The first class of mutation is probably a promoter mutation that prevents RNA polymerase binding and thus prevents expression of the entire lac operon. The first class of mutations affect a DNA-binding site for RNA polymerase. Because this DNA sequence is not transcribed or translated, any mutation in the sequence will not result in translation termination and thus is not a nonsense mutation. The first class of mutations result in polarity because they directly prevent transcription of the lac operon. The second class of mutations result in polarity because they cause translation termination which, because Rho binds to the untranslated sequences, results in transcription termination.
Many antibiotics act by binding to bacterial ribosomes and inhibiting translation.
Resistance to such antibiotics is often due to mutations that produce specific nucleotide changes in one of the ribosomal subunits which prevent the antibiotic from binding to the ribosome. In such cases, the antibiotic resistant alllele is often recessive to the antibiotic sensitive allele. If the antibiotic stops the ribosomes in their tracks, it will prevent subsequent ribosomes from transcribing that message. Thus, the sensitive phenotype is dominant to the resistant phenotype. The hisD gene encodes the enzyme which catalyzes the last step of histidine biosynthesis, the conversion of histidinol to histidine.