Rifampin inhibits the â subunit of the E. coli RNA polymerase. A typical rifR mutant contains a mutant gene that produces a â subunit that no longer binds rifampin. Propose one other genetic alteration by which an E. coli might become resistant to the drug rifampin (without mating with other bacteria) and the molecular basis for this other resistant phenotype. What is your evidence this other type doesn’t exist?

To propose another genetic alteration by which an E. coli can become resistant to rifampin, we need to consider the mechanism of action of the drug and identify potential targets for alteration. Rifampin specifically inhibits the β (beta) subunit of the RNA polymerase enzyme in E. coli, which is essential for transcription. Hence, a possible alteration that could confer rifampin resistance would involve a mutation in the β subunit that prevents rifampin from binding.

The molecular basis for this resistant phenotype would be a mutation in the rpoB gene, which encodes the β subunit of RNA polymerase. This mutation could result in amino acid substitutions within the β subunit, leading to structural changes that prevent rifampin from binding effectively. Consequently, the RNA polymerase enzyme would remain functional even in the presence of rifampin, allowing transcription to proceed.

As for evidence that this other type of resistance doesn't exist, we can examine existing literature and experimental studies. Researchers have extensively studied the mechanisms of rifampin resistance in E. coli and other bacteria, and the mutation in the rpoB gene leading to amino acid substitutions in the β subunit is well-documented and widely acknowledged as the primary mechanism of resistance.

Furthermore, studies conducted to investigate the genetic basis of rifampin resistance in E. coli have consistently found mutations in the rpoB gene as the prominent genetic alteration. These findings provide strong evidence that this mutation represents the main mechanism of rifampin resistance in E. coli, supporting the assertion that other types of resistance without mutations in the rpoB gene are highly unlikely.