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Baculoviral IAP repeat proteins (BIRPs) may affect cell death, cell division, and tumorigenesis. The C. elegans BIRP BIR-1 was localized to chromosomes and to the spindle midzone. Embryos and fertilized oocytes lacking BIR-1 had defects in chromosome behavior, spindle midzone formation, and cytokinesis. We observed indistinguishable defects in fertilized oocytes and embryos lacking the Aurora-like kinase AIR-2. AIR-2 was not present on chromosomes in the absence of BIR-1. Histone H3 phosphorylation and HCP-1 staining, which marks kinetochores, were reduced in the absence of either BIR-1 or AIR-2. We propose that BIR-1 localizes AIR-2 to chromosomes and perhaps to the spindle midzone, where AIR-2 phosphorylates proteins that affect chromosome behavior and spindle midzone organization. The human BIRP survivin, which is upregulated in tumors, could partially substitute for BIR-1 in C. elegans. Deregulation of bir-1 promotes changes in ploidy, suggesting that similar deregulation of mammalian BIRPs may contribute to tumorigenesis.

Type

Journal article

Publication Date

08/2000

Volume

6

Pages

211 - 223

Keywords

Animals, Aurora Kinase B, Aurora Kinases, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Cell Cycle, Cell Division, Chromosome Mapping, Chromosomes, Embryo, Nonmammalian, Female, Genes, Helminth, Helminth Proteins, Humans, Inhibitor of Apoptosis Proteins, Male, Microtubule-Associated Proteins, Molecular Sequence Data, Neoplasm Proteins, Oocytes, Protein-Serine-Threonine Kinases, Proteins, Spermatozoa, Spindle Apparatus