RETRACTED: WHAT DETERMINES SEX ROLES IN MATE SEARCHING?

In a seminal paper, Hammerstein and Parker (1987) described how sex roles in mate searching can be frequency dependent: the need for one sex to perform mate searching is diminished when the opposite sex takes on the greater searching effort. Intriguingly, this predicts that females are just as likely to search as males, despite a higher potential reproductive rate by the latter sex. This prediction, however, is not supported by data: male mate searching prevails in nature. Counterexamples also exist in the empirical literature. Depending on the taxon studied, female mate searching can arise in either low- or high-density conditions, and suggested explanations differ accordingly. We examine these puzzling observations by building two models (with and without sperm competition). When sperm competition is explicitly included, male mate searching becomes the dominant pattern; when it is excluded, male mate searching predominates only if we assume that costs of searching are higher for females. Consequently, two hypotheses emerge from our models. The multiple-mating hypothesis explains male searching on the basis of the ubiquity of sperm competition, and predicts that female searching can arise in low-density situations in which sperm can become limiting. It can also explain cases of female pheromone production, where males pay the majority of search costs. The sex-specific cost hypothesis predicts the opposite pattern of female searching in high-density conditions, and it potentially applies to some species in which sperm limitation is unlikely.     

TO WHAT EXTENT DO DIFFERENT TYPES OF SEX RATIO DISTORTERS INTERFERE?

Within the Diptera, two different selfish genetic elements are known to cause the production of female-biased sex ratios: maternally inherited bacteria that kill male zygotes (male-killers), and X chromosomes causing the degeneration of Y-bearing sperm in males (meiotic drive). We here develop a mathematical model for the dynamics of these two sex-ratio distorters where they co-occur. We show that X chromosome meiotic drive elements can be expected to substantially lower the equilibrium frequency of male-killers and can even lead to their extinction. Conversely, male-killers can also decrease the equilibrium frequency of X drivers and cause their extinction. Thus, we predict that there will be some complementarity in the incidence of X chromosome meiotic drive and male-killing in natural populations, with a lower than expected number of species bearing both elements.     

IS LIFE IMPOSSIBLE? INFORMATION,SEX, AND THE ORIGIN OF COMPLEX ORGANISMS

The earliest organisms are thought to have had high mutation rates. It has been asserted that these high mutation rates would have severely limited the information content of early genomes. This has led to a well‐known “paradox” because, in contemporary organisms, the mechanisms that suppress mutations are quite complex and a substantial amount of information is required to construct these mechanisms. The paradox arises because it is not clear how efficient error‐suppressing mechanisms could have evolved, and thus allowed the evolution of complex organisms, at a time when mutation rates were too high to permit the maintenance of very substantial amounts of information within genomes. Here, we use concepts from the formal theory of information to calculate the amount of genomic information that can be maintained. We identify conditions under which much higher levels of genomic information can be maintained than previously considered possible among origin‐of‐life researchers. In particular, we find that the highest levels of information are maintained when many genotypes produce identical phenotypes, and when reproduction occasionally involves recombination between multiple parental genomes. There is a good reason to believe that these conditions are relevant for very early organisms, and thus the results presented may provide a solution to a long‐standing logical problem associated with the early evolution of life.     

SEX HORMONE STUDIES—The Effects on the Cellular Membrane Potentials and Contractility of lsolated Rat Atrium

The effects of estradiol, testosterone and progesterone on the electrical and mechanical characteristics of rat atria were determined. Cellular membrane potentials were obtained with microelectrodes and the contractility recorded from a sensitive strain gauge. All three steroids at concentrations near 10⁻⁵ M produced characteristic changes in the membrane potentials, the most striking effect being a pronounced slowing of the depolarization of the action potential, without simultaneously reducing the magnitudes of the resting or action potentials. As a result, there was slower impulse conduction in the atria, a lengthening of the action potential and a consequent increase in the refractory period. The repolarization rate was slowed. These changes are due to effects on the transmembrane fluxes of Na⁺ and K⁺, a decrease in permeability being assumed.These effects are similar to those produced by the standard antiarrhythmic drugs, such as quinidine; and these steroids, particularly testosterone, have been found to be potent in the prevention and abolishment of atrial arrhythmias, both in vitro and in vivo. The steroids also block the effects of acetylcholine on the atria and this may play a role in the reduction in excitability and automaticity.Testosterone, but not estradiol nor progesterone, exerts a temporary stimulation of the atrial contractility, which is not due to any effect on the membrane, but is related in some manner more directly to the contractile systems.     

