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. 1991 May;173(9):2733–2738. doi: 10.1128/jb.173.9.2733-2738.1991

Interference with phage lambda development by the small subunit of the phage 21 terminase, gp1.

G Johnson 1, W Widner 1, W N Xin 1, M Feiss 1
PMCID: PMC207852  PMID: 1826903

Abstract

Bacteriophage lambda development is blocked in cells carrying a plasmid that expresses the terminase genes of phage 21. The interference is caused by the small subunit of phage 21 terminase, gp1. Mutants of lambda able to form plaques in the presence of gp1 include sti mutants. One such mutation, sti30, is an A. T-to-G.C transition mutation at base pair 184 on the lambda chromosome. The sti30 mutation extends the length of the ribosome-binding sequence of the Nul gene that is complementary to the 3' end of the 16S rRNA from GGA to GGAG. The sti30 mutation causes a approximately 50-fold increase in the level of expression of a Nul-lacZ reporter gene, indicating that the sti30 mutation overcomes the gp1 inhibition by increasing the level of expression of gpNul. Although the Nul and A genes of lambda overlap, the sti30 mutation has little effect on the level of gpA expression, indicating that translational coupling does not occur.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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