Last Updated: 24/02/2026
Epigenetic regulation of the malaria parasite in the mosquito gut
Objectives
This project will undertake a comprehensive investigation aiming to unravel the regulatory mechanisms underlying gene expression in the developing zygote/ookinete and how this might be related to the parasite transmission strategies through the vector.
Malaria is a widespread parasitical disease occurring in tropical and sub-tropical countries with approximately half of the world’s population being at risk. If left untreated, malaria can become life threatening and took about 627’000 lives in 2012, the majority being children and pregnant women in sub-Saharan Africa. It is caused by apicomplexan parasites of the genus Plasmodium, which are transmitted by female Anopheles mosquitoes. When sexual stages of Plasmodium are taken up during a mosquito blood meal, male and female gametes fuse in the mosquito midgut to form a tetraploid zygote. The Plasmodium zygote then develops into a motile stage called the ookinete, which migrates through the mosquito midgut wall and forms an asexually growing sporulation oocyst at the basal lamina. It is known that this journey through the mosquito acts as a bottleneck in the parasite’s life cycle where numbers decrease drastically. Therefore, this is a favourable stage for an intervention to take effect. In the last decade, it has become increasingly clear that epigenetic mechanisms are a very important hallmark in the parasite’s survival strategy within the human host. However, current knowledge of epigenetic orchestration of gene expression in the mosquito-stage parasites is virtually absent. The belief is that detailed understanding of the molecular mechanisms controlling malaria parasite development in the mosquito midgut will add substantially to the understanding of malaria transmission biology. This study will expand current understanding of epigenetics in Plasmodium sexual stages and can pave the way for the testing of epigenetic drugs towards blocking malaria transmission.
Feb 2015 — Jan 2017
$108,552


