We identified 24 rnr1 mutant alleles resulting in diverse mutator phenotypes linked in most cases to imbalanced dNTPs. Among the identified rnr1 alleles the strongest mutators presented a dNTP imbalance in which three out of the four dNTPs were elevated (dCTP dTTP and dGTP) particularly if dGTP levels were highly increased.
Multiple turnover kinetics show that Sml1 inhibition of dGTP/ADP- and ATP/CDP-bound ScRR follows a mixed inhibition mechanism. However Sml1 cooperatively binds to the ES complex in the dGTP/ADP form whereas with ATP/CDP Sml1 binds weakly and noncooperatively
there is a directed orientation of the RNR beta and beta' C-terminal tails relative to alpha within the holoenzyme consistent with a docking model of the two subunits and argue against RT across the beta beta' interface
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