methyl
radicals generated by lipid eroxidation. The primary sites of alkylation are
the O? and N-atoms of nucleobases (Dexheimer,

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case study of Deinococcus radiodurans;
this microorganism has the ability to repair its genome after it has been
blasted apart by a high dose of radiation might be a contender. Surprisingly,
this ability is primarily related to the resistance of D. radiodurans proteins and the structure of its genome, rather
than to its DNA repair mechanisms. Its radiation-resistant proteins are able to
begin repairing the genome quickly. Repair is aided by the genome consisting of
two chromosomes, each having numerous areas of homology. This allows the DNA
fragments to anneal to each other, facilitating the piecing together of the
shattered genome. Other than this, D.
radiodurans uses almost the same DNA repair mechanisms as other microorganisms.
Clearly, mutations can have disastrous effects. Therefore it is imperative that
a microorganism be able to repair changes. E.
coli is another example of microorganism that carryout DNA repairs (Willey, et al,

to properly manage deleterious consequences of DNA damage, the cells developed
several repair mechanisms which eliminates genomes mis-instructive or
non-instructive elements, as well as seal DNA breaks (Dexheimer, 2013). The cells initiate processes such as Proofreading, Mismatch repair, Excision
repair, Direct repair and Recombinant repair.

which is a function of DNA polymerase III checks for errors such as mismatches
of nucleotide bases and corrects them (Kornberg and Maki, 1987).  This mechanism also acts as the first line of
defense. DNA polymerases have the ability to evaluate the hydrogen bonds formed
between the newly added nucleotide and the template nucleotide, and correct any
errors immediately. When a DNA polymerase detects that a mistake has been made,
it backs up, removing the incorrect nucleotide with its 3′ to 5′ exonuclease
activity. It then restarts DNA replication, this time inserting the correct
nucleotide. Proofreading is very efficient, but it does not always correct
errors in replication. Furthermore, it is not useful for correcting induced
mutations (Willey, et al, 2014).

repair is essential to all organisms because it
maintains the stability of the genome during repeated duplication (Jun, et al, 2006). When proofreading by
replicative DNA polymerases fails, mismatched bases are usually detected and
repaired by the mismatch repair system. In E. coli the enzyme MutS scans the
newly replicated DNA for mismatched pairs. Another enzyme, MutH, removes a
stretch of newly synthesized DNA around the mismatch. A DNA polymerase then replaces
the excised nucleotides, and the resulting nick is sealed by DNA ligase (Willey, et al,

 Excision repair corrects
damage that causes distortions in the double helix. Two types of excision
repair systems have been described: nucleotide excision repair and base
excision repair. They both use the same approach to repair: Remove the damaged portion
of a DNA strand and use the intact complementary strand as the template for
synthesis of new DNA. They are distinguished by the enzymes used to correct DNA
damage. Nucleotide excision repair uses UvrABC endonuclease, which base
excision repair uses DNA glycosylase. Both enzymes and repairs are applicable
to E.coli repair mechanism (Willey, et al,

repair corrects Thymine dimers and alkylated
bases. Thus, damage to guanine from mutagens such as methyl-nitrosoguanidine can
be repaired directly. For instance, photoreactivation repairs thymine dimers
(figure 16.5) by splitting them apart with the help of visible light. This
photochemical reaction is catalyzed by the enzyme photolyase (Willey, et al,

Recombinant repair
corrects damaged DNA in which both bases of a pair are missing or damaged, or
where there is a gap opposite a lesion. In this type of repair, a protein
called RecA cuts a piece of template DNA from a sister molecule and puts it
into the gap or uses it to replace a damaged strand (Willey, et al, 2014).



genetic and biological significance of DNA repair mechanisms is underscored by
the fact that their deregulation of DNA repairs can lead to the initiation and
progression of genetic disorders. On the other hand, DNA repair can confer
resistance to front line antibiotics, cancer treatments (i.e. chemotherapy and
radiation), which rely on the generation of DNA damage to kill pathogenic live
forms or cancerous cells. The repair mechanisms serve as a method of survival
to the cell and also a way of retaining or attaining the normal state of
cellular stability. However, DNA repair mechanisms sometimes are not be able to
correct errors and breaks especially when these errors and breaks are induced.