
An essential role of the basal body protein SAS ‐6 in P lasmodium male gamete development and malaria transmission
Author(s) -
Marques Sara R.,
Ramakrishnan Chandra,
Carzaniga Raffaella,
Blagborough Andrew M.,
Delves Michael J.,
Talman Arthur M.,
Sinden Robert E.
Publication year - 2015
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12355
Subject(s) - biology , gametogenesis , gamete , basal body , gametocyte , plasmodium (life cycle) , flagellum , centriole , plasmodium berghei , microbiology and biotechnology , zygote , plasmodium falciparum , malaria , genetics , immunology , microtubule , parasite hosting , gene , embryo , embryogenesis , sperm , world wide web , computer science
Summary Gametocytes are the sole P lasmodium parasite stages that infect mosquitoes; therefore development of functional gametes is required for malaria transmission. Flagellum assembly of the P lasmodium male gamete differs from that of most other eukaryotes in that it is intracytoplasmic but retains a key conserved feature: axonemes assemble from basal bodies. The centriole/basal body protein SAS ‐6 normally regulates assembly and duplication of these organelles and its depletion causes severe flagellar/ciliary abnormalities in a diverse array of eukaryotes. Since basal body and flagellum assembly are intimately coupled to male gamete development in P lasmodium , we hypothesized that SAS ‐6 disruption may cause gametogenesis defects and perturb transmission. We show that P lasmodium berghei sas6 knockouts display severely abnormal male gametogenesis presenting reduced basal body numbers, axonemal assembly defects and abnormal nuclear allocation. The defects in gametogenesis reduce fertilization and render Pbsas6 knockouts less infectious to mosquitoes. Additionally, we show that lack of Pbsas6 blocks transmission from mosquito to vertebrate host, revealing an additional yet undefined role in ookinete to sporulating oocysts transition. These findings underscore the vulnerability of the basal body/ SAS ‐6 to malaria transmission blocking interventions.