llar transport and consequentially very rapid; all eight axonemes reaching 14 m in length in just 10 min, when formed, lay coiled around the persistent envelope of the single nucleus. Axonemes are largely of conventional 9 + 2 design. The formation of the central pair is severely, although incompletely, disrupted when the armadillo repeat protein PF16 is deleted. At the onset of exflagellation, the axonemes become motile and swim basal body first out of the parental cell. The prior attachment of each basal body to a mitotic spindle pole `ensures’ each basal body drags a haploid genome into the gamete; the gamete then swims through the dense mosquito bloodmeal using alternating periods of fast and slow rotary `ambidextrous’ sinusoidal waves. Microgamete motility is entirely dependent on the import of hexose from the bloodmeal. Protein remodelling of the gamete surfaces The surface proteins of the male and female gametes differ both from each other and from that of the parental gametocytes. Sexual differences between gametes, e.g. expression of P48/45, P230 and HAP2 in male and P47 and the LAP/CCCP proteins in female, may reflect functions in fertilization, and differences between gametocyte and gametes may indicate functions related to gamete survival in the challenging environment of the bloodmeal. Expression of some 169731 proteins in the female gamete, including the surface proteins P25 and P28 on the fertilized zygote, is dependent on the release of their mRNA from translation repression, a process in part regulated by CDPK1. Early defence of the gametes/zygote by expression of a complement regulator factor H-like protein inactivates complement ingested in the bloodmeal; however, the gametes have no defence against antibody attack targeted against proteins secreted onto the gamete surface, making these molecules excellent targets for `contraceptive’ vaccines. P230 is reportedly responsible for the attachment of the male gametes to RBCs in the bloodmeal, although what possible advantage this is to the parasite escapes this writer. Fertilization Fertilization of malaria gametes was first recognized in 1897 and described at the ultrastructural level some 40 years ago. Gamete recognition and binding is mediated through GPI-anchored P47 on female interacting with P230, complexed to GPI-anchored P48/45 on the male cell. The `ambidextrous’ ability of P230 to bind both male- and female-specific moieties may explain the formation of intimately bound same-sex and mixed-sex clusters of gametes/gametocytes in vitro. The fusion of the gamete membranes is now known to be mediated by male-specific HAP2/CSC1 and can PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19822626 be severely disrupted by anti-HAP2 antibodies. Fusion of the gamete nuclei occurs within 1 h of plasma membrane fusion, and is preceded by the decondensation of the chromosomes in the male nucleus. There is substantial transcriptional up-regulation of the zygote genome via AP2O. We do not yet have definitive evidence as to when expression of male-inherited genes begins, but zygote development reportedly can progress in the absence of RNA Danoprevir site polymerase II mediated transcription. Within the mosquito the parasite is from the time of zygote formation until budding of daughter sporozoites from the oocyst a polyploid cell, but cytological study shows that the genetic organization of the parasite, fol- 2014 The Author. Cellular Microbiology published by John Wiley & Sons Ltd, Cellular Microbiology, 17, 451466 Malaria infection 
of the mosquito lowi