E. coli strain lactose |-lactose | +lactose |+lactose - glucose +glucose glucose
ID: 211161 • Letter: E
Question
E. coli strain lactose |-lactose | +lactose |+lactose - glucose +glucose glucose+ glucose 10 |100 mut1 100 mut1 / F' lac from wt 100 100 100 100 100 100 100 wt / F' lac from mut1 00 mut2 100 mut2I F lac from wt 100 wt /F' lac from mut2 100 mut3 mut3 / F' lac from wt 0 wt / F' lac from mut3 0 100 100 mut4 mut4/ F lac from wt 00 Continued be 100 100 wt / F lac from mut4 0 Identify the defect in each mutant. Not all defects will be placed Mutant 1: Mutant 2: Mutant 3: Mutant 4 deletion of repressor gene super-repressor deletion of operator defective CAP-binding site deletion of CAP geneExplanation / Answer
Answer:
Mutant 1: Deletion of repressor gene
The wt cell contains all the genes that are important to test the questions for the lac permease protein (that's why it is used in the experiment). With the wt cells the table shows that there was only, and always, lac permease production when lactose was present.
The fact that, when considering the mut1 cells or the wt cells with the mut1 lac operon plasmid (F' lac from wt/mut1), there was always lac permease production regardless of the presence or absence of lactose, and in the F' lac from mut1/wt cells there wasn't, tells us that there is a deletion of the repressor gene operator in the mut1 cells.
That repressor binds to the operator when lactose is absent. This is a gene that is outside the operon and therefore there is no repression when considering mut1 cells.
Mutant 2: Deletion of operator
There is always production of lac permease protein, even when there isn't lactose, which means that there isn't an operator for the repressor to bind to. The operator is part of the operon lac and therefore, if it is not present in mut2's operon lac, there won't ever be repression of this operon.
Mutant 3: Defective promoter
Because there seems to be no problem with the regulation of the operon lac when lactose is absent, and there isn't any production of lac permease even when lactose is present, the problem is the activation of the operon by the promotor. When the promotor wt is present there is no problem and the lac permease production occurs normally.
Mutant 4: Deletion of CAP gene
When there is a defective CAP-binding site, the CAP protein cannot bind to the operon. The CAP protein binds to the lac operon whenever glucose is low so that the lac operon is activated. When considering only mut4 cells this activation is not present which indicates a problem with this activation process.
If there is normal production of lac permease whenever wt lac operon is present, it means that the problem is on the actual binding site of the mut4 operon and not in the CAP protein.
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