Alp system has a key role in cell lysis of pyocin-producing Pseudomonas aeruginosa cells

Abstract

Pseudomonas aeruginosa produces intraspecific bacteriophage-like killing complexes, called pyocins, in response to DNA damage. The pyocins are only capable of killing nearby, susceptible P. aeruginosa cells. However, to permit the relatively large pyocin complexes to escape the cell, producer cells must die via programmed cell lysis. The canonical pathway induced by DNA damage is dependent on recA and unlocks a cascade of events that activates a cluster of pyocin-encoding genes, including genes encoding auto-lysing holin and lysin enzymes. In regard to the subset of pyocin producing cells, it was previously thought that these two enzymes were the main regulators of pyocin release via lysis. Indeed, pyocin-producing cells lyse in a wild-type background after DNA damage and also in a xerC mutant strain that produces pyocins without DNA damage and independently of recA. However, additional genes found outside of the pyocin cluster, the alp genes, are also involved in mediating cell lysis in the presence of DNA damage. My research is aimed at understanding if and how the alp system is involved in the lysis of pyocin producing cells in the wild-type PA14 background or the ΔxerC mutant background. I present evidence that the alpBCDE genes, which include the holin-encoding alpB gene, have a key role in the cell lysis that releases pyocins.