2016ToxinsOpen access

Mechanisms that Determine the Differential Stability of Stx+ and Stx− Lysogens

Michael Colon, Dolonchapa Chakraborty, Yonatan Pevzner, Gerald B. Koudelka

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Abstract

Phages 933W, BAA2326, 434, and λ are evolutionarily-related temperate lambdoid phages that infect Escherichia coli. Although these are highly-similar phages, BAA2326 and 933W naturally encode Shiga toxin 2 (Stx⁺), but phage 434 and λ do not (Stx(-)). Previous reports suggest that the 933W Stx⁺ prophage forms less stable lysogens in E. coli than does the Stx(-) prophages λ, P22, and 434. The higher spontaneous induction frequency of the Stx⁺ prophage may be correlated with both virulence and dispersion of the Stx2-encoding phage. Here, we examined the hypothesis that lysogen instability is a common feature of Stx⁺ prophages. We found in both the absence and presence of prophage inducers (DNA damaging agents, salts), the Stx⁺ prophages induce at higher frequencies than do Stx(-) prophages. The observed instability of Stx⁺ prophages does not appear to be the result of any differences in phage development properties between Stx⁺ and Stx(-) phages. Our results indicate that differential stability of Stx⁺ and Stx(-) prophages results from both RecA-dependent and RecA-independent effects on the intracellular concentration of the respective cI repressors.

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Phages 933W, BAA2326, 434, and λ are evolutionarily-related temperate lambdoid phages that infect Escherichia coli. Although these are highly-similar phages, BAA2326 and 933W naturally encode Shiga toxin 2 (Stx⁺), but phage 434 and λ do not (Stx(-)). Previous reports suggest that the 933W Stx⁺ prophage forms less stable lysogens in E. coli than does the Stx(-) prophages λ, P22, and 434. The higher spontaneous induction frequency of the Stx⁺ prophage may be correlated with both virulence and dispersion of the Stx2-encoding phage. Here, we examined the hypothesis that lysogen instability is a common feature of Stx⁺ prophages. We found in both the absence and presence of prophage inducers (DNA damaging agents, salts), the Stx⁺ prophages induce at higher frequencies than do Stx(-) prophages. The observed instability of Stx⁺ prophages does not appear to be the result of any differences in phage development properties between Stx⁺ and Stx(-) phages. Our results indicate that differential stability of Stx⁺ and Stx(-) prophages results from both RecA-dependent and RecA-independent effects on the intracellular concentration of the respective cI repressors.

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Available abstract

Phages 933W, BAA2326, 434, and λ are evolutionarily-related temperate lambdoid phages that infect Escherichia coli. Although these are highly-similar phages, BAA2326 and 933W naturally encode Shiga toxin 2 (Stx⁺), but phage 434 and λ do not (Stx(-)). Previous reports suggest that the 933W Stx⁺ prophage forms less stable lysogens in E. coli than does the Stx(-) prophages λ, P22, and 434. The higher spontaneous induction frequency of the Stx⁺ prophage may be correlated with both virulence and dispersion of the Stx2-encoding phage. Here, we examined the hypothesis that lysogen instability is a common feature of Stx⁺ prophages. We found in both the absence and presence of prophage inducers (DNA damaging agents, salts), the Stx⁺ prophages induce at higher frequencies than do Stx(-) prophages. The observed instability of Stx⁺ prophages does not appear to be the result of any differences in phage development properties between Stx⁺ and Stx(-) phages. Our results indicate that differential stability of Stx⁺ and Stx(-) prophages results from both RecA-dependent and RecA-independent effects on the intracellular concentration of the respective cI repressors.

Key concepts: Prophage, Lysogen, Shiga toxin, Biology, Lysogenic cycle, Escherichia coli, STX2, Microbiology

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