Temperate phage immunity: The prophage-encoded repressor renders the host cell resistant to lysis initiated by which source?

Introduction:
Temperate phages can integrate into the host genome as prophages under lysogeny. A key feature is “superinfection immunity,” where a prophage-encoded repressor protects the lysogen from subsequent infection by the same or closely related phages that attempt to enter the lytic program.

Given Data / Assumptions:

• A temperate phage encodes a repressor protein.
• We must identify what lytic trigger the repressor blocks.
• Induction of the resident prophage is a distinct process regulated by repressor stability.

Concept / Approach:
The repressor binds operator sites of lytic promoters, preventing expression of lytic genes. This blocks incoming phages of the same immunity group from initiating lytic growth, thereby conferring immunity to superinfection. However, under stress (e.g., DNA damage), repressor cleavage can induce the prophage, allowing it to enter the lytic cycle; this is not “blocked” by the repressor.

Step-by-Step Solution:
Recognize that superinfection immunity targets external lytic attempts by related phages. Differentiate induction of the resident prophage (repressor inactivation) from blocking of superinfecting phages (repressor active). Choose resistance to lytic infection by other related phages as the correct outcome.

Verification / Alternative check:
Lambda phage immunity system (cI repressor) exemplifies how lysogens resist superinfection by lambda-like phages while remaining inducible under SOS conditions.

Why Other Options Are Wrong:

• The resident prophage: Induction occurs when repressor is inactivated; immunity does not prevent this.
• Both (a) and (b): Incorrect because (a) is not blocked under induction.
• None / Environmental lysozyme: Do not represent the genetic immunity mechanism.

Common Pitfalls:
Confusing superinfection immunity with resistance to prophage induction; they are mechanistically distinct.

Final Answer:
The repressor protects against lytic infection by superinfecting related phages.