Caenorhabditis elegans in the study of SMN-interacting proteins: A role for SMI-1, an orthologue of human Gemin2 and the identification of novel components of the SMN complex

Emma C. Burt, Paula R. Towers, David B. Sattelle

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Spinal muscular atrophy is a common neuromuscular disorder caused by mutations in the survival motor neuron (SMN) gene. In mammals, SMN is tightly associated with Gemin2. To gain further insight into the functions of SMN and Gemin2, we have cloned and sequenced smi-1 (Survival of Motor neuron-Interacting protein 1), a C. elegans homologue of the human Gemin2 gene. We show that the SMI-1 expression pattern and RNA interference phenotype show considerable overlap with that previously reported for SMN-1. Finally, we demonstrate that the SMN-1 and SMI-1 proteins directly interact. Having demonstrated the utility of the C. elegans genetic model for investigating genes encoding SMN-interacting proteins, we have undertaken a yeast two-hybrid screen of a C. elegans cDNA library to identify novel proteins that interact with SMN-1. We show the direct interaction of SMN-1 with nine novel proteins, several of which may be involved in RNA metabolism. © 2006 Springer-Verlag.
    Original languageEnglish
    Pages (from-to)145-159
    Number of pages14
    JournalInvertebrate Neuroscience
    Volume6
    Issue number4
    DOIs
    Publication statusPublished - Dec 2006

    Keywords

    • C. elegans
    • RNA interference
    • smi-1 gene
    • SMN-interacting proteins
    • Spinal muscular atrophy
    • Yeast two-hybrid assay

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