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Abstract:
Evidence that optimum repair depends on adequate pools of deoxynucleotide triphosphates (dNTPs) comes from the study of pyrimidine auxotrophs of Ustilago maydis. These strains are sensitive to UV light and X-rays, and for pyr1-1 it has been shown that the intracellular concentration of dTTP is reduced about 7-fold. Evidence has been published that DNA repair synthesis may require higher concentrations of dNTPs, than chromosome replication. The survival curve of pyr1-1 after UV-treatment, and split dose experiments with wild-type cells, provide evidence for an inducible repair mechanism, which probably depends on genetic recombination. Although inducible repair saves cellular resources, it has the disadvantage of becoming ineffective at doses which are high enough to inactivate the repressed structural gene(s) for repair enzymes. To ensure survival it is vital for organisms to preserve the integrity of their DNA, and this is accomplished both by accurate replication and by repair. It is clear that a wide variety of repair mechanisms have evolved to remove lesions which arise either spontaneously (such as the deamination of cytosine to uracil) or as a result of damage from external agents. Nevertheless, it would be incorrect to assume that all species require all possible pathways of repair. It is now well established that the accuracy of DNA and protein synthesis depends on proof-reading or editing mechanisms (for a review, see Ref. 5). These consume energy and may slow down the rate of synthesis, therefore organisms must invest metabolic resources to achieve any given level of accuracy. Optimum accuracy levels will evolve from the balance between error avoidance in macromolecular synthesis and physiological efficiency in growth and propagation [11, 12, 22].(ABSTRACT TRUNCATED AT 250 WORDS)