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What does T-T stand for?

T-T stands for cis-syn thymine-thymine

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Translesion polymerases frequently introduce mutations at pyrimidine dimers, both in prokaryotes (SOS mutagenesis) and in eukaryotes. 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. On the other hand, any C involved in CPDs is prone to be deaminated, inducing a C to T transition.
The most well known example of the latter is synthesis involving 8-oxy-G, a common by-product of oxidative metabolism. With many polymerases, 8-oxy-dG in a syn conformation forms a Hoogsteen pair with adenine, ultimately generating transversion mutations (reviewed in Refs. 44 and 45). However, Pol ß avoids this inaccurate reaction by flipping the 5'-phosphate backbone of the templating nucleotide 180°, relieving a steric clash with the oxygen at C-8 and allowing non-mutagenic pairing of incoming dCTP with 8-oxy-dG in the Watson-Crick anti conformation (46). Yet a different, non-mutagenic example of Hoogsteen base pairing is seen for Sso Dpo4 bypass of a cis-syn thymine-thymine.
Rochette, P. J. , J. P. Therrien, R. Drouin, D. Perdiz, N. Bastien, E. A. Drobetsky, and E. Sage. 2003. UVA-induced cyclobutane pyrimidine dimers form predominantly at thymine-thymine dipyrimidines and correlate with the mutation spectrum in rodent cells. Nucleic Acids Res. 31:2786-94.
cerevisiae DNA polymerase ?, determined at 2. 25Å resolution. The structure reveals a novel polydactyl right hand-shaped molecule with a unique polymerase-associated domain. We identify the catalytic residues and show that the fingers and thumb domains are unusually small and stubby. In particular, the unexpected absence of helices “O” and “O1” in the fingers domain suggests that openness of the active site is the critical feature which enables DNA polymerase ? to replicate through DNA lesions such as a UV-induced cis-syn thymine-thymine.
This polymerase is coded by the XPV gene, which is defective in persons with XP variant cells (Johnson et al. 1999; Masutani et al. 1999). Although these cells possess NER capability, they carry a predisposition to skin cancer on exposure to sunlight. The discovery that polη is able to bypass the cis-syn thymine-thymine dimer efficiently and accurately (Masutani et al. 1999) indicates that this polymerase plays a very important role in protection from the deleterious effects of unrepaired UV photoproducts.
can efficiently bypass a thymine thymine.