Journal
MOLECULAR MICROBIOLOGY
Volume 60, Issue 6, Pages 1355-1363Publisher
WILEY
DOI: 10.1111/j.1365-2958.2006.05189.x
Keywords
-
Categories
Funding
- MRC [G120/746] Funding Source: UKRI
- Medical Research Council [G120/746] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
Ask authors/readers for more resources
Apicomplexan parasites critically depend on a unique form of gliding motility to colonize their hosts and to invade cells. Gliding requires different stage and species-specific transmembrane adhesins, which interact with an intracellular motor complex shared across parasite stages and species. How gliding is regulated by extracellular factors and intracellular signalling mechanisms is largely unknown, but current evidence suggests an important role for cytosolic calcium as a second messenger. Studying a Plasmodium berghei gene deletion mutant, we here provide evidence that a calcium-dependent protein kinase, CDPK3, has an important function in regulating motility of the ookinete in the mosquito midgut. We show that a cdpk3(-) parasite clone produces morphologically normal ookinetes, which fail to engage the midgut epithelium, due to a marked reduction in their ability to glide productively, resulting in marked reduction in malaria transmission to the mosquito. The mutant was successfully complemented with an episomally maintained cdpk3 gene, restoring mosquito transmission to wild-type level. cdpk3(-) ookinetes maintain their full genetic differentiation potential when microinjected into the mosquito haemocoel and cdpk3(-) sporozoites produced in this way are motile and infectious, suggesting an ookinete-limited essential function for CDPK3.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available