Phage-Host Genomics

Phage and host genome evolution and CRISPR spacer dynamics

Keywords: Bacteriophages - Population genomics - Convergence evolution - CRISPR-Cas immunity

Whole-Genome Sequence of Myxococcus Phage Mx9

Here, we characterize the genome of Myxococcus phage Mx9, a lysogenic, short-tailed phage (genus Lederbergvirus) phage infecting the bacterial host Myxococcus xanthus, a model for bacterial evolution and development. The 53.5-kb genome has a GC content of 67.5% and contains 98 predicted protein-coding genes, including the previously characterized site-specific integrase gene (int).

Complete Genome Sequence of Myxococcus Phage Mx4

Myxococcus xanthus is a bacterial model in microbial developmental biology and social evolution. Here, I present the 57.0-kb circular genomic sequence of the wild-type Myxococcus phage Mx4, with a GC content of 70.1%. Annotation predicted 97 protein-coding genes. Head-neck-tail protein classification assigns Mx4 to the tailed, Mu-like members of the family Myoviridae of group type 1 (cluster 8).

Review:

Bacteriophages of Myxococcus xanthus, a Social Bacterium

Bacteriophages have been used as molecular tools in fundamental biology investigations for decades. Beyond this, however, they play a crucial role in the eco-evolutionary dynamics of bacterial communities through their demographic impact and the source of genetic information they represent. The increasing interest in describing ecological and evolutionary aspects of bacteria–phage interactions has led to major insights into their fundamental characteristics, including arms race dynamics and acquired bacterial immunity. Here, we review knowledge on the phages of the myxobacteria with a major focus on phages infecting Myxococcus xanthus, a bacterial model system widely used to study developmental biology and social evolution. In particular, we focus upon the isolation of myxophages from natural sources and describe the morphology and life cycle parameters, as well as the molecular genetics and genomics of the major groups of myxophages. Finally, we propose several interesting research directions which focus on the interplay between myxobacterial host sociality and bacteria–phage interactions.

Adaptation to parasites and costs of parasite resistance in mutator and non-mutator E. coli bacteria

Parasitism creates selection for resistance mechanisms in host populations and is hypothesized to promote increased host evolvability. However, the influence of these traits on host evolution when parasites are no longer present is unclear. We used experimental evolution and whole-genome sequencing of Escherichia coli to determine the effects of past and present exposure to parasitic viruses (phages) on the spread of mutator alleles, resistance and bacterial competitive fitness. We found that mutator alleles spread rapidly during adaptation to any of four different phage species, and this pattern was even more pronounced with multiple phages present simultaneously. However, hypermutability did not detectably accelerate adaptation in the absence of phages and recovery of fitness costs associated with resistance. Several lineages evolved phage resistance through elevated mucoidy, and during subsequent evolution in phage-free conditions they rapidly reverted to non-mucoid, phage-susceptible phenotypes. Genome sequencing revealed that this phenotypic reversion was achieved by additional genetic changes rather than by genotypic reversion of the initial resistance mutations. Insertion sequence (IS) elements played a key role in both the acquisition of resistance and adaptation in the absence of parasites; unlike single nucleotide polymorphisms (SNPs), IS insertions were not more frequent in mutator lineages. Our results provide a genetic explanation for rapid reversion of mucoidy, a phenotype observed in other bacterial species including human pathogens. Moreover, this demonstrates that the types of genetic change underlying adaptation to fitness costs, and consequently the impact of evolvability mechanisms such as increased point-mutation rates, depend critically on the mechanism of resistance. Figure (left): Position of genetic changes associated with phage resistance and reversion of mucoidy in genes for which high parallelism was detected (adapted from Wielgoss et al. 2016).