Final answer:
Site-specific recombination with inverted loxP sites can result in gene inversion or excision, generating a knockout mouse. In the lac operon, a mutation in the operator that prevents repressor binding leads to continuous gene transcription. DNA replication requires 3'-OH groups on deoxyribonucleotides, and mutations in a promoter can inhibit transcription.
Step-by-step explanation:
If loxP sites are oriented as inverted repeats and a site-specific recombination system is used, the effect on the resulting DNA would usually involve either the inversion of the DNA segment flanked by the loxP sites or the excision of this segment depending on the orientation and location of the loxP sites. The Cre recombinase enzyme recognizes these sequences and mediates the recombination event. In a typical genetic knockout scenario in mice, the loxP sites would flank a gene of interest, and when recombination occurs, the gene would be excised, effectively creating a knockout mouse lacking that specific gene's function.
Concerning the lac operon, if a mutation occurred in the operator sequence preventing the repressor protein from binding, the result would be the continuous transcription of the operon's genes regardless of the presence of lactose. In contrast, mutations preventing DNA binding proteins from being produced, like those involved with RNA polymerase or retroviral integration, would have broad implications, potentially stopping transcription or integration of viral DNA into the host genome.
Regarding DNA replication, if deoxyribonucleotides lacking a 3'-OH group were introduced, DNA synthesis would halt because the 3'-OH group is essential for forming the phosphodiester bond with the incoming nucleotide. Mutations in the -35 region of a bacterial promoter would likely reduce or prevent the binding of RNA polymerase, leading to decreased or absent transcription of the associated genes.