THE DISAPPEARANCE OF THYMINE DIMERS FROM DNA: AN ERROR-CORRECTING MECHANISM

THE DISAPPEARANCE OF THYMINE DIMERS FROM DNA: AN ERROR-CORRECTING MECHANISM

December 11, 1963 | BY R. B. SETLOW AND W. L. CARRIER
The article by R. B. Setlow and W. L. Carrier investigates the disappearance of thymine dimers from DNA as an error-correcting mechanism following ultraviolet (UV) irradiation. UV radiation causes intrastrand thymine dimers, which are stable and block DNA synthesis. The study uses several strains of Escherichia coli to examine the fate of these dimers during recovery from UV damage. Key findings include: 1. **Recovery Mechanisms**: The recovery processes, such as photoreactivation, heat reactivation, and host-cell reactivation, are likely enzymatic and overlap, indicating they act on the same UV lesions. 2. **Thymine Dimer Splitting**: Dimer-splitting by 330-450 mμ radiation in yeast extract can explain the biological effects of photoreactivation on transforming DNA. 3. **In Vitro and In Vivo Blockage**: Thymine dimers block DNA synthesis both in vitro and in vivo, and radiation-resistant cells can recover in the dark from these blocks. 4. **State of Dimers**: In resistant cells, thymine dimers disappear from the acid-insoluble fraction and appear in the acid-soluble fraction, suggesting their removal from the polynucleotide chain. 5. **Strain-Specific Differences**: Different strains of E. coli show varying rates of dimer removal, with sensitive strains retaining dimers in the acid-insoluble fraction and resistant strains removing them. 6. **Oligonucleotides**: The dimers in the acid-soluble fraction are likely in oligonucleotides, as they migrate on DEAE paper at similar rates to trinucleotides containing dimers. 7. **Mechanism of Recovery**: The removal of thymine dimers from DNA chains may be a crucial step in the recovery of cells from UV irradiation, but it is not the only factor. Other processes, such as slow random polymerization and nuclease degradation, also play roles. The study suggests that the removal of thymine dimers is a key mechanism in the recovery of cells from UV damage, potentially applicable to other types of DNA damage or random errors in double-stranded DNA.The article by R. B. Setlow and W. L. Carrier investigates the disappearance of thymine dimers from DNA as an error-correcting mechanism following ultraviolet (UV) irradiation. UV radiation causes intrastrand thymine dimers, which are stable and block DNA synthesis. The study uses several strains of Escherichia coli to examine the fate of these dimers during recovery from UV damage. Key findings include: 1. **Recovery Mechanisms**: The recovery processes, such as photoreactivation, heat reactivation, and host-cell reactivation, are likely enzymatic and overlap, indicating they act on the same UV lesions. 2. **Thymine Dimer Splitting**: Dimer-splitting by 330-450 mμ radiation in yeast extract can explain the biological effects of photoreactivation on transforming DNA. 3. **In Vitro and In Vivo Blockage**: Thymine dimers block DNA synthesis both in vitro and in vivo, and radiation-resistant cells can recover in the dark from these blocks. 4. **State of Dimers**: In resistant cells, thymine dimers disappear from the acid-insoluble fraction and appear in the acid-soluble fraction, suggesting their removal from the polynucleotide chain. 5. **Strain-Specific Differences**: Different strains of E. coli show varying rates of dimer removal, with sensitive strains retaining dimers in the acid-insoluble fraction and resistant strains removing them. 6. **Oligonucleotides**: The dimers in the acid-soluble fraction are likely in oligonucleotides, as they migrate on DEAE paper at similar rates to trinucleotides containing dimers. 7. **Mechanism of Recovery**: The removal of thymine dimers from DNA chains may be a crucial step in the recovery of cells from UV irradiation, but it is not the only factor. Other processes, such as slow random polymerization and nuclease degradation, also play roles. The study suggests that the removal of thymine dimers is a key mechanism in the recovery of cells from UV damage, potentially applicable to other types of DNA damage or random errors in double-stranded DNA.
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