Premium
Morphogenesis of P lasmodium zoites is uncoupled from tensile strength
Author(s) -
Tremp Annie Z.,
Carter Victoria,
Saeed Sadia,
Dessens Johannes T.
Publication year - 2013
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12297
Subject(s) - biology , morphogenesis , cytoskeleton , motility , microbiology and biotechnology , plasmodium berghei , mutant , actin , null allele , microtubule , cell , gene , genetics , immunology , malaria
Summary 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. P lasmodium 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 P lasmodium berghei ookinetes and sporozoites named G 2 (glycine at position 2), which is structurally unrelated to alveolins. G 2 knockout abolishes parasite transmission and causes zoite malformations and motility defects similar to those observed in alveolin null mutants. Unlike alveolins, however, G 2 contributes little to tensile strength, arguing against a cause‐effect relationship between tensile strength and cell shape. We also show that G 2 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.