1. Viral gene expression after T3 bacteriophage infection is controlled by:
(1) Repressor molecule.
(2) Modification of RNA polymerase
(3) Slow injection of nucleic acid.
(4) DNA polymerase.

Bacteriophage T3 is a well-studied virus that infects Escherichia coli and is closely related to phage T7. A key aspect of T3’s successful infection strategy is its ability to precisely control the timing and specificity of viral gene expression. Understanding the molecular mechanism behind this control reveals insights into both phage biology and the broader field of gene regulation.

Mechanism of Gene Expression Control in T3 Bacteriophage

After T3 infects a bacterial cell, the phage must quickly redirect the host’s transcription machinery to prioritize viral gene expression over the host’s own genes. This is achieved through a sophisticated mechanism centered on modification of RNA polymerase.

Stepwise Control:

1. Early Gene Expression Using Host RNA Polymerase:
   Immediately after infection, T3 utilizes the host’s E. coli RNA polymerase to transcribe its early genes. These early gene products are essential for taking over the host cell and preparing for viral replication.

2. Phage-Encoded RNA Polymerase for Middle and Late Genes:
   One of the early gene products is the T3-encoded RNA polymerase. This phage-specific enzyme is highly selective, recognizing only T3-specific promoter sequences. As infection progresses, this RNA polymerase takes over, transcribing the middle and late genes required for phage assembly and lysis1246.

3. Modification of Host RNA Polymerase:
   T3 also produces protein factors that modify the host RNA polymerase, changing its promoter specificity or inhibiting its activity. This ensures that host transcription is suppressed and the cellular machinery is redirected toward viral gene expression16.

Why RNA Polymerase Modification is Central

• Temporal Regulation:
  By switching from host to phage RNA polymerase, T3 achieves precise temporal control—early genes are transcribed first, followed by middle and late genes as the infection advances124.

• Promoter Specificity:
  The T3 RNA polymerase is uniquely tailored to recognize T3 promoters, ensuring only viral genes are expressed during the later stages of infection34.

• Host Takeover:
  Modification of the host RNA polymerase shuts down host gene expression, freeing up resources for phage replication16.

Why Other Options Are Incorrect

• Repressor molecule:
  While repressors are used by some phages (like lambda), T3 relies on polymerase modification and its own RNA polymerase for gene regulation16.

• Slow injection of nucleic acid:
  This is a characteristic of phage T5, not T3.

• DNA polymerase:
  DNA polymerase is essential for replication, not for the regulation of gene expression.

Summary Table: Control Mechanisms in T3 Phage Infection

Conclusion

After T3 bacteriophage infects a bacterial cell, viral gene expression is controlled by modification of RNA polymerase. This ensures a tightly regulated transcriptional program, allowing the phage to efficiently hijack the host’s machinery and produce new viral particles. This strategy is a hallmark of T3 and T7 phages and is central to their success as infectious agents