The replication of damaged DNA by synthesis across a lesion in the template strand; a specialized DNA polymerase or replication complex inserts a defined nucleotide across from the lesion which allows DNA synthesis to continue beyond the lesion. This process can be mutagenic depending on the damaged nucleotide and the inserted nucleotide.

The process of restoring DNA after damage. Genomes are subject to damage by chemical and physical agents in the environment (e.g. UV and ionizing radiations, chemical mutagens, fungal and bacterial toxins, etc.) and by free radicals or alkylating agents endogenously generated in metabolism. DNA is also damaged because of errors during its replication. A variety of different DNA repair pathways have been reported that include direct reversal, base excision repair, nucleotide excision repair, photoreactivation, bypass, double-strand break repair pathway, and mismatch repair pathway.

The process of restoring DNA after damage. Genomes are subject to damage by chemical and physical agents in the environment (e.g. UV and ionizing radiations, chemical mutagens, fungal and bacterial toxins, etc.) and by free radicals or alkylating agents endogenously generated in metabolism. DNA is also damaged because of errors during its replication. A variety of different DNA repair pathways have been reported that include direct reversal, base excision repair, nucleotide excision repair, photoreactivation, bypass, double-strand break repair pathway, and mismatch repair pathway.

The nucleotide-excision repair process that carries out preferential repair of DNA lesions on the actively transcribed strand of the DNA duplex. In addition, the transcription-coupled nucleotide-excision repair pathway is required for the recognition and repair of a small subset of lesions that are not recognized by the global genome nucleotide excision repair pathway.

The endonucleolytic cleavage of the damaged strand of DNA 5' to the site of damage. The incision occurs at the junction of single-stranded DNA and double-stranded DNA that is formed when the DNA duplex is unwound. The incision follows the incision formed 3' to the site of damage.

Repair of the gap in the DNA helix by DNA polymerase and DNA ligase after the portion of the strand containing the lesion has been removed by pyrimidine-dimer repair enzymes.

Repair of the gap in the DNA helix by DNA polymerase and DNA ligase after the portion of the strand containing the lesion has been removed by pyrimidine-dimer repair enzymes.

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a stimulus indicating damage to its DNA from environmental insults or errors during metabolism.

A process that results in the endonucleolytic cleavage of the damaged strand of DNA. The incision occurs at the junction of single-stranded DNA and double-stranded DNA that is formed when the DNA duplex is unwound.

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of an ultraviolet radiation (UV light) stimulus. Ultraviolet radiation is electromagnetic radiation with a wavelength in the range of 10 to 380 nanometers.

The conversion of DNA-damage induced single-stranded gaps into large molecular weight DNA after replication by using a specialized DNA polymerase or replication complex to insert a defined nucleotide across the lesion. This process does not remove the replication-blocking lesions and causes an increase in the endogenous mutation level. For example, in E. coli, a low fidelity DNA polymerase, pol V, copies lesions that block replication fork progress. This produces mutations specifically targeted to DNA template damage sites, but it can also produce mutations at undamaged sites.

The conversion of DNA-damage induced single-stranded gaps into large molecular weight DNA after replication by using a specialized DNA polymerase or replication complex to insert a defined nucleotide across the lesion. This process does not remove the replication-blocking lesions and causes an increase in the endogenous mutation level. For example, in E. coli, a low fidelity DNA polymerase, pol V, copies lesions that block replication fork progress. This produces mutations specifically targeted to DNA template damage sites, but it can also produce mutations at undamaged sites.

That part of the nuclear content other than the chromosomes or the nucleolus.

Extra-nucleolar nuclear domains usually visualized by confocal microscopy and fluorescent antibodies to specific proteins.

That part of the nuclear content other than the chromosomes or the nucleolus.