Oxidative stress protection of Trypanosomes requires selenophosphate synthase

• Published in: Molecular and biochemical parasitology 2011-11, Vol.180 (1), p.47-50
• Main Authors: Costa, F.C., Oliva, M.A.V., de Jesus, T.C.L., Schenkman, S., Thiemann, O.H.
• Format: Article
• Language: English
• Subjects: bacteria; cell death; eukaryotic cells; Oxidation-Reduction; Oxidative Stress; parasites; parasitology; phenotype; Phosphotransferases - genetics; Phosphotransferases - metabolism; Protozoan Proteins - genetics; Protozoan Proteins - metabolism; RNA interference; Selenium - metabolism; Selenocysteine; Selenophosphate synthetase; selenoproteins; stop codon; Trypanosoma; Trypanosoma brucei; Trypanosoma brucei brucei - enzymology; Trypanosoma brucei brucei - genetics; Trypanosoma brucei brucei - metabolism
• ISSN: 0166-6851; 1872-9428
• DOI: 10.1016/j.molbiopara.2011.04.007

RNA interference of the selenophosphate synthetase (SPS2) mRNA from Trypanosoma brucei reveals that the selenocysteine synthesis pathway is essential for the parasite survival to oxidative stress. [Display omitted] ► The selenocysteine synthesis pathway confers oxidative protection to Trypanosoma brucei cells. ► Knockdown of T. brucei SPS2 by RNA interference result in cell death. ► T. brucei SPS2 knockdown cells present an apoptotic phenotype. Selenoproteins are characterized by the incorporation of at least one amino acid selenocysteine (Sec-U) encoded by in-frame UGA stop codons. These proteins, as well as the components of the Sec synthesis pathway, are present in members of the bacteria, archaea and eukaryote domains. Although not a ubiquitous pathway in all organisms, it was also identified in several protozoa, including the Kinetoplastida. Genetic evidence has indicated that the pathway is non-essential to the survival of Trypanosoma growing in non-stressed conditions. By analyzing the effects of RNA interference of the Trypanosoma brucei selenophosphate synthetase SPS2, we found a requirement under sub-optimal growth conditions. The present work shows that SPS2 is involved in oxidative stress protection of the parasite and its absence severely hampers the parasite survival in the presence of an oxidizing environment that results in an apoptotic-like phenotype and cell death.