PERSPECTIVE: SEX,RECOMBINATION, AND THE EFFICACY OF SELECTION—WAS WEISMANN RIGHT?

The idea that sex functions to provide variation for natural selection to act upon was first advocated by August Weismann and it has dominated much discussion on the evolution of sex and recombination since then. The goal of this paper is to further extend this hypothesis and to assess its place in a larger body of theory on the evolution of sex and recombination. A simple generic model is developed to show how fitness variation and covariation interact with selection for recombination and illustrate some important implications of the hypothesis: (1) the advantage of sex and recombination can accrue both to reproductively isolated populations and to modifiers segregating within populations, but the former will be much larger than the latter; (2) forces of degradation that are correlated across loci within an individual can reduce or reverse selection for increased recombination; and (3) crossing-over (which can occur at different places in different meioses) will create more variability than having multiple chromosomes and so will have more influence on the efficacy of selection. Several long-term selection experiments support Weismann's hypothesis, including those showing a greater response to selection in populations with higher rates of recombination and higher rates of recombination evolving as a correlated response to selection for some other character. Weismann's hypothesis is also consistent with the sporadic distribution of obligate asexuality, which indicates that clones have a higher rate of extinction than sexuals. Weismann's hypothesis is then discussed in light of other patterns in the distribution of sexuality versus asexuality. To account for variation in the frequency of obligate asexuality in different taxa, a simple model is developed in which this frequency is a function of three parameters: the rate of clonal origin, the initial fitness of clones when they arise, and the rate at which that fitness declines over time. Variation in all three parameters is likely to be important in explaining the distribution of obligate asexuality. Facultative asexuality also exists, and for this to be stable it seems there must be ecological differences between the sexual and asexual propagules as well as genetic differences. Finally, the timing of sex in cyclical parthenogens is most likely set to minimize the opportunity costs of sex. None of these patterns contradict Weismann's hypothesis, but they do show that many additional principles unrelated to the function of sex are required to fully explain its distribution. Weismann's hypothesis is also consistent with what we know about the mechanics and molecular genetics of recombination, in particular the tendency for chromatids to recombine with a homolog rather than a sister chromatid at meiosis, which is opposite to what they do during mitosis. However, molecular genetic studies have shown that cis-acting sites at which recombination is initiated are lost by gene conversion as a result, a factor that can be expected to affect many fine details in the evolution of recombination. In summary, although Weismann's hypothesis must be considered the leading candidate for the function of sex and recombination, nevertheless, many additional principles are needed to fully account for their evolution.     

ARE RELATIONSHIPS BETWEEN POLLEN–OVULE RATIO AND POLLEN AND SEED SIZE EXPLAINED BY SEX ALLOCATION?

Positive correlations between pollen-ovule ratio and seed size, and negative correlations between pollen-ovule ratio and pollen grain size have been noted frequently in a wide variety of angiosperm taxa. These relationships are commonly explained as a consequence of sex allocation on the basis of a simple model proposed by Charnov. Indeed, the theoretical expectation from the model has been the basis for interest in the empirical pattern. However, the predicted relationship is a necessary consequence of the mathematics of the model, which therefore has little explanatory power, even though its predictions are consistent with empirical results. The evolution of pollen-ovule ratios is likely to depend on selective factors affecting mating system, pollen presentation and dispensing, patterns of pollen receipt, pollen tube competition, female mate choice through embryo abortion, as well as genetic covariances among pollen, ovule, and seed size and other reproductive traits. To the extent the empirical correlations involving pollen-ovule ratios are interesting, they will need explanation in terms of a suite of selective factors. They are not explained simply by sex allocation trade-offs.     

SEX RATIO VARIATION AMONG GYNODIOECIOUS POPULATIONS OF SEA BEET: CAN IT BE EXPLAINED BY NEGATIVE FREQUENCY‐DEPENDENT SELECTION?

