What happens if a thymine dimer is not repaired

This repair mechanism does not require light and instead of just breaking the bonds of the T-T dimer as was done by photolyase, it excises the region of damaged nucleotides. Generally, the nicks are 12 nucleotides apart and the DNA between the nicks is removed. In addition, other mechanisms such as mutagenic repair or dimer bypass, recombinational repair, cell-cycle checkpoints, apoptosis, and certain alternative repair pathways are also operative in various organisms for the removal or correction of T-T dimers Ref.

The UV component of sunlight is responsible for the induction of skin tumors, most notably basal cell and squamous cell carcinomas and melanomas Ref. The presence of UV induced dimers in the DNA is damaging, and it may cause a mispairing as the strand is being copied or may stop replication altogether.

Unless repaired, pyrimidine dimers may lead to blockage of transcription, mutations, cell death and cancer Ref. Can't read the image? Tel : Fax : Email : support abeomics.

Toggle navigation. Recombinant Proteins. Immune-Check Point. Tissue Microarray. DNA polymerase has trouble reading the dimer, since it doesn't fit smoothly in the active site. TT dimers like the ones shown here are not the major problem, since they are usually paired correctly with adenine when the DNA is replicated.

But CC dimers do not fare as well. DNA polymerase often incorrectly pairs adenine with them instead of guanine, causing a mutation. If this happens to be in an important gene that controls the growth of cells, such as the genes for Src tyrosine kinase or p53 tumor suppressor , the mutation can lead to cancer. We spend a lot of time in the sun, so it will come as no surprise that we have a powerful mechanism for correcting these problems.

Our cells use a process called nucleotide excision repair, which requires the concerted effort of a large collection of proteins that recognize the corrupted bases, clip out the section of DNA with the error, and then build a new copy of the damaged area. Other organisms have additional correction mechanisms. For instance, the enzyme on the left PDB entry 1vas is an endonuclease that clips out the damaged bases, making the site available for repair.

Surprisingly, this endonuclease doesn't recognize the thymine dimer directly. You can see in this picture that the thymine dimer colored magenta doesn't touch the enzyme at all. Instead, the enzyme recognizes one of the adenines that is paired with the dimer.

Since the base pair is weakened by the contorted shape of the dimer, the adenine is easily flipped out and bound to a pocket in the enzyme. The enzyme on the right PDB entry 1tez is a photolyase that directly breaks the bonds connecting the dimer, correcting the error in place.

Ironically, photolyases use visible light to power this process. This structure captures the DNA after the thymine dimer has been fixed. Notice that the two thymine bases colored magenta are flipped out of the normal DNA helix and are bound in a pocket on the enzyme surface. It has a loose active site, so it can easily accommodate the stiff thymine dimer. Bottom line: Casual sun exposure is OK. Sunburns are not. This dramatically increases your risk of skin cancer.

Here are some abstracts of papers that describe the link between UV light and skin cancer:. A paper on cytosine dimers and different wavelengths of UV light. Here is a good general review of the subject. UV light causes a crosslink in the DNA.