Mismatch excision and possible polarity effects result in preferred deoxyribonucleic acid strand of integration in pneumococcal transformation.
Heteroduplex deoxyribonucleic acid molecules having a drug resistance marker on one strand and its wild-type allele on the other have been used as donors in pneumococcal transformation. Opposite strands are not equally effective in producing transformants, and this strand bias is not the same, either in direction or magnitude, for various different genetic markers. Selective excision of mismatched base pairs is probably responsible for the large differences in strand efficiency seen with discriminating (hex+) strains, for when the recipient is nondiscriminating (hex-), and therefore presumably lacking an excision enzyme system, strand bias is drastically reduced or altered. The evidence also indicates that excision occurs after integration, as it is provoked by specific donor-recipient mismatch and not by the same mismatch when introduced within donor heteroduplex molecules. Excision can extend to include a neighboring linked marker which would otherwise not be excised, thus altering its intrinsic strand bias as well as its efficiency in transformation. There is a small bias in relative strand efficiency for some markers, not caused by mismatch excision, which perhaps is due to polarity in the integration process itself.
D000630:Aminopterin / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D004269:DNA, Bacterial / Q000378:metabolism / Q000502:physiology*; D004352:Drug Resistance, Microbial; D004917:Erythromycin / Q000494:pharmacology; D005796:Genes; D013296:Streptococcus pneumoniae / Q000502:physiology*; D013424:Sulfanilamides / Q000494:pharmacology; D014170:Transformation, Genetic
D000900:Anti-Bacterial Agents; D004269:DNA, Bacterial; D013424:Sulfanilamides; D004917:Erythromycin; D000630:Aminopterin