This study is devoted to assess sex ratio variation among 33 populations of the gynodioecious Beta vulgaris ssp. maritima in Brittany (France) and to explore the causes of this variation. We showed that three different CMS (cytoplasmic male sterility) cytotypes occurred in populations, but strongly differed for their frequencies and the frequency of their associated nuclear restorer alleles (which counteract the effect of CMS and restore male fertility). No correlation was found between CMS and restorer frequencies within populations, which has been previously interpreted as a result of stochasticity. However, neutral genetic variation did not indicate recent population bottlenecks in studied populations. Moreover, no significant correlation was found between female frequency or variance and current population size. Consequently, stochastic processes could not be the major cause of sex ratio variation. Alternatively, empirical estimations of the variation of females, CMS genes and nuclear restorer allele's frequencies were compared to theoretical predictions based on a frequency‐dependent selection model of gynodioecy. In particular, we showed that an absence of correlation between CMS and restorer frequencies could also occur without stochasticity. The large variation of sex ratio in Beta vulgaris could thus be explained by frequency‐dependent selection acting on CMS genes and restorer alleles.     

Does differential selection on the 5S rDNA explain why the rainbow trout sex chromosome heteromorphism is not linked to the SEX locus?

Many but not all rainbow trout strains have morphologically distinguishable sex chromosomes. In these strains, the short arm of the X has multiple copies of 5S rDNA and a bright DAPI band near the centromere, both of which are missing from the Y chromosome, which has a very small short arm. We examined the presence of these markers using fluorescence in situ hybridization (FISH) in four different YY clonal lines derived from different strains and compared the results with sexed fish of the Donaldson strain with the normal X/Y heteromorphism. The Y chromosome in two of the YY clonal lines (Arlee and Swanson) is indistinguishable from the X chromosome and it is positive for 5S rDNA and the DAPI bright band. On the other hand, both 5S rDNA sequences and the DAPI band were not found on the Y chromosome in Hot Creek and Clearwater which have the normal Y. Thus the presence of these two cytogenetic markers may account for the size difference between the short arm of the X and Y chromosome found in most rainbow trout strains. In fishes the expression of one type of 5S rRNA is restricted to oocytes and previous work suggests that although XX males are fairly common, XY females are rare, implying a selective disadvantage for XY females. A hypothesis is presented to explain why this sex chromosome heteromorphism is not closely linked to the SEX locus, which is found on the long arm of the Y chromosome in rainbow trout.     

HOW CAN SEX RATIO DISTORTERS REACH EXTREME PREVALENCES? MALE‐KILLING WOLBACHIA ARE NOT SUPPRESSED AND HAVE NEAR‐PERFECT VERTICAL TRANSMISSION EFFICIENCY IN ACRAEA ENCEDON

Abstract.— Maternally transmitted bacteria that kill male hosts early in their development are found in many insects. These parasites typically infect 1–30% of wild females, but in a few species of insects, prevalences exceed 95%. We investigated one such case in the butterfly Acraea encedon , which is infected with a male-killing Wolbachia bacterium. We measured three key parameters that affect the prevalence of the parasite: transmission efficiency, rate of survival of infected males, and the direct cost of infection. We observed that all wild females transmit the bacterium to all their offspring and that all infected males die in wild populations. We were unable to detect any physiological cost to infection in lab culture. These observations explain the high prevalence of the A. encedon male killer, as theory predicts that under these conditions the parasite will spread to fixation. This will occur provided the death of males provides some benefit to the surviving infected females. The problem therefore becomes why the bacterium has not reached fixation and driven the butterfly extinct due to the shortage of males. We therefore investigated whether males choose to mate with uninfected rather than infected females, as this would prevent the bacterium from reaching fixation. We tested this hypothesis in the "lekking swarms" of virgin females found in the most female-biased populations, and were unable to detect any evidence of mate choice. In conclusion, this male killer has spread to high prevalence because it has a high transmission efficiency and low cost, but the factors maintaining uninfected females in the population remain unknown.     

The Laforin-Like Dual-Specificity Phosphatase SEX4 from Arabidopsis Hydrolyzes Both C6- and C3-Phosphate Esters Introduced by Starch-Related Dikinases and Thereby Affects Phase Transition of α-Glucans

