Question at position 6 The arbinose BAD operon (araBAD) is required for the breakdown of the sugar arabinose and is regulated by AraC. There is no expression of araBAD in E. coli that harbor either wild type AraC in the absence of arabinose or an AraC operator binding mutant in the presence or absence of arabinose. Which of the following best explains these observations?AraC promotes transcription in absence of arabinose.AraC promotes transcription in the absence of arabinose, but blocks transcription in the presence of arabinose.AraC promotes transcription in the presence of arabinose.AraC blocks transcription in the absence of arabinose and promotes transcription in the presence of arabinose.AraC blocks transcription in the presence of arabinose.

Question

Question at position 6 The arbinose BAD operon (araBAD) is required for the breakdown of the sugar arabinose and is regulated by AraC. There is no expression of araBAD in E. coli that harbor either wild type AraC in the absence of arabinose or an AraC operator binding mutant in the presence or absence of arabinose. Which of the following best explains these observations?AraC promotes transcription in absence of arabinose.AraC promotes transcription in the absence of arabinose, but blocks transcription in the presence of arabinose.AraC promotes transcription in the presence of arabinose.AraC blocks transcription in the absence of arabinose and promotes transcription in the presence of arabinose.AraC blocks transcription in the presence of arabinose.

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Question context: The arabinose operon (araBAD) in E. coli is regulated by AraC, and the observed phenotype is that there is no expression of araBAD when either wild-type AraC is present without arabinose or an AraC operator-binding mutant is present with or without arabinose. We must evaluate the options to explain this behavior.
Option 1: 'AraC promotes transcription in absence of arabinose.' This would predict some transcription when arabinose is absent, which contradicts the observation of no expression under that condition. Therefore this statement is incorrect.
Option 2: 'AraC promotes transcription in the absence of arabinose, but blocks transcription in the presence of arabinose.' Here, AraC would activate without arabinose and repress with arabinose, which is the opposite of the known mechanism where arabinose presence relieves repression and activates transcription. This makes the option inconsistent with the established model.
Option 3: 'AraC promotes transcription in the presence of arabinose.' While this captures part of the activating role, it ignores the fact that in the absence of arabinose AraC can repress the operon by forming a loop, leading to no transcription. Thus this option is incomplete and not accurate on its own.
Option 4: 'AraC blocks transcription in the absence of arabinose and promotes transcription in the presence of arabinose.' This aligns with the classic mechanism: without arabinose, AraC binds to the operator in a way that represses transcription; when arabinose is present, AraC undergoes a conformational change that promotes transcription of araBAD. This matches the observed lack of expression in the absence of arabinose and wild-type AraC, and the proper induction in its presence.
Option 5: 'AraC blocks transcription in the presence of arabinose.' This directly contradicts the inducer role of arabinose and would not explain induced expression when arabinose is present. Therefore it is incorrect.
In summary, the only option that coherently explains both the repression in the absence of arabinose and the activation in its presence, including how an operator-binding mutant could fail to express under all conditions, is the scenario where AraC blocks transcription without arabinose and promotes transcription with arabinose. The reasoning hinges on AraC’s dual role as a repressor in the absence of inducer and as an activator in the presence of inducer, enabling arabinose metabolism only when the sugar is available.

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