Abstract
A shared feature of the motile stages (zoites) of malaria parasites is a cortical cytoskeletal structure termed subpellicular network (SPN), thought to define and maintain cell shape. Plasmodium alveolins comprise structural components of the SPN, and alveolin gene knockout causes morphological abnormalities that coincide with markedly reduced tensile strength of the affected zoites, indicating the alveolins are prime cell shape determinants. Here, we characterize a novel SPN protein of Plasmodium berghei ookinetes and sporozoites named G2 (glycine at position 2), which is structurally unrelated to alveolins. G2 knockout abolishes parasite transmission and causes zoite malformations and motility defects similar to those observed in alveolin null mutants. Unlike alveolins, however, G2 contributes little to tensile strength, arguing against a cause-effect relationship between tensile strength and cell shape. We also show that G2 null mutant sporozoites display an abnormal arrangement of their subpellicular microtubules. These results provide important new understanding of the factors that determine zoite morphogenesis, as well as the potential roles of the cortical cytoskeleton in gliding motility.