The female reproductive tract is where competition between the sperm of different males takes place, aided and abetted by the female herself. Intense postcopulatory sexual selection fosters inter-sexual conflict and drives rapid evolutionary change to generate a startling diversity of morphological, behavioural and physiological adaptations. We identify three main issues that should be resolved to advance our understanding of postcopulatory sexual selection. We need to determine the genetic basis of different male fertility traits and female traits that mediate sperm selection; identify the genes or genomic regions that control these traits; and establish the coevolutionary trajectory of sexes.

In this paper, I consider the criteria necessary to demonstrate the postcopulatory ability of females to favor the sperm of one conspecific male over another, that is, sperm choice. In practice it is difficult to distinguish between sperm competition and sperm choice, and sperm choice can be demonstrated only if the effects of sperm competition can be controlled. Few studies have used experimental protocols that do this, so evidence for sperm choice is limited. Moreover, in those studies in which sperm choice occurs, it does so to avoid incompatible genetic combinations and is therefore unlikely to result in directional sexual selection.

Human chorionic gonadotropin (hCG) is a heterodimeric molecule consisting of an α-chain common to all members of the glycoprotein hormone family (luteinizing hormone (LH), folliclestimulating hormone (FSH) and thyroid-stimulating hormone (TSH)) non-covalently associated with a β-chain unique to each hormone. However, there is extensive sequence homology between the different β-chains, with LH exhibiting 85%, TSH 46%, and FSH 36% homology with the first 114 of the 145 amino acid residues of hCG. Both the α-and the β-chains are composed of three loops held in place by a cystine knot of three disulfide bonds (Lapthorn et al., 1994; Wu et al., 1994), a structural motif also found in transforming growth factor β (TGF-β), neuronal growth factor (NGF), platelet-derived growth factor β (PDGF-β) and various other growth hormones. One end of both of the subunits comprises loops 1 and 3, which in the β-subunit are stabilized by a fourth disulfide bond, while loop 2 forms the other end of each of the subunits. The α-and β-subunits are oriented opposite to each other in such a way that the paired loops 1 and 3 form each end of a cigar-like molecule ( Fig. 1) with the α-subunit held in place by an additional loop structure in the β-subunit containing two disulfide bonds and referred to as the 'seat belt ' (β91-110). The seat belt is also important in the receptor binding. The unique C-terminal peptide (CTP, β113-145) of the hCGβ-subunit protrudes from the compact molecule without any obviously constrained structure. The hormone is extensively glycosylated, having two N-linked oligosaccharides on each chain and, in addition, four O-linked oligosaccharides located on the serine rich CTP of the β-chain. Although receptor binding requires intact holo-hormone, hCG can be extracted from urine and serum in several different molecular species, reflecting different glycoforms, proteolytic fragments and sometimes the presence of free β-chain.After fertilization, hCG is produced from the eight-cell blastocyst stage onwards, and is initially detectable at days 7-12 after fertilization. Production of hCG is continued by trophoblast cells and promotes the secretion of progesterone from the corpus luteum. After 7 weeks, the synthesis of hCG is switched to the placenta, where the production remains constant until 14-15 weeks, after which time secretion begins to decline. The function of the placenta-derived hCG is not known. While expression of dimeric hCG is associated with trophoblastic neoplasia, non-trophoblastic tumours can express hCG ectopically but, in these tumours, only the β-chain is produced. Therefore, increased serum concentrations of the hormone are used both as an aid to diagnosis and as a marker of established disease. Generation of immune responsesA prerequisite for the induction of an immune response against a protein antigen is that the antigen is taken up by specialized antigen-presenting cells (APC), such as dendritic cells. After proteolytic degradation, selected peptide fragments (T cell epitopes) are expressed on the...

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