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6a.
The nucleotide excision repair or NER is mechanism that has capacity to repair the damaged
nucleotide bases which are formed due to covalent interaction with large hydrocarbons and due
to formation of pyrimidine dimers (T-T, T-C or CC), this mechanism of DNA repair is present in
bacteria, yeast and mammalian cells.
The damaged bases are first cut out within a string of nucleotides, and replaced with new DNA
using undamaged strand as a complementary strand with the assistance of DNA polymerase and
DNA ligase.
In prokaryotes, the enzymes that perform NER because of UV damage or pyrimidine dimers are
UvrABC excinuclease and the UvrD helicase. The genes responsible for their formation are
named as uvrA, uvrB, uvrC and uvrD. The UvrABC complex first recognizes the damaged part
of DNA, followed by cleavage on both sides of the demage, this damaged part is released by
UvrD helicase that unwinds DNA using ATP molecules. The gap so created is filled by new
DNA using DNA polymerase and the nick so created is later joined with main DNA on either by
DNA ligase.
In eukaryotes, it has been reported that Pol II (polB ) and Pol IV (dinB) does not affect them
after UV irradiation or dimmer formation and only affects Pol V (umuC)
Solution
6a.
The nucleotide excision repair or NER is mechanism that has capacity to repair the damaged
nucleotide bases which are formed due to covalent interaction with large hydrocarbons and due
to formation of pyrimidine dimers (T-T, T-C or CC), this mechanism of DNA repair is present in
bacteria, yeast and mammalian cells.
The damaged bases are first cut out within a string of nucleotides, and replaced with new DNA
using undamaged strand as a complementary strand with the assistance of DNA polymerase and
DNA ligase.
In prokaryotes, the enzymes that perform NER because of UV damage or pyrimidine dimers are
UvrABC excinuclease and the UvrD helicase. The genes responsible for their formation are
named as uvrA, uvrB, uvrC and uvrD. The UvrABC complex first recognizes the damaged part
of DNA, followed by cleavage on both sides of the demage, this damaged part is released by
UvrD helicase that unwinds DNA using ATP molecules. The gap so created is filled by new
DNA using DNA polymerase and the nick so created is later joined with main DNA on either by
DNA ligase.
In eukaryotes, it has been reported that Pol II (polB ) and Pol IV (dinB) does not affect them
after UV irradiation or dimmer formation and only affects Pol V (umuC)

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6a.The nucleotide excision repair or NER is mechanism that has cap.pdf

  • 1. 6a. The nucleotide excision repair or NER is mechanism that has capacity to repair the damaged nucleotide bases which are formed due to covalent interaction with large hydrocarbons and due to formation of pyrimidine dimers (T-T, T-C or CC), this mechanism of DNA repair is present in bacteria, yeast and mammalian cells. The damaged bases are first cut out within a string of nucleotides, and replaced with new DNA using undamaged strand as a complementary strand with the assistance of DNA polymerase and DNA ligase. In prokaryotes, the enzymes that perform NER because of UV damage or pyrimidine dimers are UvrABC excinuclease and the UvrD helicase. The genes responsible for their formation are named as uvrA, uvrB, uvrC and uvrD. The UvrABC complex first recognizes the damaged part of DNA, followed by cleavage on both sides of the demage, this damaged part is released by UvrD helicase that unwinds DNA using ATP molecules. The gap so created is filled by new DNA using DNA polymerase and the nick so created is later joined with main DNA on either by DNA ligase. In eukaryotes, it has been reported that Pol II (polB ) and Pol IV (dinB) does not affect them after UV irradiation or dimmer formation and only affects Pol V (umuC) Solution 6a. The nucleotide excision repair or NER is mechanism that has capacity to repair the damaged nucleotide bases which are formed due to covalent interaction with large hydrocarbons and due to formation of pyrimidine dimers (T-T, T-C or CC), this mechanism of DNA repair is present in bacteria, yeast and mammalian cells. The damaged bases are first cut out within a string of nucleotides, and replaced with new DNA using undamaged strand as a complementary strand with the assistance of DNA polymerase and DNA ligase. In prokaryotes, the enzymes that perform NER because of UV damage or pyrimidine dimers are UvrABC excinuclease and the UvrD helicase. The genes responsible for their formation are named as uvrA, uvrB, uvrC and uvrD. The UvrABC complex first recognizes the damaged part of DNA, followed by cleavage on both sides of the demage, this damaged part is released by UvrD helicase that unwinds DNA using ATP molecules. The gap so created is filled by new DNA using DNA polymerase and the nick so created is later joined with main DNA on either by DNA ligase.
  • 2. In eukaryotes, it has been reported that Pol II (polB ) and Pol IV (dinB) does not affect them after UV irradiation or dimmer formation and only affects Pol V (umuC)