Gene Structure

The genes that code for many proteins are broken into pieces. These pieces—the exons—are separated by stretches of noncoding DNA—the introns

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#Unit 3. Fundamental Processes

Even if cells cannot repair these lesions, there is a fail-safe mechanism that allows the replication machinery to bypass these sites of damage or tolerate the DNA damage. One mechanism of DNA damage tolerance is translesion synthesis. Although this mechanism is, as we shall see, highly error-prone and thus likely to introduce mutations, translesion synthesis spares the cell the worse fate of an incompletely replicated chromosome. A key feature of DNA damage tolerance is that the DNA lesion remains in the genome. DNA repair pathways can subsequently correct the lesion.

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#Unit 3. Fundamental Processes

Translesion synthesis is catalyzed by a specialized class of DNA polymerases that synthesize DNA directly across the site of the damage. In E. coli, DNA Pol IV (DinB) or DNA Pol V (a complex of the proteins UmuC and UmuD’) performs translesion synthesis.  DinB and UmuC are members of a distinct family of DNA polymerases found in many organisms known as the Y family of DNA 

polymerases. There are five translesion polymerases known in humans, four of which belong to the Y family.

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#Unit 3. Fundamental Processes

DinB and UmuC are members of a distinct family of DNA polymerases found in many organisms known as the Y family of DNA polymerases. There are five translesion polymerases known in humans, four of which belong to the Y family. 

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#Unit 3. Fundamental Processes

These polymerases are template-dependent, they incorporate nucleotides in a manner that is independent of base pairing.

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#Unit 3. Fundamental Processes

Human member of the Y family of translesion polymerases (DNA Pol n) correctly inserts two A residues opposite a thymine dimer. 

TLS Online TPP Program

#Id: 6156

#Unit 3. Fundamental Processes