African sleeping sickness is a vector-borne devastating disease caused by the parasitic protozoan Trypanosoma brucei. Sleeping sickness threatens over 60 million people in 36 countries of sub-Saharan Africa. Over 70,000 deaths every year are a result of sleeping sickness and the disease is always fatal unless treated. Of great importance is the fact that, as opposed to other parasitic organisms, trypanosomes synthesize phospholipids de novo. This makes the trypanosome phospholipids biosynthesis machinery a very attractive target for new drug design. We recently identified TbLpn, a protein homologous to yeast and human lipin, a phosphatidate phosphatase involved in membrane biogenesis, energy metabolism, and adipose tissue development. In yeast and mammals, lipin catalyzes the dephosphorylation of phosphatidic acid (PA) to diacylglycerol (DAG) which, in turn, is used for the synthesis of phospholipids. We have recently shown that, as predicted by the presence of conserved domains, TbLpn displays phosphatidic acid phosphatase activity in vitro, and that the two conserved aspartic acid residues present in the C-LIP domain, are essential for enzymatic activity. The aim of this work is to observe the effect of TbLpn down-regulation by RNA interference on cellular growth and morphology in T. brucei. Preliminary data suggests that, although TbLpn is not essential for growth, its expression is necessary for cell morphology.
|Presenter:||Elizabeth Snyder (Graduate Student)|
|Time:||9:30 am (Session I)
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