Conference Agenda
Overview and details of the sessions of this conference. Please select a date or location to show only sessions at that day or location. Please select a single session for detailed view (with abstracts and downloads if available).
|
Daily Overview |
| Session | ||
CP4.2: Cells, Molecules and Genes – Tribute to Bob Sinden - 5 min talks
| ||
    | ||
Investigating the role of Kelch13 in Plasmodium falciparum gametocytes University of Melbourne, Australia Resistance of Plasmodium falciparum to artemisinin, the current frontline anti-malarial, greatly threatens global malaria control. Mutations in the parasites' Kelch13 (K13) protein is the major driver behind this resistance. In asexual stages, K13 forms ring at neck of parasites' cytostome, the membrane invagination responsible for haemoglobin uptake from RBC. Activation of artemisinin requires reaction with haem released from digested haemoglobin. K13 mutation is thought to cause resistance through decreasing haemoglobin uptake, causing reduced activation of artemisinin. How K13 modulates this process is undetermined. Despite continued spread of resistance in endemic regions, the role of K13 and K13 mutations on parasite transmission remain unresolved. Using an endogenously tagged version of K13, we imaged K13 throughout gametocyte development, using standard fixes as well as expansion microscopy. Similar to its asexual counterpart, K13 was found to form ring structures throughout gametocyte development, though the amount and the location of these rings varies across stages. In late-stage gametocytes, K13 also forms a hollow tubular structure, likely serving a distinct function compared to the rings. To test if K13 modulates gametocyte sensitivity to artemisinin, we have employed the Knock sideway (KS) system and KS of K13 potentially increases gametocyte survival under artemisinin treatment. Exploring the regulation of sex ratios in Plasmodium berghei. The University of Melbourne, Australia Malaria, caused by single-cell parasites of the genus Plasmodium, currently has a widespread impact on global public health security. As a sexually reproducing species, understanding the sexual biology of Plasmodium is fundamental to developing approaches to control malaria transmission. It is widely accepted that Plasmodium exhibits a female-biased sex ratio (male to female is <1) during gametocyte development and actively adjusts this ratio to promote outcrossing. However, due to the lack of straightforward research models, how Plasmodium controls and changes its sex ratio is still unclear. By genetically manipulating sexual differentiation in Plasmodium berghei, we could artificially bias sex ratio. Using this system, we found that, contrary to existing evidence, when the growth of the parasite stabilizes, the sex ratio of the gametocytes (male to female) is close to 1:1. Furthermore, isogenic parasite lines do not modify sex ratio in response to an overabundance of one sex. | ||