A theory worked out by Brian Charlesworth to describe the population genetics of Drosophila transposons as an equilibrium provides a mathematically formal framework for dealing with transposons. I have summarized the application of equilibrium theory to LINE-1 in a lecture to the 18th International Congress of Genetics. The basic theory has a net increase in copy number of a transposon family balanced by an increasingly negative selective pressure based on the accumulated copy number. More generally, the mathematical description is a starting point for conversion of most any model into a mathematical form.
Unfortunately we've gotten in the rut of starting out by saying "selfishness" means that the transposon does nothing for the host. Actually, selfishness springs from the transposon's ability to replicate itself, providing a selective pressure to do so more efficiently. Whether or not is does anything for the host is irrelevant for most of what follows from the ability to self replicate, except perhaps for some protection against stochastic loss.
Emergence in host-transposon relationships
This presentation from a poster at the 1998 SMBE meeting is an attempt to find a conceptual framework less restrictive than equilibrium and more reflective of the role of adaptation by both the host and transposon.
This presentation from a poster at the 1998 SMBE meeting is an attempt to find a conceptual framework less restrictive than equilibrium and more reflective of the role of adaptation by both the host and transposon.
Stochastic loss in its purest sense is when the transposon is lost when it does less well than average in some stochastic process, usually drift. LINE-1 should be vulnerable to that process, since it passes through low population size bottlenecks in a variety of mammalian species. The term "stochastic loss" has been applied less rigorously to virtually any circumstance where the transposon is lost. Other causes of loss could be inability to cope with some adaptive response by the host, competitiion with some other transposon, or a negative interfering interaction with its own defective copies. Whereas complete loss of LINE-1 from a genome appears to be a rare occurance, loss of individual lineages occurs more commonly.
Self-restraint originally implied that the transposon down-regulated itself at high copy number to spare the host from deleterious effects. This thinking always runs afoul of the question "why don't mutant transposons that ignore the regulation overrun the system?". I've found this apparent paradox, reinforced by the observation of transposons that clearly do self-regulate, to be like a wad of chewing gum in the conceptual machinery for over a decade. I think that the only way to resolve it is to say that what happens at high copy number is directly determined by negative selection on the host, like the equilibrium model says. The value of the self-regulation to the transposon is that it turns its rate of transposition up at low copy number to avoid loss. I'm dropping the term "self-restraint" in favor of "self-regulation".
Langley and Charlesworth (1983) have shown how to merge self regulation with their basic fitness function, and to judge whether self regulation is stable. In this scheme, a self-regulated transposon wouldn't be stable unless the unregulated transposon would also come to equilibrium. However, self regulation would alter the equilibrium copy number and fitness of the host, perhaps obscuring the underlying form of the negative selection that maintains the system.