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Malaria parasites lacking eef1a have a normal S/M phase yet grow more slowly due to a longer G 1 phase
Author(s) -
Janse Chris J.,
Haghparast Alireza,
Sperança Márcia A.,
Ramesar Jai,
Kroeze Hans,
Del Portillo Hernando A.,
Waters Andrew P.
Publication year - 2003
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 - 10.1046/j.1365-2958.2003.03820.x
Subject(s) - biology , gametocyte , cell cycle , plasmodium berghei , parasite hosting , gene , microbiology and biotechnology , mutant , flow cytometry , plasmodium (life cycle) , apicomplexa , genetics , malaria , virology , plasmodium falciparum , immunology , world wide web , computer science
Summary Eukaryotic elongation factor 1A (eEF1A) plays a central role in protein synthesis, cell growth and morphology. Malaria parasites possess two identical genes encoding eEF1A (e ef1aa and eef1ab ). Using pbeef1a – Plasmodium berghei mutants that lack an eEF1a gene, we demonstrate that the level of eEF1A production affects the proliferation of blood stages and parasite fitness. Pbeef1a – parasites can complete the vertebrate and mosquito phases of the life cycle, but the growth phase of the asexual blood stages is extended by up to 20%. Analysis of the cell cycle by flow cytometry as well as transcriptional analyses revealed that the duration of the S and M phases and the number of daughter cells produced were not detectably affected, but that the G 1 phase is elongated. Thus, as in budding yeast, a growth threshold must be achieved by blood‐stage Plasmodium parasites to permit transition from G 1 into S/M phase. Initial analyses indicate that transcriptional events associated with gametocyte development were not remarkably retarded. Insight into protein synthesis and its influence on cell proliferation might be used to generate slow‐growing (attenuated) parasites.