I'm Probably Greatly Oversimplifying this, but How Does RNA Pol II (Eukaryotes) Interpret Thymine Dimers?

Question

Involved:

http://www.cem.msu.edu/~reusch/VirtualText/photchem.htm

Answer 1

AS RNA poly II is transcribing a gene, it stops transcribing when it reaches a thymine dimer.  Then nucleotide excision repair proteins must repair the strand.

Hope this helps.

Answer 2

Well, as said above, it either causes a mis-read or a drop off. Repair is carried out by DNA excision and replacement. THis is carried out by NER proteins, which have a helicase activity and excise the DNA from the error marker to the nearest conserved DNA region - I forget the generic sequence- and then pol δ or ε fill in the gaps.

Dimerisation is a problem with any pyrimidines (i.e C or U) however, TT is on of the least problematic as it still has a fairly strong propensity to form translate as AA, although misrepair/translation of dimer lesions is still possible.

Answer 3

simplified:

the dimer confuses the transcription process because it makes it more difficult for the dual chain to split at the point of the dimer.  think of a zipper getting stuck.  the result is that the RNA Pol II misreads the 'dimed' base as a different base, so copies it incorrectly.

Answer 4

The thymine dimers offer no complementary nucleotide for normal Watson-Crick base pairing. As a result several things can happen:

1) Pol II can fall off the template strand. Pol II can re-start replication at this site, however the dimers can slow replication. If there are enough dimers, this can inhibit DNA synthesis, which is lethal (to the cell).  

2) If Pol II stays on the template it will randomly insert nucleotides where the two adenines should have been. There seems to be a preference for inserting a T or G in place of A, however the constitution of the nucleotide pool will play a role (i.e. if there is a lot of extra cytosine as compared to T or G, expect more C misinsertions)