Impact of spontaneous prophage induction on the fitness of bacterial populations and host-microbe interactions

Abstract

Bacteriophages and genetic elements, such as prophage-like elements, pathogenicity islands, and phage morons, make up a considerable amount of bacterial genomes. Their transfer and subsequent activity within the host's genetic circuitry have had a significant impact on bacterial evolution. In this review, we consider what underlying mechanisms might cause the spontaneous activity of lysogenic phages in single bacterial cells and how the spontaneous induction of prophages can lead to competitive advantages for and influence the lifestyle of bacterial populations or the virulence of pathogenic strains.

FIG 1

SOS-dependent SPI. A host of extrinsic and intrinsic factors have an influence on the host genome and can lead to spontaneous DNA lesions or stalled polymerases laying bare single-stranded DNA bound by polymerizing RecA proteins. The nucleoprotein filament in turn triggers the autocatalytic cleavage of LexA or CI-like phage repressors. Alleviation of LexA repression leads to the expression of SOS genes—initiating cell growth inhibition and DNA repair. An alternative route is the inactivation of the phage repressor by binding to antirepressor proteins. Inactivation of phage repressors leads to the derepression of the lytic promoters which facilitate the excision of the prophage from the host genome and its packaging into virions and release from the cell by holin- and lysin-mediated cell lysis.

FIG 2

Impact of SPI on host physiology. Spontaneous induction of lysogenic prophages can have manifold effects, such as enhancing biofilm formation, playing a vital role in bacterial virulence or leading to horizontal gene transfer of its own DNA (including virulence factors) and of host genes.