The evolution of repeated mating under sexual conflict

In insects, repeated mating by females may have direct effects on female fecundity, fertility, and longevity. In addition, a female's remating rate affects her fitness through mortality costs of male harassment and ecological risks of mating such as predation. We analyse a model where these female fitness factors are put into their life-history context, and traded against each other, while accounting for limitations because of mate availability. We solve analytically for the condition when female multiple mating will evolve. We show that the probability that a female mates with a courting male decreases with increases in population density. The extent of conflict between the sexes thus automatically becomes larger at higher densities. However, because at higher densities females meet males at a higher rate, the resulting ESS female remating rate is independent of population density. The female remating probability is in conflict with male adaptations that increase male mating rate by persuading or forcing females to mate, and also in conflict with male adaptations for protecting the own sperm from being removed by future female mates. We show that the relative importance of these conflicts depends on population density

Base of Pore Loop Is Important for Rectification, Activation, Permeation, and Block of Kir3.1/Kir3.4

The Kir3.1/Kir3.4 channel is an inward rectifier, agonist-activated K(+) channel. The location of the binding site within the channel pore that coordinates polyamines (and is thus responsible for inward rectification) and the location of the gate that opens the channel in response to agonist activation is unclear. In this study, we show, not surprisingly, that mutation of residues at the base of the selectivity filter in the pore loop and second transmembrane domain weakens Cs(+) block and decreases selectivity (as measured by Rb(+) and spermine permeation). However, unexpectedly, the mutations also weaken inward rectification and abolish agonist activation of the channel. In the wild-type channel and 34 mutant channels, there are significant (p < 0.05) correlations among the K(D) for Cs(+) block, Rb(+) and spermine permeation, inward rectification, and agonist activation. The significance of these findings is discussed. One possible conclusion is that the selectivity filter is responsible for inward rectification and agonist activation as well as permeation and block

Base of Pore Loop Is Important for Rectification, Activation, Permeation, and Block of Kir3.1/Kir3.4

The Kir3.1/Kir3.4 channel is an inward rectifier, agonist-activated K(+) channel. The location of the binding site within the channel pore that coordinates polyamines (and is thus responsible for inward rectification) and the location of the gate that opens the channel in response to agonist activation is unclear. In this study, we show, not surprisingly, that mutation of residues at the base of the selectivity filter in the pore loop and second transmembrane domain weakens Cs(+) block and decreases selectivity (as measured by Rb(+) and spermine permeation). However, unexpectedly, the mutations also weaken inward rectification and abolish agonist activation of the channel. In the wild-type channel and 34 mutant channels, there are significant (p < 0.05) correlations among the K(D) for Cs(+) block, Rb(+) and spermine permeation, inward rectification, and agonist activation. The significance of these findings is discussed. One possible conclusion is that the selectivity filter is responsible for inward rectification and agonist activation as well as permeation and block