This damage is mainly the formation of a thymine dimer.

The error is called a thymine dimer.

Such damages can include the thymine dimers created by UV rays.

Several substances are known to increase the amount of direct DNA damage (thymine dimers).

Overexposure to sun leads to the formation of thymine dimers, a form of DNA damage.

The few that survived had developed enzymes which verified the genetic material and broke up thymine dimer bonds, known as excision repair enzymes.

The tanning activator coumarin is known to induce thymine dimers (cyclobutane pyrimidine dimers).

This thymine dimer prevents enzymes from "reading" the DNA and copying it, thus neutering the microbe.

For example, UV light can damage DNA by producing thymine dimers, which are cross-links between pyrimidine bases.

Thymine dimers (T-T dimers) formed in between two thymines are the most abundant of the CPDs.

Two common UV products are cyclobutane pyrimidine dimers (CPDs, including thymine dimers) and 6,4 photoproducts.

If added to a topical preparation of ascorbic acid and vitamin E, ferulic acid may reduce oxidative stress and formation of thymine dimers in skin.

UV rays in the middle range can irreparably damage the complex DNA molecules in the cells producing thymine dimers making it a very potent mutagen.

UV DNA damage results in bulky DNA adducts - these adducts are mostly thymine dimers and 6,4-photoproducts.

The dimerization of alkenes is relevant to the photodamage of DNA, where thymine dimers are observed upon illuminating DNA to UV radiation.

DNA molecules may be directly or indirectly damaged by UV radiation carrying enough energy to excite certain molecular bonds to form thymine dimers (pyrimidine dimers) (this causes sunburn).

Translesion synthesis is a DNA damage tolerance process that allows the DNA replication machinery to replicate past DNA lesions such as thymine dimers or AP sites.

UVB light causes thymine base pairs next to each other in genetic sequences to bond together into thymine dimers, a disruption in the strand that reproductive enzymes cannot copy (see picture above).

In his inaugural article in the PNAS, Sançar captures the elusive photolyase radicals he has chased for nearly 20 years, thus providing direct observation of the photocycle for thymine dimer repair.

Many other deoxyribozymes have since been developed that catalyse DNA phosphorylation, DNA adenylation, DNA deglycosylation, porphyrin metalation, thymine dimer photoreversion and DNA cleavage.

Although the thymine-thymine CPDs (thymine dimers) are the most frequent lesions caused by UV light, translesion polymerases are biased toward introduction of As, so that TT dimers are often replicated correctly.

One of the common mutations of DNA involves two adjacent thymines or cytosine, which, in presence of ultraviolet light, may form thymine dimers, causing "kinks" in the DNA molecule that inhibit normal function.

At a wavelength of 2,537 Angstroms (254 nm) UV will break the molecular bonds within micro-organismal DNA, producing thymine dimers in their DNA thereby destroying them, rendering them harmless or prohibiting growth and reproduction.

Following irradiation by the UV laser we observed that the presence of both wild type polymerase and CRP inhibits the formation of the thymine dimer between T-50 and -51 on the template strand (Fig. 4, lane 6)[20].

However, it accurately replicates UV-damaged DNA; when thymine dimers are present, this polymerase inserts the complementary nucleotides in the newly synthesized DNA, thereby bypassing the lesion and suppressing the mutagenic effect of UV-induced DNA damage.