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Describe the phenotype of the following E. coli mutants when grown in two different media: glucose only and lactose only. Explain the reasoning behind your answer. a. A strain with a mutation in the gene encoding the lac repressor; the mutant repressor cannot bind allolactose. b. A strain with a mutation in the gene encoding CAP; the mutant form of CAP binds but cannot release cAMP. c. A strain in which the Shine-Dalgarno sequence has been deleted from the gene encoding adenyl cyclase.

What would be the phenotype of an E. coli strain in which the tandem trp codons in the leader region were mutated so that they coded for serine instead?

Propose a mechanism by which a cell might sense and respond to levels of \(\mathrm{Na}^{+}\)in its environment.

The extracytoplasmic sigma factor (ECF) \(\sigma^{\mathrm{E}}\) is required for full virulence in Mycobacterium tuberculosis, which causes tuberculosis. Many stimuli induce \(\sigma^{\mathrm{E}}\) production, including detergent stress to the cell surface, alkaline pH, heat shock, and oxidative stress. Unlike most ECF sigma factors, \(\sigma^{\mathrm{E}}\) does not regulate its own transcription. Because it is so important in \(M\). tuberculosis pathogenicity, microbiologists want to understand what controls \(\sigma^{\mathrm{E}}\) production. They have discovered that at least three different types of regulation are in play. (1) A two-component regulatory system consisting of MprA and MprB (signal kinase and response regulator, respectively) activates transcription of the \(\sigma^{\mathrm{F}}\) structural gene \(\operatorname{sig} E\) in response to cell surface stress and increases in pH. (2) The \(M\). tuberculosis heatshock sigma factor, \(\sigma^{\mathrm{H}}\), activates transcription of \(\operatorname{sig} E\) in response to heat shock and oxidative stress, and (3) an antisigma factor RsrA binds to and inactivates \(\sigma^{\mathrm{E}}\). Sketch this regulatory network using arrows to represent induction and cross- hatched lines to indicate repression. How might RsrA be regulated so that it is not always bound to \(\sigma^{E}\) ? Suggest an explanation for why \(M\). tuberculosis uses three different regulatory mechanisms to control \(\operatorname{sig} E\) expression. Is this type of regulatory layering unusual in bacterial cells? Explain your answer.