This might come as a shock to many, but mosquitoes, which are by far the most prevalent agents of malaria in the world, are not big fans of the parasite themselves. In fact, members of the Anopheles genus have developed an immune pathway to fend-off infection by the Plasmodium, similar to that employed by eukaryotes. However, an alternative agenda of males has resulted in a peculiar evolution of the gene, leaving the system less robust.
The main genetic culprit responsible for the immune response to Plasmodium falciparum in mosquitoes is a polymorphic gene TEP1, which has its counterparts in the complement system of eukaryotes – one of the most important (and complex) parts of our immune system. TEP1 protein is able to recognize and mark Plasmodium cells for destruction, thus reducing the likelihood that the she-mosquito will be infected herself.
TEP1 gene consists of multiple alleles, and, perhaps most curiously, not all of them contribute to the fitness of the mosquito. For example, R1 and R2 classes of alleles ensure efficient elimination of the parasite; however S1 and S2 determine quite the opposite – sensitivity to the Plasmodium infection. This, naturally, begs a question – if the alleles result in reduced fitness of the mosquito, how are they maintained during the course of evolution?
Pompon and Levashina (2015), who reported their results in PLOS Biology last month, have set out to solve the puzzle by thinking outside the box, and looking at the role of TEP1 not only in female mosquitos, which are the main carriers of the Plasmodium, but males as well, and found the counter-intuitive nature of TEP1 might have evolved due to its dual role in Anopheles.
According to their research, TEP1, along with other players of the complement-like cascade, is also prevalent in the testes of Anopheles gambiae males, where it helps to destroy defective sperm cells during the most active stage of reproduction. This thus increases the male fecundity, ensuring that even otherwise unfavorable alleles of TEP1 are maintained in the population.
The defective spermatozoids are purified by exactly the same mechanism as the one used to kill malaria parasites – by labelling the cells for destruction. This is by far the first report of mosquito complement-like system involved in fertility as well, and explains the evolutionary peculiarity of the gene.
Unfortunately for us humans, however, the alternative role of TEP1 in male reproduction also means more infected females and increased likelihood of malaria transmission to people.
Written by Eglė Marija Ramanauskaitė