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Characterization of putative mitochondrial processing peptidase α‐subunit in Trypanosoma brucei
Author(s) -
Mak Ivy Lynn,
Lu Zhiquan,
Mehta Vaibhav N,
Salavati Reza
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.987.1
Subject(s) - trypanosoma brucei , protein subunit , mitochondrion , biology , rna editing , rna interference , rna , biochemistry , nadh dehydrogenase , gene , microbiology and biotechnology
Trypanosoma brucei , the causative agent of African sleeping sickness, contains a single mitochondrion which imports proteins responsible for RNA editing process. Using RNA interference (RNAi), this study aims to characterize the gene Tb 11.02.1480, annotated as mitochondrial processing peptidase α‐subunit (MPP‐α) that is believed to cleave mitochondrial import signal to aid protein maturation. Severe growth inhibition resulted from RNAi. Analysis of transcript level by RT‐PCR showed a 2–8 fold accumulation in pre‐edited mRNAs that encode electron transport chain components apocytochrome b, ATP synthase subunit 6 and NADH‐ubiquinone oxidoreductase subunit 3 (ND3), along with relatively unchanged levels of never‐edited mRNAs ND4 and cytochrome oxidase 1. Mitochondrial extract prepared from glycerol gradient fractionation suggest disruption of editosome integrity, although maturation of editosome subunit KREL1 was unaffected. These observations suggest that the proposed MPP‐α in T brucei might not be involved in protein import as reported in other species; but impaired RNA editing activity suggest this protein contributes to editosome stability. This was supported by computational analysis where this protein appears to interact with editosome accessory proteins MRP. Ongoing work on identification of protein interacting partners would allow further elucidation of gene function.