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An Haemophilus influenzae mutant which inhibits the growth of HP1c1 phage
Abstract:
A strain of Haemophilus influenzae, called hpm- inhibits the growth of phage HP1c1 but not S2. This inhibition is overcome by HP1c1ph mutants. Phage HP1c1 adsorbs normally to hpm- cells but only a small fraction of infected cells produce phage with a normal burst size or become lysogenic. When hpm- strains lysogenic for HP1c1 are induced, 100 percent of the cells yield phage. There is no degradation of phage DNA after infection of hpm- cells and HP1c1 can normally grow when its DNA is introduced into hpm- by transfection. The most probable explanation is that in hpm- cells the penetration of phage DNA is blocked. The hpm- property behaves as as unstable mutation.
Insights
A specific Haemophilus influenzae strain (hpm-) blocks phage HP1c1 DNA penetration, preventing its growth. This bacterial mutation is unstable and can be overcome by specific phage mutants.
Area of Science:
- Microbiology
- Bacteriology
- Virology
Background:
- Haemophilus influenzae is a significant human pathogen.
- Bacteriophages are viruses that infect bacteria and play roles in bacterial evolution and gene transfer.
- Understanding phage-host interactions is crucial for both basic research and potential therapeutic applications.
Purpose of the Study:
- To investigate the mechanism by which a specific strain of Haemophilus influenzae, designated hpm-, inhibits the growth of bacteriophage HP1c1.
- To characterize the nature of the hpm- mutation and its effect on phage infection dynamics.
Main Methods:
- Comparative growth studies of phage HP1c1 and S2 on wild-type and hpm- Haemophilus influenzae strains.
- Adsorption assays to determine phage binding efficiency.
- Burst size determination and lysogenization frequency analysis.
- Transfection experiments to assess the viability of phage DNA in hpm- cells.
Main Results:
- The hpm- strain specifically inhibited HP1c1 growth, while phage S2 remained unaffected.
- Phage HP1c1 adsorption to hpm- cells was normal, but phage production and lysogenization were significantly reduced.
- Induced lysogenic hpm- strains yielded 100% phage production, indicating the defect was not in phage replication post-induction.
- No degradation of phage DNA was observed, and transfection with HP1c1 DNA into hpm- cells resulted in normal phage growth.
- The hpm- mutation was found to be unstable.
Conclusions:
- The primary mechanism of inhibition by the hpm- strain is the blockage of phage HP1c1 DNA penetration into the bacterial cell.
- This defect in DNA entry is specific to HP1c1 and does not affect phage S2 or the integrity of phage DNA once inside the cell.
- The unstable nature of the hpm- mutation suggests a potential role in bacterial defense mechanisms or genetic instability.