Perturbation of phosphatidylethanolamine synthesis affects mitochondrial morphology and cell-cycle progression in procyclic-form Trypanosoma brucei

Signorell, A. , Gluenz, E. , Rettig, J. , Schneider, A. , Shaw, M. K. , Gull, K. and Bütikofer, P. (2009) Perturbation of phosphatidylethanolamine synthesis affects mitochondrial morphology and cell-cycle progression in procyclic-form Trypanosoma brucei. Molecular Microbiology, 72(4), pp. 1068-1079. (doi: 10.1111/j.1365-2958.2009.06713.x) (PMID:19400804)

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Abstract

Phosphatidylethanolamine (PE) and phosphatidylcholine (PC) are the two major constituents of eukaryotic cell membranes. In the protist Trypanosoma brucei, PE and PC are synthesized exclusively via the Kennedy pathway. To determine which organelles or processes are most sensitive to a disruption of normal phospholipid levels, the cellular consequences of a decrease in the levels of PE or PC, respectively, were studied following RNAi knock‐down of four enzymes of the Kennedy pathway. RNAi against ethanolamine‐phosphate cytidylyltransferase (ET) disrupted mitochondrial morphology and ultrastructure. Electron microscopy revealed alterations of inner mitochondrial membrane morphology, defined by a loss of disk‐like cristae. Despite the structural changes in the mitochondrion, the cells maintained oxidative phosphorylation. Our results indicate that the inner membrane morphology of T. brucei procyclic forms is highly sensitive to a decrease of PE levels, as a change in the ultrastructure of the mitochondrion is the earliest phenotype observed after RNAi knock‐down of ET. Interference with phospholipid synthesis also impaired normal cell‐cycle progression. ET RNAi led to an accumulation of multinucleate cells. In contrast, RNAi against choline‐/ethanolamine phosphotransferase, which affected PC as well as PE levels, caused a cell division phenotype characterized by non‐division of the nucleus and production of zoids.

Item Type:Articles
Additional Information:The work was supported by Swiss National Science Foundation Grant 3100A0‐116627 to P.B. and The Wellcome Trust and EP Abraham Trust.
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Gluenz, Dr Eva
Authors: Signorell, A., Gluenz, E., Rettig, J., Schneider, A., Shaw, M. K., Gull, K., and Bütikofer, P.
College/School:College of Medical Veterinary and Life Sciences > Institute of Infection Immunity and Inflammation
Journal Name:Molecular Microbiology
Publisher:Wiley
ISSN:0950-382X
ISSN (Online):1365-2958
Published Online:28 April 2009

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