The biochemical function of the Laforin-like dual-specific phosphatase AtSEX4 (EC 3.1.3.48) has been studied. Crystalline maltodextrins representing the A- or the B-type allomorph were prephosphorylated using recombinant glucan, water dikinase (StGWD) or the successive action of both plastidial dikinases (StGWD and AtPWD). AtSEX4 hydrolyzed carbon 6-phosphate esters from both the prephosphorylated A- and B-type allomorphs and the kinetic constants are similar. The phosphatase also acted on prelabeled carbon-3 esters from both crystalline maltodextrins. Similarly, native starch granules prelabeled in either the carbon-6 or carbon-3 position were also dephosphorylated by AtSEX4. The phosphatase did also hydrolyze phosphate esters of both prephosphorylated maltodextrins when the (phospho)glucans had been solubilized by heat treatment. Submillimolar concentrations of nonphosphorylated maltodextrins inhibited AtSEX4 provided they possessed a minimum of length and had been solubilized. As opposed to the soluble phosphomaltodextrins, the AtSEX4-mediated dephosphorylation of the insoluble substrates was incomplete and at least 50% of the phosphate esters were retained in the pelletable (phospho)glucans. The partial dephosphorylation of the insoluble glucans also strongly reduced the release of nonphosphorylated chains into solution. Presumably, this effect reflects fast structural changes that following dephosphorylation occur near the surface of the maltodextrin particles. A model is proposed defining distinct stages within the phosphorylation/dephosphorylation-dependent transition of α-glucans from the insoluble to the soluble state.The metabolism of starch, the most prominent storage carbohydrate in plants, is assumed to require approximately 30 to 40 distinct (iso)enzymes (Deschamps et al., 2008), but, presumably, the list of the starch-related proteins is not yet complete. Several novel proteins (and protein functions) essential for the normal starch metabolism have recently been identified among which are two α-glucan phosphorylating dikinases. One dikinase (glucan, water dikinase [GWD], EC 2.7.9.4) utilizes ATP as dual phosphate donor and esterifies the C6 position of amylopectin-related glucosyl residues, whereas the other dikinase (phosphoglucan, water dikinase [PWD], EC 2.7.9.5) selectively transfers the β-phosphate group from ATP to the C3 position of glucosyl residues (Ritte et al., 2006).Two other previously unknown starch-related enzymes were designated as SEX4 protein (EC 3.1.3.48; At3g52180; previous designations PTPKIS1 and DSP4) and as Like Sex Four1 (LSF1) protein (At3g01510; previously named PTPKIS2; Comparot-Moss et al., 2010). Both proteins are predicted to contain a noncatalytic carbohydrate-binding module (CBM; Boraston et al., 2004; Shoseyov et al., 2006) and a catalytic dual-specificity phosphatase (DSP) domain. The latter is shared by the large family of DSPs that dephosphorylate distinct target phosphoproteins both at phosphotyrosine and phosphoserine/phosphothreonine residues. Some DSPs also act on various nonproteinaceous substrates, such as phospholipids or phosphorylated polyglycans (Pulido and Hooft van Huijsduijnen, 2008).Arabidopsis (Arabidopsis thaliana) mutants lacking a functional SEX4 protein contain both elevated starch levels and significant amounts of soluble phosphooligoglucans that are below the limit of detection in wild-type plants and probably originate from starch. However, the precise biochemical function of SEX4 is far from being clear (Kötting et al., 2009). The phenotype of the SEX4-deficient mutant is complex: Transitory starch possesses an elevated amylose-to-amylopectin ratio but the phosphate content of amylopectin is not increased. It has been hypothesized that SEX4 and LSF1 selectively hydrolyze C6- and C3-phosphate esters, respectively, but experimental evidence is lacking (Kötting et al., 2009). Likewise, it is unknown whether SEX4 preferentially acts on particulate starch or on soluble phosphoglucans.Crystalline maltodextrins (MD_cryst) have recently been introduced as a model mimicking some structural features of the native starch granules (Hejazi et al., 2008). They can be crystallized as either the A- or the B-type allomorph (Gallant et al., 1997; Gérard et al., 2001). Recombinant StGWD phosphorylates both maltodextrin allomorphs with a far higher rate than native starch granules and thereby initiates solubilization of both phosphorylated and nonphosphorylated maltodextrins. In vitro both allomorphs act also as substrate for PWD provided a prephosphorylation by GWD (Hejazi et al., 2009).In this study, we used the prephosphorylated A- and B-type allomorphs of MD_cryst to study biochemical functions of AtSEX4. As highly ordered α-glucans are the preferred sites of the dikinase-mediated phosphorylation, we designed experiments to answer the following questions: Does SEX4 preferentially act on phosphorylated insoluble or soluble glucans? If insoluble α-glucans are the preferred substrate, does the phosphatase distinguish between the A- and the B-type allomorph? Does SEX4 preferentially or selectively hydrolyze C6-phosphate esters? Does SEX4 also interact with nonphosphorylated oligoglucans? Finally, assuming that SEX4 acts on insoluble phosphoglucans, does the removal of phosphate esters affect the phase transition and/or the physical order of the glucans?