Q.72. The resistance of a lambda lysogenic E.coli to re-infection by lambda is mediated by
(A) blocking entry of the incoming lambda DNA
(B) degrading the incoming lambda DNA
(C) blocking transcription of the incoming lambda DNA
(D) triggering mutation of the lambda receptor of the host
The correct answer is: (C) blocking transcription of the incoming lambda DNA.
In a λ-lysogenic E. coli, the prophage expresses the CI repressor, which binds to operators on any newly entering λ DNA and prevents its transcription, thereby conferring “superinfection immunity.”
Correct Answer Explained: Option (C)
In a λ lysogen, the integrated prophage constitutively produces the CI repressor protein.
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CI binds specifically to operator sites (OL, OR) on any incoming λ DNA.
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This binding blocks transcription from the major promoters (PL, PR), so early lytic genes of the superinfecting phage cannot be expressed.
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As a result, the incoming λ genome cannot initiate lytic development or establish a new lysogen and is eventually diluted out as the host cell divides.
Thus, resistance to re‑infection in a classical λ lysogen is mediated at the level of transcriptional repression of the incoming lambda DNA, matching option (C).
Why the Other Options Are Incorrect
Option (A) Blocking entry of the incoming lambda DNA
Superinfection immunity in canonical λ lysogens is not primarily due to preventing DNA entry.
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In the standard textbook case, λ DNA does enter the lysogenic cell.
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The immunity is then enforced by CI repressor acting on this incoming DNA, not by blocking adsorption or injection.
While some naturally occurring lysogens can evolve receptor-based resistance that reduces phage adsorption or DNA entry, this is distinct from the classic immunity mechanism asked about in this question.
Option (B) Degrading the incoming lambda DNA
There is no specific λ-encoded system in the classical immunity model that degrades incoming λ DNA to confer superinfection immunity.
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Restriction–modification or CRISPR–Cas systems can degrade phage DNA in other contexts, but λ immunity is defined by CI-mediated repression, not targeted degradation.
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The incoming λ genome generally remains intact but transcriptionally silent and is lost by dilution during cell growth.
Therefore, degradation of incoming λ DNA is not the principal mechanism of λ lysogen resistance to re‑infection.
Option (D) Triggering mutation of the lambda receptor of the host
Lambda uses the LamB (maltoporin) protein of E. coli as its receptor.
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Mutations in lamB can indeed make cells resistant to λ infection by preventing adsorption, but this is a host mutation–based resistance, not the normal prophage-encoded immunity mechanism.
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The classical question on λ lysogen “resistance” refers to phage-encoded superinfection immunity via CI repressor, not to spontaneous host receptor mutations.
Thus, option (D) describes a possible evolutionary outcome but not the standard mechanistic basis of λ lysogen immunity tested in this MCQ.
Quick Exam-Oriented Summary
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Key mechanism: CI repressor from prophage binds operators on incoming λ DNA and shuts off its transcription.
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What still happens: Incoming λ can adsorb and inject DNA, but cannot express early genes needed for lytic growth or new lysogeny.
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So:
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(A) Incorrect – DNA entry is not the main blocked step.
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(B) Incorrect – no specific immunity pathway via DNA degradation.
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(C) Correct – immunity works by blocking transcription of incoming λ DNA.
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(D) Incorrect in this context – receptor mutation is host-based resistance, not classical λ immunity.
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