Competition occurs in two forms: individuals compete indirectly by consuming resources and thus depriving others of those (exploitative competition); and can compete directly by harming others through antagonistic interactions (interference competition) [ 4].
Exploitation competition is inevitable whenever parasites do not have completely separate niches within the host, while interference competition via antagonistic compounds drives, for example, the interaction between strains of entomopathogenic bacteria that produce bacteriocins [ 17].
Degeneration of gene function is a key feature of evolving Y chromosomes, and the interference generated by sexually antagonistic alleles could contribute to this process [4], [5].
Hitchhiking of deleterious mutations with sexually antagonistic alleles is a form of interference previously proposed to facilitate Y-chromosome degeneration [58].
While the three sense/antisense pairs may have the potential for RNA interference, we find no indication for antagonistic interactions of the transcript in our experimental system (Figure 3).
The mechanism of competition can be: (1) exploitation, with parasites competing for resources, (2) interference, with parasites, for example, producing antagonistic compounds, or (3) apparent, being mediated by the host immune system [ 5].
These results suggest that NO effects on cell cycle genes are independent of its interference with cAMP signaling, since cAMP analog (the opposite signal) was not antagonistic to the actions of NO.
With the exception of a moderate effect on the antisense gene of pair 1 (Figure 3A), none of these lines showed antagonistic changes in transcript levels of the partner genes, which does not argue for RNA interference or other quantitative effects regulating transcript levels (Figure 3).
On the other hand, if antagonistic interactions are prevailing and shared preference entails net costs due to increased exploitation or interference competition [ 20],[ 26] avoidance of boxes with symbols previously associated to conspecifics and/or heterospecifics is expected.
Thus, assuming that selection fluctuates to some degree through time (which it always will, unless coevolution is a pure GFGM and resistance and infectivity evolution is cost-free) during antagonistic coevolution, we predict unimodal relationships between the rate of evolution and migration rate when clonal interference can occur.
