Table 1.
Mechanisms selecting gene-prophage associations plus primarily benefiting entities.
| Selecting mechanism | Benefiting entities | ||||
|---|---|---|---|---|---|
| gene | bacterium | bacter. pop. | phage | ||
| 1 | Gene survival via greater mobility | ✓a | ✗b | ✗c | ✗ |
| 2 | Genetic hitchhiking on more-fit bacterial lineages | ✓ | ✗ | ✗ | ✗ |
| 3 | Gene escape from immune surveillance | ✓ | ✗ | ✗ | ✗ |
| 4 | Gene extrabacterial survival | ✓ | ✗ | ✗c | —d |
| 5 | Faster gene evolution | ✓ | —e | —e | — |
| 6 | Epistasis linking VF and phage genes | — | ✓f | ✓g | — |
| 7 | Dissemination of an effective toxin dose | —h | ✗i | ✓g | — |
| 8 | Lysogen allelopathy | — | ✗i | ✓j | — |
| 9 | Direct enhancement of phage fitness | — | ✗ | ✗ | ✓ |
| 10 | Indirect enhancement of phage fitness | — | ✗ | ✗ | ✓k |
In constructing this table we assume that if at any time a gene/allele contributes to the fitness of a harboring organism, then that gene is under positive natural selection. We indicate (with a tick) that the gene is a primarily benefiting entity only when gene benefits cannot be explained solely on the basis of enhancing the fitness of a or the harboring organism.
We employ a cross to indicate a relative lack of benefits to the indicated entity. We do not distinguish in this table between selection acting on prophage versus uninduced bacterial lysogens.
An alternative view is that gene mobility and extra-bacterial survival (ie, as within phage virions) can be beneficial to bacterial populations or communities by retaining a reserve of functions among bacteria, but we would view hypotheses based solely on such a perspective to be inherently group selectionist, especially given arguments that bacteria do not retain gene exchange mechanisms for the sake of gene exchange (Redfield 1993; Redfield 2001) and therefore likely do not contribute greatly to a retention of gene-prophage associations.
Phage fitness-enhancing effects we consider solely in rows 9 and 10. We indicate absence of any comment on utility with the symbol —.
Our arguments assume that faster gene evolution requires gene mobility (see c, above).
Such linkage can contribute to VF survival independent of bacterial fitness (as indicated in row 4), but in other cases may be considered to contribute to VF expression and thereby to bacterial fitness.
Because VF deployment in some instances requires expressing-bacteria death, we also invoke “bacterial population” as a potential beneficiary of this deployment.
Dissemination should contribute to gene mobility, but gene mobility we cover in rows 1–3.
Since these mechanisms involve phage-induced lysis of phage-producing bacteria, the benefiting entity would be the bacterial population rather than the producing bacterium.
Lysogen allelopathy we speculate can augment the fitness advantages associated with gene-prophage associations rather than representing a mechanism sufficient to explain such associations.
This enhancement could occur in terms of phage replication or dissemination, and mechanisms which may enhance phage dissemination within or between environments could presumably also enhance bacterial dissemination within or between environments.