Please explain clear and different to the answers that arealready in other websites. Thank you
1. An interesting mutation in lacI results inrepressors with 110-fold increased binding to both operator andnonoperator DNA. These repressors display a “reverse†inductioncurve, allowing β-galactosidase synthesis in the absence of aninducer (IPTG) but partly repressing β-galactosidase expression inthe presence of IPTG. How can you explain this? (Note that, whenIPTG binds a re- pressor, it does not completely destroy operatoraffinity, but rather it reduces affinity 110-fold. Additionally, ascells divide and new operators are generated by the synthesis ofdaughter strands, the repressor must find the new operators bysearching along the DNA, rapidly binding to nonoperator sequencesand dissociating from them.)
2. Certain lacI mutations eliminate operator binding by the Lacrepressor but do not affect the aggregation of subunits to make atetramer, the active form of the re- pressor. These mutations arepartly dominant over wild type. Can you explain the partly dominantI− pheno- type of the I−/I+ heterodiploids?
3. You are examining the regulation of the lactose operon in thebacterium Escherichia coli. You isolate seven new inde- pendentmutant strains that lack the products of all three structuralgenes. You suspect that some of these muta- tions are lacISmutations and that other mutations are al- terations that preventthe binding of RNA polymerase to the promoter region. Usingwhatever haploid and partial diploid genotypes that you think arenecessary, describe a set of genotypes that will permit you todistinguish be- tween the lacI and lacP classes of uninduciblemutations.
