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Plasmodium GPI-anchored micronemal antigen is essential for parasite transmission through the mosquito host
Charlie Jennison1, Janna M Armstrong1, Dorender A Dankwa1
1Center for Global Infectious Disease Research, Seattle Children's Research Institute, Washington, Seattle, USA.
Abstract:
Plasmodium parasites, the eukaryotic pathogens that cause malaria, feature three distinct invasive forms tailored to the host environment they must navigate and invade for life cycle progression. One conserved feature of these invasive forms is the micronemes, apically oriented secretory organelles involved in egress, motility, adhesion, and invasion. Here we investigate the role of GPI-anchored micronemal antigen (GAMA), which shows a micronemal localization in all zoite forms of the rodent-infecting species Plasmodium berghei. ∆GAMA parasites are severely defective for invasion of the mosquito midgut. Once formed, oocysts develop normally, however, sporozoites are unable to egress and exhibit defective motility. Epitope-tagging of GAMA revealed tight temporal expression late during sporogony and showed that GAMA is shed during sporozoite gliding motility in a similar manner to circumsporozoite protein. Complementation of P. berghei knockout parasites with full-length P. falciparum GAMA partially restored infectivity to mosquitoes, indicating conservation of function across Plasmodium species. A suite of parasites with GAMA expressed under the promoters of CTRP, CAP380, and TRAP, further confirmed the involvement of GAMA in midgut infection, motility, and vertebrate infection. These data show GAMA's involvement in sporozoite motility, egress, and invasion, implicating GAMA as a regulator of microneme function.
Insights
The GPI-anchored micronemal antigen (GAMA) is crucial for malaria parasite invasion of mosquito midguts and sporozoite motility. Its absence severely impairs parasite infectivity and transmission.
Area of Science:
- Malariology
- Parasitology
- Cell Biology
Background:
- Plasmodium parasites, the causative agents of malaria, possess specialized invasive forms.
- Micronemes are apical secretory organelles essential for parasite egress, motility, adhesion, and invasion.
- GPI-anchored micronemal antigen (GAMA) is localized to micronemes in all Plasmodium zoite forms.
Purpose of the Study:
- To investigate the function of GAMA in Plasmodium berghei.
- To determine GAMA's role in parasite invasion, motility, and egress.
- To assess the conservation of GAMA function across Plasmodium species.
Main Methods:
- Generation and analysis of GAMA knockout (∆GAMA) Plasmodium berghei parasites.
- Epitope-tagging of GAMA to study its expression and shedding.
- Complementation studies using Plasmodium falciparum GAMA in P. berghei knockout parasites.
- Expression of GAMA under heterologous promoters (CTRP, CAP380, TRAP).
Main Results:
- ∆GAMA parasites exhibited severe defects in mosquito midgut invasion.
- Sporozoites lacking GAMA were unable to egress from oocysts and showed defective motility.
- GAMA is expressed late during sporogony and shed during sporozoite gliding.
- Complementation with P. falciparum GAMA partially restored mosquito infectivity.
- Heterologous GAMA expression confirmed its role in midgut infection, motility, and vertebrate infection.
Conclusions:
- GAMA is essential for Plasmodium sporozoite motility, egress, and invasion.
- GAMA plays a critical role in the transmission of malaria parasites to mosquitoes.
- GAMA functions as a regulator of microneme-mediated processes in Plasmodium parasites.
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