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Functions and cellular localization of cysteine desulfurase and selenocysteine lyase in Trypanosoma brucei

SYSNO ASEP	0342953
Document Type	J - Journal Article
R&D Document Type	Journal Article
Subsidiary J	Článek ve WOS
Title	Functions and cellular localization of cysteine desulfurase and selenocysteine lyase in Trypanosoma brucei
Author(s)	Poliak, Pavel (BC-A) Van Hoewyk, D. (US) Oborník, Miroslav (BC-A)_{RID, ORCID} Zíková, Alena (BC-A)_{RID, ORCID} Stuart, K. D. (US) Tachezy, J. (CZ) Pilon, M. (US) Lukeš, Julius (BC-A)_{RID, ORCID}
Source Title	FEBS Journal - ISSN 1742-464X Roč. 277, č. 2 (2010), s. 383-393
Number of pages	11 s.
Language	eng - English
Country	GB - United Kingdom
Keywords	Fe–S cluster ; mitochondrion ; RNAi ; selenoprotein ; Trypanosoma
Subject RIV	EB - Genetics ; Molecular Biology
R&D Projects	GA204/09/1667 GA ČR - Czech Science Foundation (CSF)
CEZ	AV0Z60220518 - PAU-O, BC-A (2005-2011)
UT WOS	000273396000013
DOI	10.1111/j.1742-4658.2009.07489.x
Annotation	It was shown previously that the Nfs-like protein called Nfs from the parasitic protist Trypanosoma brucei is a genuine CysD. A second Nfs-like protein is encoded in the nuclear genome of T. brucei. We called this protein selenocysteine lyase (SCL) because phylogenetic analysis reveals that it is monophyletic with known eukaryotic selenocysteine lyases. The Nfs protein is located in the mitochondrion, whereas the SCL protein seems to be present in the nucleus and cytoplasm. Unexpectedly, downregulation of either Nfs or SCL protein leads to a dramatic decrease in both CysD and selenocysteine lyase activities concurrently in the mitochondrion and the cytosolic fractions. Because loss of Nfs causes a growth phenotype but loss of SCL does not, we propose that Nfs can fully complement SCL, whereas SCL can only partially replace Nfs under our growth conditions.
Workplace	Biology Centre (since 2006)
Contact	Dana Hypšová, eje@eje.cz, Tel.: 387 775 214
Year of Publishing	2011

Number of the records: 1