Entry of λ phage lysogen to lytic phase is triggered by loss of co-operativity in binding of λ repressor, making option (B) correct. This occurs during SOS response when RecA cleaves CI repressor, disrupting its cooperative binding to operator sites.

Option Analysis

(A) Mutation in the λ genome

Mutations could affect lysogeny maintenance but don’t represent the primary physiological trigger for induction. Natural prophage activation relies on host DNA damage response, not spontaneous genome changes.

(B) Loss of co-operativity in binding of λ repressor

DNA damage activates RecA, which cleaves CI repressor dimers. Cleaved monomers lose cooperative binding to OR1/OR2 operator sites, derepressing PR/PL promoters and allowing Cro expression that commits to lytic cycle.

(C) Increase in the λ repressor concentration

Higher CI levels strengthen lysogeny by repressing lytic genes more effectively. This maintains prophage repression, opposite of induction.​

(D) Decrease in recA function

RecA is essential for induction; its inactivation prevents CI cleavage, blocking lysogen-to-lytic switch. Mutants with reduced RecA maintain stable lysogeny.​

λ Phage Lysogen Lytic Phase Induction Mechanism

λ phage lysogen to lytic phase transition occurs when DNA damage triggers RecA-mediated cleavage of CI repressor, causing loss of co-operativity in binding to operator sites OR1/OR2. This derepresses lytic promoters PR and PL.

Repressor Binding Co-operativity Breakdown

Intact CI dimers bind cooperatively: CI at OR1 recruits additional CI to OR2, maintaining lysogeny. SOS-induced cleavage produces monomers that bind only weakly, allowing Cro transcription and lytic commitment.