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Published May 2015 | Published + Supplemental Material
Journal Article Open

Flatworms have lost the right open reading frame kinase 3 gene during evolution


All multicellular organisms studied to date have three right open reading frame kinase genes (designated riok-1, riok-2 and riok-3). Current evidence indicates that riok-1 and riok-2 have essential roles in ribosome biosynthesis, and that the riok-3 gene assists this process. In the present study, we conducted a detailed bioinformatic analysis of the riok gene family in 25 parasitic flatworms (platyhelminths) for which extensive genomic and transcriptomic data sets are available. We found that none of the flatworms studied have a riok-3 gene, which is unprecedented for multicellular organisms. We propose that, unlike in other eukaryotes, the loss of RIOK-3 from flatworms does not result in an evolutionary disadvantage due to the unique biology and physiology of this phylum. We show that the loss of RIOK-3 coincides with a loss of particular proteins associated with essential cellular pathways linked to cell growth and apoptosis. These findings indicate multiple, key regulatory functions of RIOK-3 in other metazoan species. Taking advantage of a known partial crystal structure of human RIOK-1, molecular modelling revealed variability in nucleotide binding sites between flatworm and human RIOK proteins.

Additional Information

© 2015 The Authors. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ Received 28 November 2014; Accepted 26 February 2015; Published 15 May 2015. This project was funded by the National Health and Medical Research Council (NHMRC) of Australia and the Australian Research Council (ARC). This project was also supported by a Victorian Life Sciences Computation Initiative (VLSCI) grant number VR0007 on its Peak Computing Facility at the University of Melbourne, an initiative of the Victorian Government. Other support from the Australian Academy of Science, the Australian-American Fulbright Commission, Alexander von Humboldt Foundation, Melbourne Water Corporation (R.B.G.) is gratefully acknowledged, as is funding from the Howard Hughes Medical Institute (HHMI) and National Institutes of Health (NIH) (P.W.S.). N.D.Y. is an NHMRC Early Career Research (ECR) Fellow. We acknowledge the staff at WormBase (www.wormbase.org) and Wellcome Trust Sanger Institute (http://www.ebi.ac.uk/ena/data/view/PRJEB2709) for their support or provision of data. We acknowledge the use of the program I-TASSER – © 2013 The Regents of the University of Michigan.

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